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Biomedical subjects

J Scheuer

Publications and source records attributed to J Scheuer.

At least 55 records · Page 3Linked to original sources
PubMed1986

Chronic swimming reverses cardiac dysfunction and myosin abnormalities in hypertensive rats.

The purpose of this study was to determine whether a chronic swimming program could reverse the decreased cardiac function and altered myosin biochemistry found in hearts of rats with established renal hypertension. Ten wk after the onset of hypertension [midpoint (m)], hearts from normotensive controls (C) and hypertensives (H) were studied in an isolated working heart apparatus, and myosin biochemistry was analyzed. Half of the control and hypertensive animals were then subjected to a 10-wk swimming program (Sw) and their hearts were compared with those from age-matched sedentary rats. Body weight was no different at the midpoint of the study between Cm and Hm or at the end point (e) of the study among Ce, Swe, He, or H-Swe. Swimming had no effect on blood pressure in either normotensive or hypertensive rats. Dry heart weight was increased by 46% in Hm compared with Cm and by 36% in He, 21% in Swe, and 61% in H-Swe when compared with Ce. Hypertension was associated in both the mid- and end-point studies, with decreases in coronary flow, stroke work (both per gram left ventricle), ejection fraction, and midwall fractional shortening. In addition, actin-activated myosin adenosinetriphosphatase (ATPase) activity was decreased in Hm and He associated with an increase in the content of the V3 myosin isoenzyme. Although the coronary deficit was not corrected in H-Swe, stroke work, ejection fraction, and fractional midwall shortening were normalized compared with control hearts. Myosin ATPase activity and the myosin isoenzyme distribution were similarly restored in H-Swe.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1986

Myocardial biochemical, contractile, and electrical performance after imposition of hypertension in young and old rats.

The effects of renovascular hypertension on the biochemical, contractile, and electrical performance of myocardial tissue from rats of various ages has been examined. Male Fischer rats, 2, 7, 12, and 17 months old, were made hypertensive by constriction of the left renal artery. Ten weeks after the onset of hypertension, left ventricular papillary muscles were isolated from those four groups when 5, 10, 15, and 20 months old, respectively. Mechanical performance and transmembrane electrical events were recorded simultaneously. Contractile protein enzyme activity was determined in the same hearts from which papillary muscles were used for acquisition of mechanical and electrical information. There was a slight increase in blood pressure in control groups as a function of age while blood pressure maintained a range of approximately 179-188 mm Hg for all hypertensive groups. Heart weight of control animals increased significantly from 5 months to 20 months of age from 539 +/- 26 to 1088 +/- 56 mg, representing an increase of 101%. In hypertensive animals, heart weight increased 50% in 5-month-, 15% in 10-month-, 50% in 15-month-, and 11.7% in 20-month-old animals. Although control groups revealed alterations in mechanical, electrical, and biochemical parameters that increased as a function of age, the magnitude of the biochemical, contractile, and electrical response to hypertension varied monotonically with the extent of myocardial hypertrophy, rather than age per se. Adaptation to the stress of hypertension was observed in each age group, and was revealed as prolongation of mechanical and electrical timing parameters, depression of the load-velocity relation, and contractile protein enzyme activity. Thus, the stress of hypertension, which was tolerated by the 10- and 20-month-old animals with lesser relative hypertrophy and lesser changes in measured parameters, may represent a differential adaptation to the stress of hypertension.

Action Potentials↗
PubMed1985

Multiple cardiac contractile protein abnormalities in myopathic Syrian hamsters (BIO 53 : 58).

Hearts of genetically myopathic male hamsters (BIO 53 : 58) were studied at 1 month, 2 months, 3 months, 4 to 5 months and 7 months of age. The time course of alterations in the cardiac myofibrillar ATPase activity, the relationship of myofibrillar ATPase activity to free [Ca2+], myosin ATPase activity and the distribution of heavy chain myosin isoenzymes were evaluated. Mg2+-Ca2+ ATPase activity of cardiac myofibrils in myopathics was increased in 4 month and 7 month-old hamsters. Elevated Mg2+ ATPase activity was found as early as in 2-month-old hamster. However, there was no loss in the regulation of the myopathic myofibrillar assembly as measured by the PCa response (10(-7) M to 10(-4) M Ca2+). Scans of SDS electrophoresis slab gels of cardiac myofibrillar proteins from control (C) and myopathic animals (M) did not show any differences at any age group (1, 4 and 7 months). There was a significant decrease in myosin Ca2+ ATPase activity and actin activated Mg2+-ATPase activity at 4 to 5 months and 7 months of age in the myopathic hearts. At all ages in normal and myopathic animals cardiac myosin consisted of three isoenzymes, V1, V2 and V3. At all ages in controls and at 1 to 3 months in myopathics, V1 predominated and the isoenzyme distribution was V1 greater than V2 greater than V3. However, in myopathics at 4 to 5 months, the distribution was V1 = V3 greater than V2 and at 7 months was V3 greater than V2 greater than V1. Our experiments suggest alterations in different components of the contractile protein system that occur at different stages of myopathy.

