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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 56:B108-B115 (2001)
© 2001 The Gerontological Society of America

Effects of Food Restriction on Systolic Mechanical Behavior of the Ventricular Pump in Middle-aged and Senescent Rats

Kuo-Chu Changa, Ying-I Penga, Fong-Chu Leea and Yung-Zu Tsengb

a Departments of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan
b Departments of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan

Kuo-Chu Chang, Department of Physiology, College of Medicine, National Taiwan University, No. 1, Sec. 1, Jen-Ai Rd., Taipei, Taiwan E-mail: kcchang{at}ha.mc.ntu.edu.tw.

Decision Editor: John A. Faulkner, PhD


   Abstract
Top
 Abstract
Materials and Methods
 Results
 Discussion
 References
 
Previous work from our laboratory has revealed that the intrinsic contractility of the left ventricle is depressed in rats at 24 months, and the ventricular internal resistance shows declines with age. The aim of this study was to determine whether food restriction (FR) delays the development of age-related changes in left ventricular (LV) contractility and internal resistance. Male Fischer 344 rats that began FR at the ages of 12 and 18 months were fed on alternate days for 6 months and compared with age-matched ad libitum (AL)-fed rats. Rats studied at the ages of 18 and 24 months were referred to as middle-aged and senescent rats, respectively, and were anesthetized and thoracotomized. We measured LV pressure and ascending aortic flow waves by using a high-fidelity pressure sensor and an electromagnetic flow probe, respectively. The elastance–resistance model was used to generate Emax and Qmax to describe the physical properties of the left ventricle; Emax is the maximal systolic elastance to represent the myocardial contractility; Qmax is the theoretical maximal flow to be inversely related to the LV internal resistance. Neither age nor diet affected basal heart rate, LV end-systolic pressure, or cardiac output. Emax normalized to LV weight (Emaxn) exhibited a decline from 941.9 ± 62.7 mmHg/ml-g to 690.2 ± 57.5 mmHg/ml-g with age in AL-fed rats but not FR rats. Qmax showed an increase with age from 36.55 ± 2.78 ml/s to 44.22 ± 2.62 ml/s in AL-fed rats or from 36.01 ± 2.09 ml/s to 43.52 ± 2.74 ml/s in FR rats. There was no effect of diet on Qmax. In conclusion, FR prevents or delays the reduction in myocardial contractility that occurred between 18 and 24 months of age in AL rats. However, FR does not affect the age-related changes in ventricular internal resistance.

FOOD restriction (FR) not only increases the life span of rodents (1)(2), but also reduces the incidence of a broad spectrum of age-related pathologies, including cardiovascular diseases (3)(4)(5). There is evidence suggesting that FR may have the potential to maintain the cardiac neurotransmitter content and reuptake (6) and to alter the cellular calcium handling process (7). FR may increase the inotropic and chronotropic responsiveness of the isolated working heart preparation to ß–adrenergic agnoists (7)(8). However, not all changes induced by FR retard the aging phenotypes. Both short- (9)(10) and long-term (11)(12) FR induce a shift in the myosin isoenzyme profile from the fast V1 isoform toward the slow V3 isoform, a shift that accentuates rather than retards the age-related changes.

The elastance–resistance model can be used to quantify the physical properties of the left ventricle, when the specific contractile proteins and the calcium metabolism have been changed (13)(14). This model to characterize the cardiac mechanics generates both Emax and Qmax; Emax is the maximal systolic elastance; Qmax is the theoretical maximal flow. Emax is considered the elasticity most sensitive to changes in contractile state and independent of preload, afterload, and heart rate in a given contractile state of the heart (15)(16)(17). These support the view that Emax serves in a given heart to quantify the intrinsic contractility of the left ventricle. The quantity in Qmax is the amount of outflow generated by the ventricle if it were to eject under zero load condition and is inversely related to the ventricular internal resistance (13)(18). An inverse relation between Qmax and percent slow myosin has been observed, suggesting that isomyosin composition is one of the determinants of ventricular resistive behavior (18). It is clear that the systolic elastance and resistance can describe two independent facets of the left ventricle as a mechanical pump (13).

Previous work from our laboratory has revealed that the intrinsic contractility of the left ventricle is depressed in rats at 24 months, and the ventricular internal resistance shows declines with age (14). The aim of the present study was to determine whether FR delays the development of age-related changes in left ventricular (LV) contractility and internal resistance in male Fischer 344 rats. Those two parameters that describe the cardiac mechanics were obtained by the use of fitting the elastance–resistance model. Although others have shown the reduced myocardial contractility with age (19) and the altered myocardial mechanics by FR (7), the novel aspect of this study is that the elastance–resistance model can describe the two independent facets of the left ventricle, affected by age and diet.


   Materials and Methods
Top
 Abstract
 Materials and Methods
Results
 Discussion
 References
 
Experimental Preparations
The specific pathogen-free male Fischer 344 rats used in this study were obtained from the colony maintained in the barrier facilities at the Animal Center of Medical College, National Taiwan University. Rats aged 18 and 24 months were individually referred to as middle-aged and senescent rats. The middle-aged (n = 9) and senescent (n = 9) ad libitum-fed groups were allowed free access to the Purina chow and water and housed two to three per cage in a 12-h light/dark cycle animal room. Periodic checks of the cages and body weights ensured that the food was administered properly. Rats that started FR at the ages of 12 and 18 months were fed on alternate days until middle age (n = 9) and senescence (n = 9), respectively. Animals at the ages of 18 and 24 months were anesthetized and thoracotomized for the study of changes in cardiac systolic mechanics caused by FR. The animal experiments were conducted according to the Guide for the Care and Use of Laboratory Animals of the American National Council and approved by the Animal Care and Use Committee of the National Taiwan University.

Measurements of Hemodynamic Data
Each rat was anesthetized with sodium pentobarbital (35 mg/kg, i.p.). The femoral vein was cannulated for the administration of supplemental pentobarbital (30 mg/kg every 2 h). We monitored animal's rectal temperature and used a heater to maintain the rat's body temperature. Tracheotomy was performed to provide artificial ventilation with a tidal volume of 5–6 ml/kg and respiratory rate of 50–70 breaths/min. The chest was opened through the right second intercostal space. An electromagnetic flow probe (model 100 series, internal circumference 8–10 mm, Carolina Medical Electronics, King, NC) was positioned around the ascending aorta to measure the pulsatile aortic flow. A Millar catheter with a high-fidelity pressure sensor (model SPC 320, size 2F, Millar Instruments, Houston, TX) was used to measure the pulsatile LV pressure. Before inserting the catheter, the pressure sensor was prewarmed in 37°C saline for at least 1 h. The catheter was inserted via the isolated right carotid artery into the left ventricle. After withdrawing the catheter from each rat, the technician reimmersed the catheter in the bath to check for baseline drift. At the end of the experiment, the pressure reading from the sensor submerged in the saline of less than 10 mm in depth was used as the zero pressure reference. The electrocardiogram (ECG) of lead II was recorded with a Gould ECG/Biotach amplifier (Gould Electronics, Cleveland, OH).

The analogue waveforms were sampled at 500 Hz using a 12-bit simultaneously sampling analog-to-digital (A/D) converter interfaced to a personal computer. Selection of signals of 5–10 beats at steady state was made on the basis of the following criteria: (i) recorded beats with optimal velocity profile that is characterized by a steady diastolic level, maximal systolic amplitude, and minimal late systolic negative flow; (ii) beats with a cardiac cycle length less than 5% different from the average value for all recorded beats; (iii) exclusion of ectopic and postectopic beats. The selected beats were averaged in the time domain, using the peak R wave of ECG as a fiducial point. The resulting LV pressure and ascending aortic flow signals were subjected to further analysis using the procedure previously described (20)(21). First, the isovolumic pressure curve is obtained from the instantaneous pressure of an ejecting contraction by a curve-fitting technique. Next, the elastance–resistance model with the estimated isovolumic pressure is applied to measure the systolic mechanical properties of the ventricular pump.