Adenosine Triphosphatases↗
PubMed1985

Early increases in coronary vascular reserve in exercised rats are independent of cardiac hypertrophy.

To evaluate the relationship between the physiological cardiac hypertrophy associated with physical training and the increases in vascular capacitance associated with this stimuli, male and female rats trained by a swimming program were studied. Both sexes were used so that the coronary vascular response to exercise could be studied in the presence (females) and absence (males) of cardiac hypertrophy. Coronary vascular reserve was assessed in isolated retrograde buffer-perfused hearts under conditions of minimal coronary resistance (15 microM adenosine or anoxia). Both groups demonstrated an increase in coronary vascular reserve after 8 wk of exercise swim training, male animals increasing flow (per g of myocardium) by 15% and females by 18%. When the time course of this response was compared in female animals with the time course of the development of myocardial hypertrophy, it was evident that the vascular changes occurred early, greater than 80% of the response was seen within the first 10 days of exercise, compared with an approximately 35% increase in cardiac mass. These data suggest that the vascular response to exercise swim training is independent of the hypertrophic response and further that the increase in coronary vascularity is an early event in the cardiac adaptation to a physiological load.

Animals↗
PubMed1984

Radionuclide ventriculographic responses to graded supine and upright exercise: critical role of the Frank-Starling mechanism at submaximal exercise.

To assess the influence of work load and posture on the response to exercise, 25 patients with coronary artery disease (CAD) and 17 normal subjects underwent graded supine and upright exercise radionuclide ventriculography. In both groups, end-diastolic counts increased with supine exercise (p less than 0.001). The ejection fraction and peak systolic pressure-end-systolic volume relation increased in normal subjects (p less than 0.02), but not in patients with CAD. At upright rest, end-diastolic counts decreased in both groups (p less than 0.001) and then increased with exercise (p less than 0.001). The increase in end-diastolic counts was most pronounced on the transition from upright rest to the 150-kpm work load and resulted in a significant increase in stroke counts (p less than 0.05) for both patients with CAD and normal subjects, without a measurable change in the ejection fraction or the peak systolic pressure-end-systolic volume relation. Later in exercise, end-diastolic counts plateaued, and the ejection fraction and the peak systolic pressure, end-systolic volume relation increased only among normal subjects. Thus, low-level upright exercise is highly dependent on the Starling mechanism in both normal subjects and patients with CAD, with enhanced contractility apparent only during more vigorous exercise in normal subjects.

Blood Pressure↗
PubMed1984

Correlation of myosin isoenzyme alterations with myocardial function in physiologic and pathologic hypertrophy.

To explore the interactions of physiologic and pathologic hypertrophy, four groups of hearts were studied in an isolated working rat heart apparatus. Cardiac contractile proteins were also evaluated. The groups were hearts of female control sedentary rats; rats subjected to a 10-week swimming programme; rats with renal hypertension; and hypertensive rats subjected to a 10-week swimming programme. The swimming programme in normotensive female rats caused a 30% cardiac hypertrophy, in hypertensive animals 46% hypertrophy, and in combined hypertension and swimming 70% hypertrophy. Ca2+-myosin ATPase activity and actin-activated myosin ATPase were elevated in hearts of swimmers, depressed in hearts of hypertensive sedentary animals and similar to control values in hearts of hypertensive swimmers. Myosin V1 isoenzyme content was increased in hearts of swimmers, depressed in hearts of hypertensives, but normal in hearts of hypertensive swimmers. Reciprocal relationships were seen with the V3 isoenzyme. Stroke work, mean velocity of circumferential fibre shortening, and per cent fractional shortening at the midwall showed increased values for hearts of swimmers, depressed values for hearts of hypertensives, and normal values or values above the control for hearts of hypertensive swimmers. Myocardial flow measured with microspheres was increased in the left ventricle of swimmers, depressed in hearts of hypertensives and still depressed in hypertensive swimmers, but significantly higher than in the hypertensives alone. The correlation of actin-activated ATPase activity and of fractional shortening was linear among the four groups. These studies demonstrate that physiologic and pathologic hypertrophy in the rat have distinctly opposite effects on contractile proteins and contractile performance. When one type of hypertrophy is superimposed on the other the effects are additive.