Estimation of the Isovolumic Pressure From an Ejecting Contraction
To estimate the isovolumic pressure curve Piso(t) from an ejecting beat, a nonlinear least-squares approximation technique derived by Sunagawa and colleagues (22) is used:

(1)
where Pidmax is an estimated peak developed isovolumic pressure, {omega} is an angular frequency, c is a phase shift angle of the sinusoidal curve, and Pd is the LV end-diastolic pressure. The parameter Pisomax is the estimated peak isovolumic pressure that is the sum of Pidmax and Pd. Piso(t) is obtained by fitting the measured LV pressure curve segments from the end-diastolic pressure point to the peak positive dP/dt and from the pressure point of the peak negative dP/dt to the same level as the end-diastolic pressure of the preceding beat (23). The peak of the ECG R wave is used to identify the LV end-diastolic point.

Prediction of the LV Pressure Using an Elastance–Resistance Model
Model-derived pressure of the left ventricle P(t) can be calculated by using the elastance–resistance model if the model parameters are previously identified (13)(24). The relationship between instantaneous LV pressure, flow, and isovolumic pressure can be written as follows:

(2)
where Vej(t) is instantaneously ejected volume computed by numerically calculating the running integral of the aortic flow signal Q(t); Veed is an effective end-diastolic volume that is the difference between LV end-diastolic volume (Ved) and the zero-pressure volume axis intercept (V0); Qmax is the theoretical maximum flow (i.e., the amount of outflow generated by the ventricle if it were to eject under zero load condition). Piso(t) is the isovolumic pressure obtained by occluding the ascending aorta near the sinuses of Valsalva at the end of diastole. Herein, Piso(t) is replaced with Piso(t) that is derived from the measured pressure of an ejecting contraction by making use of 1.

Both Veed and Qmax are the model parameters that remain to be determined by curve-fitting techniques. Campbell and colleagues (24) found that 2 can be used to fit the measured LV pressure of an ejecting beat very well, if the fitting interval is tej < t < tpisomax, where tej is the onset of ventricular ejection and tpisomax is the time of peak isovolumic pressure. The normalized root-mean-square ep is 3

(3)
where P(i) and P(i) are the sampled values of observed and model-calculated pressure of the left ventricle, respectively (24). Initial values of Veed and Qmax are chosen first. The Nelder-Meade simplex algorithm (25) is then used in a nonlinear least-squares parameter-estimation procedure to iteratively adjust Veed and Qmax to minimize the normalized root-mean-square value. The parameters coincident with the minimum objective function are taken as the model estimates of the systolic pumping mechanics of the left ventricle. The LV systolic elastance E(t) can be calculated by the formulation of E(t) = Piso(t)/Veed. The maximal systolic elastance Emax is, therefore, quantified in terms of its maximal value, Emax = Pisomax/Veed and the internal resistance R in terms of the theoretical maximal flow Qmax, R(Piso) = Piso(t)/Qmax.

Fitness of the data generated by the model is judged by the magnitude of ep and by indices from a linear regression of the model-generated pressure P(i) on the measured pressure P(i). Two indices are used to evaluate the goodness-of-fit: (i) the coefficient of determination, r2, and (ii) the standard error of the estimate, SEE. We look for r2 to be close to 1 and for SEE to be on the order of less than 5% when expressed relative to the mean of pressure observations confined to the fitting interval (26).

Effective Arterial Volume Elastance as Arterial Chamber Property
The effective arterial volume elastance (Ea) could be calculated by the procedure previously described (14). In brief, the peak isovolumic pressure of the left ventricle at the end-diastolic volume is estimated by 1. The pressure-ejected volume loop can be obtained by the time integration of aortic flow and the measured LV pressure. Drawing a tangential line from the estimated peak isovolumic pressure to the right corner of the pressure-ejected volume loop yields a point referred to as the end-systolic equilibrium point (27). The pressure of the left ventricle at this end-systolic equilibrium point is the LV end-systolic pressure. Therefore, the slope of the end-systolic pressure versus stroke volume relation represents the effective arterial volume elastance.

Statistics
Results are expressed as means ± SE. Because cardiac output is significantly related to body shape, this variable was normalized to body weight when comparison was made between ad libitum (AL)-fed and food-restricted rats. We also normalized Emax for LV muscle mass, i.e., Emax n = Emax/LV weight, due to alteration in LV mass by age and diet. A two-way analysis of variance (ANOVA) was employed to determine the effects of FR on cardiac mechanics in middle-aged and senescent rats. Simple effects analysis was used when significant interaction between diet and age occurred. Significant differences were assumed at the level of p < .05.


   Results
Top
 Abstract
 Materials and Methods
 Results
Discussion
 References
 
The effects of age and diet on body weight and left ventricular weight, as well as basic hemodynamic data, are shown in Table 1 . Body and heart weights were significantly lowered by FR at both ages, but unaffected by age. No interaction between the effects of age and diet on body and heart weights was detected. Neither age nor diet affected basal heart rate (HR), nor was there an Age x Diet interaction for HR. Although there was a trend toward decreasing HR by age and diet, no significant differences were observed.


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  		Table 1. Effects of Diet and Age on Basic Hemodynamic Data Measured and Calculated in Middle-aged and Senescent Ad Libitum (AL) and Food Restricted (FR) Rats

 
Neither age nor diet affected LV end-systolic pressure (Pes) as well as cardiac output (CO). As for the chamber property of the arterial system, the effective arterial volume elastance Ea was unaffected by either diet or age. Although there was a trend toward decreasing Ea by age and diet, the differences were not significant. No interaction between the effects of age and diet on Pes, CO, and Ea was detected.

The results of fitting the elastance–resistance model to LV pressure showed little distinction between the model-generated and measured signals. The averaged values for ep as an indication of the quality of fit was 0.0049 ± 0.0004, for r2 was 0.9844 ± 0.0017, and for SEE was 2.69 ± 0.20%. These data suggest that the elastance–resistance model may generate Emax and Qmax with good quality to describe the systolic mechanical behavior of the ventricular pump.

Fig. 1Fig. 2Fig. 3 show the effects of age and diet on cardiac mechanics in terms of the maximal systolic elastance, Emax, and the theoretical maximal flow, Qmax. Neither age nor diet affected the estimated peak isovolumic pressure, Pisomax, nor was there an Age x Diet interaction for Pisomax (upper panel, Fig. 1). A significant interaction between the effects of age and diet in their effects on the effective LV end-diastolic volume, Veed, was detected (lower panel, Fig. 1). While producing a rise in Veed in middle-aged rats, FR exhibited a decline in Veed in senescent rats. Moreover, Veed increased with advancing age in AL-fed rats but not FR rats.



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  		Figure 1. Upper: Effects of age and diet on Pisomax estimated by 1. Neither age nor diet affected Pisomax, nor was there an Age x Diet interaction for Pisomax. Lower: Effects of age and diet on Veed estimated by 2. There was a significant interaction between the effects of age and diet in their effects on Veed. While producing a rise in Veed in middle-aged rats, FR exhibited a decline in Veed in senescent rats. Moreover, Veed increased with advancing age in ad libitum-fed rats but not food-restricted rats. Pisomax, estimated peak isovolumic pressure of the left ventricle; Veed, effective LV end-diastolic volume; A, ad libitum; R, food restriction.

 


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  		Figure 2. Upper: Effects of age and diet on Emax computed by Pisomax/Veed. There was a significant interaction between the effects of age and diet in their effects on Emax. The significant interaction showed that FR significantly diminished Emax in middle-aged rats but not senescent rats. On the contrary, age significantly reduced Emax in ad libitum-fed rats but not food-restricted rats. Bottom: Effects of age and diet on Emaxn computed by Emax/LV weight. Both age and diet affected Emaxn, and there was an Age x Diet interaction for Emaxn. Emaxn exhibited a decline with age in ad libitum-fed rats but not food-restricted rats, as did Emax. Unlike Emax, Emaxn showed a significant rise by food restriction in senescent rats but not middle-aged rats. Emax, the maximal systolic elastance of the left ventricle; Emaxn, Emax normalized to left ventricle weight; A, ad libitum; R, food restriction.