Actins↗
PubMed1984

Effects of graded insulin therapy on cardiac function in diabetic rats.

To determine the effects of graded insulin therapy on cardiac function and biochemistry, rats were made diabetic by streptozotocin (50 mg/kg) and subsequently treated with either 3 U of insulin per day (D3) or 5 U/day (D5) and compared with untreated diabetic rats (D phi) and a nondiabetic control group (C). Blood glucose, water consumption, and heart and body weights in D3 and D5 showed dose-dependent responses between those of D phi and C. Cardiac function was studied at similar heart rates and similar left atrial and aortic pressures in an isolated working heart apparatus. Hearts from D phi showed significant decreases in end-diastolic pressure, peak left ventricular systolic pressure, and positive dP/dt, whereas these values in D3 and D5 were similar to those in C. The isovolumic relaxation period was significantly longer in the D phi group, intermediate between D phi and C in D3, and the same in D5 and C. Ca2+-ATPase activity of myosin and actin-activated Mg2+-ATPase activity was depressed in D phi, partially corrected in D3, and completely corrected in D5. Myosin isoenzyme distribution displayed a shift from the predominant V1 pattern observed in C to a predominant V3 pattern in D phi. Treatment with 3 U of insulin per day partially corrected the isoenzyme abnormality, and treatment with 5 U/day restored the isoenzyme distribution to normal. These results indicate that gross cardiac contractile function can be normalized with insulin dosages that are not sufficient to correct hyperglycemia, polydipsia, or body and heart weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Diabetic cardiomyopathy in rats: mechanical and biochemical response to different insulin doses.

Diabetes mellitus causes congestive heart failure in humans, independent of atherosclerosis. The present study extends previous work on the reversibility, with insulin, of the alterations in myocardial function and contractile protein biochemistry observed in diabetic rats. The response of these alterations to different fixed doses of insulin was explored. Diabetic rats were given 0, 0.5, 1, 1.5, 2, or 2.5 U of insulin daily for 6 wk. Papillary muscle function, actomyosin ATPase, and myosin isoenzyme distribution showed progressive normalization with increasing insulin dose as blood glucose concentration returned to normal. Thus insulin therapy in diabetic rats on a normal diet produces continuous improvement in cardiac function and biochemistry as euglycemia is approached. This study also suggests that mild diabetes results in qualitatively identical, although quantitatively less pronounced, myocardial changes compared with those observed in severely diabetic rats.

Actomyosin↗
PubMed1984

The effects of gonadectomy on left ventricular function and cardiac contractile proteins in male and female rats.

To examine the influence of the sex hormones on mechanical properties and biochemistry of the adult heart, we studied left ventricular function and cardiac contractile proteins in hearts from 20-week-old male and female rats that had been gonadectomized at 18 days of age, compared with hearts from sham-operated animals. Testosterone and estradiol were not detectable in serum from male and female gonadectomized rats, respectively. The male rats had lower body and heart weights than male sham operated rats, whereas these values were higher in female gonadectomized than in female sham-operated rats. Left ventricular function was studied in a working heart apparatus at similar heart rate and at controlled levels of aortic diastolic pressure and left atrial pressure. At moderate left atrial pressure, end-diastolic pressure and volume per gram dry left ventricle were the same in all groups, but at high left atrial pressure, end-diastolic pressure, and volume per gram dry left ventricle were lower in male and female gonadectomized than in the respective sham-operated rats. Further increases in left atrial pressure were associated with mechanical alternans in male and female gonadectomized rats. Significantly (P less than 0.05) lower values for cardiac output, peak systolic pressure, ejection fraction, and myocardial oxygen consumption occurred in male gonadectomized compared with sham-operated rats at moderate and high left atrial pressure at higher levels of aortic diastolic pressure. Decreases in these values for female gonadectomized compared with sham-operated rats occurred only at high left atrial pressure. A significant downward shift in the mean force-velocity relationship was observed in all gonadectomized rats at both moderate and high left atrial pressure. In a follow-up study, when end-diastolic pressure was kept the same at both moderate and high left atrial pressure in female sham-operated and gonadectomized rats by reducing heart rate, decreases in contractile function in gonadectomized rats were observed at all preloads. Ca++-myosin ATPase activity was significantly reduced by 34% in male and by 19% in female gonadectomized rats when compared to respective sham-operated control hearts. These alterations in myosin ATPase activity were associated with a reduction in the V1 myosin isoenzyme and an increase in the V3 isoenzyme. Thus, left ventricular filling and left ventricular function were impaired in hearts of gonadectomized rats. Alterations in function were associated with depressed cardiac myosin ATPase activity in male and female gonadectomized rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Cardiac conditioning ameliorates cardiac dysfunction associated with renal hypertension in rats.