 


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  		Figure 3. Effects of age and diet on Qmax estimated by 2. No interaction between the effects of age and diet in their effects on Qmax was detected. Age but not diet affected Qmax, causing an increase in Qmax and then a fall in LV internal resistance. Qmax, the theoretical maximal flow of the left ventricle; A, ad libitum; R, food restriction.

 
There was a significant interaction between the effects of age and diet in their effects on Emax (upper panel, Fig. 2). The interaction showed that FR significantly diminished Emax in middle-aged rats but not senescent rats. On the contrary, age significantly reduced Emax in AL-fed rats but not FR rats. When normalized to left ventricle weight, the LV maximal systolic elastance (Emaxn) was affected by both age and diet, and there was an Age x Diet interaction for Emaxn (lower panel, Fig. 2). Emaxn exhibited a decline from 941.9 ± 62.7 mmHg/ml-g to 690.2 ± 57.5 mmHg/ml-g with age in AL-fed rats but not FR rats, as did Emax. Unlike Emax, Emaxn showed a significant rise by FR from 690.2 ± 57.5 mmHg/ml-g to 944.4 ± 36.9 mmHg/ml-g in senescent rats but not middle-aged rats. On the other hand, no interaction between the effects of age and diet in their effects on Qmax was detected. Age but not diet affected Qmax, causing an increase in Qmax from 36.55 ± 2.78 ml/s to 44.22 ± 2.62 ml/s in AL-fed rats or from 36.01 ± 2.09 ml/s to 43.52 ± 2.74 ml/s in FR rats (Fig. 3). An age-related increase in Qmax suggests that the ventricular internal resistance tends to be significantly lower for senescent rats.


   Discussion
Top
 Abstract
 Materials and Methods
 Results
 Discussion
References
 
A previous study from our laboratory demonstrated that the intrinsic contractility of the left ventricle is depressed in rats at 24 months, and the ventricular internal resistance shows declines with age (14). The most striking findings of this study are that FR prevents the reduction in ventricular contractility that occurred between 18 and 24 months of age in AL-fed rats. By contrast, FR does not affect the age-related changes in ventricular resistance.

As mentioned earlier, the maximal systolic elastance, Emax, is determined by the ratio of Pisomax to Veed. Neither age nor diet affected Pisomax, nor was there an interaction by Age x Diet for Pisomax. As a result, Veed is the predominant factor responsible for the value of Emax. An age-related increase in Veed occurs in AL-fed rats (lower panel, Fig. 1), giving rise to the decline with advancing age in Emax (upper panel, Fig. 2). The finding that this age-related increase in Veed is alleviated by FR in this study is important. FR results in a fall in Veed in senescent rats, showing a little but not a significant rise in Emax. By contrast, FR produces an increase in Veed in middle-aged rats, exhibiting the Emax similar to that as seen in senescent rats with food restriction. These data suggest that there is no age-related change in the elastic chamber property of the left ventricle in FR rats. To account for differences in LV muscle mass by age and diet (Table 1 ), Emax is normalized by dividing with LV weight (i.e., Emaxn = Emax/LV weight) (13). In this study, we compare Emaxn among the four groups to determine how great the effects of FR are on delaying the development of changes in LV intrinsic contractility with age.

The properties of the contractile unit along with the activation process (i.e., availability of Ca2+) may profoundly determine the intrinsic contractility of the myocardium (13)(16). There is evidence suggesting that the abnormalities in contractile proteins and calcium metabolism occur in an aging heart and contribute to the mechanical defects of the heart with age (8)(9). In this report, only in AL-fed rats, the intrinsic contractility of the heart is depressed in rats at 24 months, as evidenced by the reduction in Emaxn. This may be due to the abnormalities in calcium metabolism in rats with advancing age. Many reports in the literature have shown that there is an age-related decline in the responsiveness of the heart to ß–adrenergic stimulation (7)(8)(28). The implication of this phenomenon is the changes in the intracellular calcium handling with age (7)(8). Although the mechanism underlying the effect of diet on the ß–adrenergic system is not known, the age-related decline in cardiac ß–adrenergic responsiveness can be retarded by FR (7)(8). Therefore, we treat rats with FR for 6 months to establish whether the changes in cardiac contractility are preventable. FR, as manifested by the increase in Emaxn, delays the reduction in myocardial contractility that occurred between 18 and 24 months of age in AL-fed rats. As suggested by others (19)(29), FR may increase the availability of calcium ion to enhance the intrinsic contractility of the left ventricle in rats with age.

Of the biochemical changes in the contractile machinery, the most prominent event in the aging myocardium is the shift of the myosin isoenzyme profile from the fast V1 isoform toward the slow V3 isoform (30)(31). It has been suggested that there is an inverse relation between Qmax and percent slow myosin composition (18). The quantity in Qmax is inversely influenced by Ea, suggesting that Ea is also one of the determinants of ventricular resistive behavior (14)(21). Our previous work has suggested that the age-related decline in Ea, but not the shift of myosin isoenzyme profile, may be the predominant factor responsible for the increased Qmax with age (14). Much evidence has shown that FR accentuated rather than retarded the age-related shift in myosin isoenzyme profile from the V1 toward the V3 isoform (9)(10)(12). One would expect that this isoenzyme shift by FR might cause a fall in Qmax and then a rise in ventricular internal resistance. By contrast, the trend in diminishing Ea by FR was supposed to contribute to an increase in Qmax. Herein, Qmax is unaffected by diet, suggesting that FR may have no impact on the age-related changes in ventricular internal resistance. It is possible that the effects of FR on myosin isoenzyme profile and arterial chamber properties counterbalance each other to cause no alterations in Qmax at both ages.

When considering the integrated cardiovascular function, one requires not only information about cardiac mechanics but also knowledge of vascular dynamics. In this study, we are treating the arterial system like an elastic chamber with Ea, just as we treat the ventricle like an elastic chamber with Emax. Thus, the ventricular performance can be determined by the chamber properties of both the ventricle and the vasculature, when the ventricle is coupled to its arterial load (32). As mentioned earlier, FR prevents the reduction in myocardial contractility that occurred between 18 and 24 months of age in AL-fed rats. However, FR does not affect the age-related changes in ventricular internal resistance. Moreover, neither HR nor Ea is affected by diet at both ages. These data suggest that FR may reserve the ventricular function in an aging heart, maintaining normal blood flow essential for the metabolic needs of tissues and/or organs.

Some limitations of the current study deserve consideration. First of all, the isovolumic beats were not obtained by occluding the ascending aorta at the end of diastole; instead, the isovolumic pressure was estimated by the use of curve fitting of the ejecting beat. With a shorter cardiac cycle length, the estimated isovolumic beat was shown to have the Pisomax quite close to the Pisomax actually measured by occluding the ascending aorta in diastole (22). The advantage of this single-beat estimation technique is that the integrated nature of the cardiodynamics can be measured without occluding the ascending aorta at the end of diastole.

Second, Emax, rather than other indices such as the maximal first derivative of LV pressure with respect to time, was used to quantify the intrinsic contractility of the left ventricle in this study. The ideal index of contractility is: (a) sensitive to alteration in inotropic state, (b) insensitive to changes in preload and afterload, (c) independent of heart rate, and (d) independent of cardiac size (15). Much evidence has shown that Emax is independent of preload, afterload, and heart rate in a given contractile state of the heart (15)(16)(17). Hunter and colleagues (16) demonstrated that Emax is considered the elasticity most sensitive to changes in contractile state, though it is not so sensitive as the pressure–volume ratio derived by Suga and colleagues (17). Thus, Emax may be used as a measure of LV intrinsic contractility in terms of the sensitivity and the specificity.

Third, the elastance–resistance model does not perfectly describe the pumping mechanical behavior of the left ventricle. Hunter and colleagues (16)(33), using the flow–pulse response technique, demonstrated that, besides elastance and resistance, there are at least two or more processes, such as the volume influence factor and deactivation factor, involved in the description of the mechanical properties of the ventricular pump. Moreover, Campbell and colleagues (34) found that the elastance–resistance model failed to describe the instantaneous LV pumping behavior, especially during the late ejection period and from the predictive point of view. However, in an earlier article (24), they showed that the elastance–resistance model could be used to fit the measured LV pressure of an ejection beat very well, if the fitting interval was from the onset of ventricular ejection to the time of peak isovolumic pressure. Shroff and colleagues (13) believe that the elastance–resistance model is useful to quantify LV systolic mechanical properties, provided one clearly understands its limitations.