To explore the effect of physiologic hypertrophy superimposed on pathologic hypertrophy, hearts from female control rats (C), renal hypertensive rats (H), rats conditioned with a 10-12 wk swimming program (Sw), and hypertensive rats trained by the swimming program (H-Sw) were perfused in an isolated working rat-heart apparatus. Systolic blood pressure was approximately 100 mmHg in C and Sw and was 160 mmHg in H and H-Sw. The swimming program had no effect on blood pressure. Compared with C, heart weight was increased by 30% in Sw, 47% in H, and 77% in H-Sw. At high preload and afterload, cardiac output (milliliters per gram dry LV weight) was decreased in H, increased in Sw, and partially restored towards normal in H-Sw. Ejection fraction, percent fractional shortening, and mean velocity of circumferential fiber shortening were enhanced in Sw, depressed in H, and normalized in H-Sw when compared with C. Coronary flow and myocardial oxygen consumption in this series of hearts were depressed in H, with no restoration in H-Sw, but coronary effluent lactate/pyruvate ratios were only elevated in the hearts of H-Sw. Coronary vascular responses were examined in a second series of experiments which used microspheres. In this series, the depressed coronary flow observed in H was partially restored towards normal in H-Sw and the inner/outer myocardial flow ratio was normal when hearts were perfused at 140 cm aortic pressure but was somewhat depressed in both H and H-Sw when the hearts were perfused at 80 cm aortic pressure. These studies demonstrate that hypertrophic hearts from renal hypertensive rats have diminished coronary flow and depressed cardiac function when they are studied in the isolated working heart apparatus, yet there is no evidence of myocardial ischemia. Superimposition of a chronic swimming program results in increased hypertrophy but restoration of cardiac function partially or completely to normal. Thus, pathologic and physiologic hypertrophy are biologically distinct entities. Physiologic hypertrophy may partially ameliorate the defects associated with pathologic hypertrophy.

Animals↗
PubMed1983

Left ventricular function after chronic insulin treatment in diabetic and normal rats.

Previous reports have documented a cardiomyopathy in rats resulting from streptozotocin-induced diabetes. In order to determine the reversibility of streptozotocin-induced cardiomyopathy to insulin therapy, hearts from rats made diabetic by streptozotocin for 6 weeks and then treated with insulin for 3 weeks were compared with untreated diabetic rats and control rats not injected with streptozotocin. When perfused in an isolated working heart apparatus with 5.5 mM glucose as substrate, hearts from untreated diabetic rats when compared to hearts from either streptozotocin-injected rats treated with insulin or control rats showed significant depressions in peak left ventricular pressure, maximal positive and negative dP/dt, oxygen extraction, lactate production and effluent lactate; pyruvate ratio. Ca2+-actomyosin ATPase was also depressed in untreated diabetics. As left atrial pressure was raised in untreated diabetic rats, a decline in cardiac output was observed, whereas in insulin-treated or control groups there was no such negative response. Indices of cardiac performance were significantly greater in insulin-treated rats when compared to control rats suggesting overcorrection with insulin therapy. To explore whether insulin treatment may have a beneficial effect on the myocardium control rats were made hyperinsulinemic for 6 to 7 weeks. Shorter isovolumic relaxation times and elevated values for Ca2+-actomyosin ATPase were observed in hearts from hyperinsulinemic animals when compared to hearts from control animals. These results demonstrate complete reversibility of streptozotocin-induced cardiomyopathy and confirm that this condition is due to insulin deficiency and not to a primary cardiotoxic effect of streptozotocin.