In summary, we determined the effects of FR on cardiac mechanics in middle-aged and senescent rats in terms of the systolic elastance and resistance. The most striking findings of this study are that FR prevents the reduction in myocardial contractility that occurred between 18 and 24 months of age in AL-fed rats. However, FR does not affect the age-related changes in ventricular internal resistance. FR may reserve the ventricular function in an aging heart, maintaining normal blood flow essential for the metabolic needs of tissues and/or organs.


   Acknowledgments
 
This study was supported by grants from the National Science Council of Taiwan (NSC 87-2314-B-002-274 and NSC 88-2314-B002-209).

Received March 30, 2000

Accepted September 14, 2000


   References
Top
 Abstract
 Materials and Methods
 Results
 Discussion
 References
 

  1. McCay CM, Cromwell MF, Maynard LA, 1935. The effect of retarded growth upon the length of life span and upon the ultimate body mass. J Nutr. 10:63-79.
  2. Masoro EJ, 1988. Minireview. Food restriction in rodents: an evaluation of its role in the study of aging. J Gerontol Biol Sci. 43:B59-B64.
  3. Weindruch R, Walford RL, 1988. The Retardation of Aging and Disease by Dietary Restriction Charles C Thomas, Springfield, IL.
  4. Yu BP, 1994. Modulation of Aging Processes by Dietary Restriction CRC, Boca Raton, FL.
  5. Chang KC, Chow CY, Peng YI, Chen TJ, Tsai YF, 1999. Effects of food restriction on mechanical properties of arterial system in adult and middle-aged rats. J Gerontol Biol Sci. 54A:B441-B447. [Abstract]
  6. Kim SW, Yu BP, Sanderford M, Herlihy JT, 1994. Dietary restriction modulates the norepinephrine content and uptake of the heart and cardiac synaptosomes. Proc Soc Exp Biol Med. 207:43-47. [Medline]
  7. Klebanov S, Herlihy JT, Freeman GL, 1997. Effect of long-term food restriction on cardiac mechanics. Am J Physiol. 273:H2333-H2342.
  8. Kelley GR, Herlihy JT, 1998. Food restriction alters the age-related decline in cardiac ß–adrenergic responsiveness. Mech Ageing Dev. 103:1-12. [Medline]
  9. Haddad F, Bodell PW, McCue SA, Herrick RE, Baldwin KM, 1993. Food restriction-induced transformations in cardiac functional and biochemical properties in rats. J Appl Physiol. 74:606-612. [Abstract/Free Full Text]
  10. Morris GS, Surdyka DG, Haddad F, Baldwin KM, 1990. Apparent influence of metabolism on cardiac isomyosin profile of food-restricted rats. Am J Physiol. 258:R346-R351. [Abstract/Free Full Text]
  11. Klebanov S, Kim IS, Herlihy JT, 1995Abstract 6(19).. Parallelism between the effects of food restriction on longevity and cardiac myosin isozyme profile. Gerontologist 35: (special issue I) 9
  12. Klebanov S, Herlihy JT, 1997. Effect of life-long food restriction on cardiac myosin composition. J Gerontol Biol Sci. 52A:B184-B189. [Abstract]
  13. Shroff SG, Janicki JS, Weber KT, 1992. Mechanical and energetic behavior of the intact left ventricle. Fozzard HA, , ed.The Heart and Cardiovascular System 2nd ed. 129-150. Raven, New York.
  14. Chang KC, Peng YI, Dai SH, Tseng YZ, 2000. Age-related changes in pumping mechanical behavior of the rat ventricle in terms of systolic elastance and resistance. J Gerontol Biol Sci. 55A:B440-B447. [Abstract/Free Full Text]
  15. Schertel ER, 1998. Assessment of left-ventricular function. Thorac Cardiovasc Surg. Suppl)46:248-254.