Animals↗
PubMed1983

Radionuclide ventriculographic study of adaptations to exercise in aortic regurgitation.

Exercise-gated radionuclide ventriculography has been proposed as a method to evaluate cardiac reserve in patients with aortic regurgitation (AR). Characterization of ventricular function, however, in AR is complicated by the dynamic nature of the leak in individual patients and by variations in severity among patients. Twenty patients with isolated AR were studied to assess the effects of exercise on the regurgitant index. The regurgitant index (left ventricular divided by right ventricular stroke counts) estimates the severity of the leak. The regurgitant index at rest was significantly higher in patients with AR than in patients without AR (3.46 +/- 1.25 versus 1.08 +/- 0.16, p less than 0.001). In patients with AR, the regurgitant index decreased during exercise to 2.6 +/- 0.8 (p less than 0.001), whereas it did not change in the control group (1.16 +/- 0.21, difference not significant). Further, in patients with AR, the greater the regurgitant index at rest, the greater the decrease during exercise (y = 0.56x -- 1.08, r = 0.78, p less than 0.001). End-diastolic counts and stroke count responses from rest to exercise were highly variable, but were explained in part by the decreasing regurgitant index. These data support previous catheterization studies and confirm gated radionuclide ventriculography as a useful tool for monitoring adaptations to exercise in AR.

Adolescent↗
PubMed1983

Impaired coronary flow and ventricular function in hearts of hypertensive rats.

Hearts of rats made hypertensive (BP greater than 150 mmHg) by left renal artery clipping and sham operated controls were studied in two series of experiments. In series I, cardiac function was studied in an isolated working heart apparatus at weeks 4, 9 to 10 and 16 to 17 post-surgery. In series II, coronary flow was studied during normoxic and anoxic retrograde perfusions at days 6 to 9 and at weeks 4 and 10 post-surgery. In series I, when compared with controls, hypertensives had lower body weights at weeks 4 and 9 to 10, and higher left ventricular weights at each period. Heart function was depressed for hypertensives when compared with controls as measured by lower stroke volume, peak left ventricular systolic pressure, stroke work, ejection fraction, positive dP/dt, peak aortic flow, and maximal flow acceleration. Relaxation rate as measured by negative dP/dt was also depressed. Hearts from hypertensives had significantly lower coronary flows and MVO2, and increased percent oxygen extraction and effluent lactate/pyruvate ratios. LVEDP was significantly elevated for hypertensives, when LVEDV (ml) was similar for hypertensives and controls. Myocardial actomyosin ATPase activity was depressed for hypertensives at weeks 9 to 10 and 16 to 17 post-surgery. In series II, when hearts were perfused retrogradely, coronary flow was lower for hypertensives than for controls during normoxia at days 6 to 9 and at week 4, and during anoxia at all time periods. The findings demonstrate that impaired coronary vascular reserve develops within days of the development of hypertension in rats, and this can be associated with impaired ventricular function.

Animals↗
PubMed1983

Effects of age on mechanical and electrical performance of rat myocardium.

Left ventricular papillary muscles were isolated from male Fischer rats at 3, 6, 12, and 24 mo of age. Mechanical performance and transmembrane action potential characteristics were recorded simultaneously. Contractile protein enzyme activity was determined in the same hearts from which papillary muscles were used for acquisition of mechanical and electrical information. There was an age-related increase in the isometric time to peak tension and time to half relaxation with no age-related change in peak isometric developed tension. Resting tension showed a significant increase at both 12 and 24 mo of age. Although no significant change was noted in peak rate of tension rise (+T') or fall (-T'), there was a significant age-related prolongation in the time to +T' and -T'. Isotonically, peak shortening decreased in 24-mo-old animals. Time to peak shortening increased, whereas peak velocity of muscle shortening decreased from 3 to 24 mo of age. A significant and progressive prolongation was noted in the duration of the transmembrane action potential at 50% and 75% repolarization. In addition an age-related progressive decline was seen in contractile protein enzyme activity. These biochemical and electrophysiological alterations may help to explain the contractile modifications during aging.

Action Potentials↗
PubMed1983

Effects of experimental diabetes on adrenergic and cholinergic receptors of rat myocardium.

To more fully characterize the alterations in myocardial adrenergic and cholinergic receptors induced by the diabetic state, we investigated the binding characteristics of (--) [3H] dihydroalprenolol to beta adrenergic receptors (bAR), [3H] prazosin to alpha adrenergic receptors (aAR), and [3H] quinuclidinyl-benzilate to muscarinic cholinergic receptors (MCR) in myocardial membranes derived from rats 8 wk after treatment with streptozotocin. We also studied an equal number of animals from three control groups: free-eating nondiabetics, pair-weighted nondiabetics, and streptozotocin-treated animals treated daily with insulin. Diabetic hearts demonstrated 27% fewer bAR (P less than 0.01) and 31% fewer aAR (P less than 0.01) than free-eating controls, without changes in MCR, and without changes in antagonist affinity, agonist affinity, or agonist slope factor (pseudo-Hill coefficient) for any class of receptors. Food restriction had no effect on receptor characteristics, and treatment of diabetic rats with insulin prevented any downregulation of cardiac bAR or aAR. The parallel decrease in both bAR and aAR suggests that streptozotocin-induced hypothyroidism is not the primary causative factor of bAR downregulation in this model, since hypothyroidism produces upregulation of aAR. Furthermore, the lack of change in cardiac MCR suggests that the adrenergic receptor alterations are not the result of nonspecific abnormalities of protein synthesis in the diabetic heart. Further studies are required to establish the physiologic significance of these receptor alterations, but these data support the hypothesis that altered adrenergic receptor properties may underlie, at least in part, the chronotropic and inotropic abnormalities of cardiac performance that are associated with the diabetic state.

Animals↗
PubMed1982

Contractile behavior of rat myocardium after reversal of hypertensive hypertrophy.

The effects of renovascular hypertension and its reversal on the contractile performance of papillary muscles from rats has been examined. Hypertension of 10 wk duration caused a 48% increase in heart weight and significant prolongations of isometric time to peak tension (TPT), time to half relaxation, and time to peak shortening (TPS). A significant depression in the velocity of shortening was observed in the 10-wk group. However, muscles from hypertensive rats were still able to maintain normal levels of peak isometric developed tension and peak shortening; this may be due to the observed prolongation of TPT and TPS, respectively. In addition, calcium-activated actomyosin ATPase activity was depressed in hearts of hypertensive animals. Reversal of hypertension was studied at 20 wk after the onset of hypertension (10 wk of hypertension followed by 10 wk of normotension). Contractile and biochemical alterations observed in hypertensive animals were reversed in rats undergoing this regime. Thus reversal of a gradually applied pressure overload resulted in the regression of mechanical and biochemical abnormalities associated with the pressure overload myocardial hypertrophy.

Adenosine Triphosphatases↗
PubMed1982

Coronary collateral stimulation by exercise in dogs with stenotic coronary arteries.

To determine the effects of an exercise-training program on coronary collateral development, we instrumented 13 1-yr-old beagles with left circumflex (LCf) coronary artery flow probes and balloon occluders and left atrial and aortic catheters. The LCf artery was constricted resulting in a 58 +/- 4% reduction of the peak reactive hyperemia response following release of a 154-s LCf occlusion. All dogs were studied during the first week of the study protocol. Resting heart rate, cardiac output, and left atrial and aortic pressures were evaluated before and during a 1-min LCf occlusion. Myocardial blood flow was also measured with radioactively-labeled microspheres injected into the left atrium during the LCf occlusion. Subsequently the dogs were exercised at 6.4 km/h and 12% grade, and all hemodynamic and blood flow measurements were repeated. The animals were then randomized to either a sedentary or exercising group. The six sedentary animals were confined to their cages, while the seven training beagles did sprint and endurance running for 75 min/day, 5 days/wk. After 12 wk the hemodynamic and blood flow studies were repeated at rest and during treadmill running. There were no statistically significant differences in resting or exercise hemodynamics, response to LCf occlusion, or myocardial blood flow in the two groups in wk 1. Hemodynamics and blood flow data were virtually unchanged in the sedentary animals after 12 wk. However, the trained dogs demonstrated less evidence of left ventricular failure following LCf occlusion while running and had significantly higher myocardial blood flows. Their resting collateral flow increased from 0.52 +/- 0.16 ml . min-1 . g-1 at wk 1 to 0.90 +/- 0.28 ml . min-1 . g-1 at wk 12 (P less than 0.05), while the ratio of collateral to normal myocardial blood flow increased from 0.46 +/- 0.12 to 0.64 +/- 0.16 (P less than 0.05). Thus chronic exercise can stimulate coronary collateral development, and the enhanced collateral flow has a salutary functional effect.

Animals↗