  16. Hunter WC, Janicki JS, Weber KT, Noordergraaf A, 1983. Systolic mechanical properties of the left ventricle: effects of volume and contractile state. Circ Res. 52:319-327. [Abstract/Free Full Text]
  17. Suga H, Sagawa K, Shoukas AA, 1973. Load independence of the instantaneous pressure-volume ratio of the canine left ventricle and effects of epinephrine and heart rate on the ratio. Circ Res. 32:314-322. [Abstract/Free Full Text]
  18. Shroff SG, Naegelen D, Clark WA, 1990. Relation between left ventricular systolic resistance and contractile rate processes. Am J Physiol. 258:H381-H394. [Abstract/Free Full Text]
  19. Lakatta EG, 1993. Cardiovascular regulatory mechanisms in advanced age. Physiol Rev. 73:413-467. [Free Full Text]
  20. Chang KC, Kuo TS, 1997. Single-beat estimation of the ventricular pumping mechanics in terms of the systolic elastance and resistance. J Theor Biol. 189:89-95. [Medline]
  21. Chang KC, 1998. Theoretical maximal flow of the left ventricle is sensitive to change in ventricular afterload. J Theor Biol. 194:409-417. [Medline]
  22. Sunagawa K, Yamada A, Senda Y, et al. 1980. Estimation of the hydromotive source pressure from ejection beats of the left ventricle. IEEE Trans Biomed Eng. 27:299-305. [Medline]
  23. Takeuchi M, Igarashi Y, Tomimoto S, et al. 1991. Single-beat estimation of the slope of the end-systolic pressure-volume relation in the human left ventricle. Circulation 83:202-212. [Abstract/Free Full Text]
  24. Campbell KB, Ringo JA, Knowlen GG, Kirkpatrick RD, Schmidt SL, 1986. Validation of optimal elastance–resistance left ventricle pump models. Am J Physiol. 251:H382-H397.
  25. Dennis JE, Woods DJ, 1987. New computing environments. Wouk A, , ed.Microcomputers in Large-Scale Computing 116-122. SIAM, Philadelphia, PA.
  26. Draper NR, Smith H, 1981:417. Applied Regression Analysis 2nd ed. John Wiley & Sons, New York.
  27. Barnea O, Jaron D, 1990. A new method for the estimation of the left ventricular pressure-volume area. IEEE Trans Biomed Eng. 37:109-111. [Medline]
  28. Xiao RP, Lakatta EG, 1992. Deterioration of beta-adrenergic modulation of cardiovascular function with aging. Ann NY Acad Sci. 673:293-310. [Medline]
  29. Orchard CH, Lakatta EG, 1985. Intracellular calcium transients and developed tension in rat heart muscle. A mechanism for the negative interval-strength relationship. J Gen Physiol. 86:637-651. [Abstract/Free Full Text]
  30. Effron MB, Bhatnagar GM, Spurgeon HA, Ruano-Arroyo G, Lakatta EG, 1987. Changes in myosin isoenzymes, ATPase activity, and contraction druation in rat cardiac muscle with aging can be modulated by thyroxine. Circ Res. 60:238-245. [Abstract/Free Full Text]
  31. Lompre AM, Mercadier JJ, Wisnewsky C, et al. 1981. Species- and age-dependent changes in the relative amounts of cardiac myosin isoenzyme in mammals. Dev Biol. 84:286-290.
  32. Shroff SG, Janicki JS, Weber KT, 1985. Evidence and quantitation of left ventricular systolic resistance. Am J Physiol. 249:H358-H370.
  33. Hunter WC, Janicki JS, Weber KT, Noordergraaf A, 1979. Flow-pulse response: a new method for the characterization of ventricular mechanics. Am J Physiol. 237:H282-H292.
  34. Campbell KB, Kirkpatrick RD, Knowlen GG, Ringo JA, 1990. Late-systolic pumping properties of the left ventricle: deviation from elastance–resistance behavior. Circ Res. 66:218-233. [Abstract/Free Full Text]




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