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Biomedical subjects

J Scheuer

Publications and source records attributed to J Scheuer.

At least 73 records · Page 4Linked to original sources
PubMed1982

Gamma camera quantitation of thallium-210 redistribution at rest in a dog model.

Defects seen at rest on thallium-201 (201TI) scintigraphy can disappear over time. We obtained sequential 5-minute scans over 127 +/- 9.4 minutes in seven open-chest dogs with fixed, stable regional flow reductions (normal zone flow 0.76 +/- 0.09 ml g-1/min, ischemic zone flow 0.49 +/- 0.04 ml g-1 min [mean +/- SEM], p less than 0.05) as determined by microsphere injection. Sequential 5-minute scans were obtained after i.v. injection of 1.5 mCi of 201TI. Data were stored in a 64 x 64 pixel computer matrix. Qualitatively, defects that showed redistribution were seen in all dogs. Quantitatively, greater count loss from peak activity distinguished the normal zone, but overlap was great. Alternate quantitative methods using background subtraction altered the characteristics of the time-activity curves, but did not enhance the separation of ischemic from normal zones. Patterns of 201TI redistribution from gamma camera imaging are profoundly influenced by the method of quantitation. No single method of quantitative analysis separated ischemic from normal zones in all dogs. The clinical significance of patterns at rest requires redefinition.

Animals↗
PubMed1982

Effects of physical training on myocardial vascularity and perfusion.

Physical training is thought to be a stimulus for coronary vascular growth and coronary collateral development. This report is a summary of knowledge in the area. Studies in experimental animals with normal hearts indicate that physical training promotes increased myocardial capillary density and also causes enlargement of the surface coronary vessels. The physiologic effect of these changes on coronary vascular reserve and protection of segments of the heart against myocardial ischemia has not been established. Physically trained dogs and pigs do not appear to be protected against the effects of coronary occlusion, in that the ischemic area appears to be as large in trained animals as in untrained animals for any given coronary lesion. One study in physically trained rats appears to show protection against myocardial infarction, but whether this is related to coronary vascular changes has not been established. Experiments in dogs subjected to chronic narrowing or gradual occlusion demonstrate that physical training in these models does promote collateral blood flow as measured by retrograde flow in open-chest experiments. Studies using the microsphere technique in closed-chest animals confirms increased collateral flow to ischemic areas in some animals, but the magnitude of the increases appears to be small and varies greatly from animal to animal. Studies in athletes suggest that myocardial blood flow is lower at any submaximal level of training in athletes than in sedentary persons. Studies in patients with coronary artery disease have generally failed to show an increase in coronary blood flow or in perfusion of ischemic areas after physical training programs, but the techniques used might not have been sensitive enough to detect changes. The evidence in the experimental animals is sufficiently promising to indicate that the search should be continued to define physical training programs that will most stimulate myocardial vascularity and coronary collaterals in humans.

Animals↗
PubMed1982

Physiologic cardiac hypertrophy corrects contractile protein abnormalities associated with pathologic hypertrophy in rats.

To evaluate the combined effects of cardiac overload imposed by hypertension and by chronic exercise, male and female rats were made hypertensive by unilateral renal artery stenoses and made to exercise in an 8-10-wk swimming program. Sedentary normotensive animals, sedentary hypertensive animals and normotensive animals exposed to the swimming program were also studied. Hypertension was associated with the development of cardiac hypertrophy, and this was exaggerated in hypertensive swimmers. Actomyosin, Ca2+-myosin, and actin-activated Mg2+-myosin ATPase activities were enhanced in normotensive swimmers, depressed in hypertensives and were normal or increased in hypertensive swimmers. Myosin isoenzyme analysis showed a predominant V1 pattern in normals; an increase in percent V1 isoenzyme is swimmers; a predominant V3 pattern in hypertensives; and a return to the predominant V1 pattern in hypertensive swimmers. These findings suggest that the hypertrophy imposed by hypertension and hypertrophy imposed by physical training using a chronic swimming program are distinctly different biological phenomena. Physical training by swimming prevents the changes in cardiac myosin induced by hypertension despite the exaggeration of hypertrophy.

Actomyosin↗
PubMed1981

Subunit function in cardiac myosin. Effects of binding phosphorylated and unphosphorylated myosin light chain 2 to light chain 2-deficient myosin.

The 20,000-dalton light chain of cardiac muscle myosin can be specifically digested and thereby removed from the rest of the myosin molecule by incubation with a myofibrillar protease (Malhotra, A., Huang, S., and Bhan, A. (1979) Biochemistry 18, 461-467). In order to study the effects of phosphorylation of the 20,000-dalton myosin light chain, experiments were carried out with cardiac muscle myosin that was made deficient in this light chain following proteolysis. Both the phosphorylated and unphosphorylated isolated 20,000-dalton myosin light chain of cardiac muscle myosin were found to bind to light chain-deficient myosin. Prior to readdition of the isolated light chains, this light chain-deficient myosin was found to have a higher MgATPase activity in the presence and absence of actin, than native myosin. Binding of the unphosphorylated myosin light chain restored the MgATPase activity of light chain-deficient myosin to that of native cardiac myosin. In contrast, the binding of 2 mol of the previously phosphorylated myosin light chain did not lower the actin-activated MgATPase activity. The results suggest that while phosphorylation of the 20,000-dalton light chain of cardiac muscle myosin is not essential for the actin-activated MgATPase activity, it may have a modulatory role.

Animals↗
PubMed1981

Contractile proteins and sarcoplasmic reticulum in physiologic cardiac hypertrophy.

To study effects of physiologic hypertrophy on contractile protein ATPases and sarcoplasmic reticulum, hypertrophy was caused in female Wistar rats by a chronic swimming program. Nonhypertrophied hearts of female control sedentary rats and rats made to run on a treadmill program were also examined. The swimming program, but not the running program, resulted in a significant increase in heart weight. Actomyosin ATPase activity was also increased by 15% in the hearts of swimmers but not runners. Similar increases were observed for Ca2+-activated myosin ATPase activity and actin-activated ATPase of myosin. Sarcoplasmic reticulum from the hearts of swimmers showed increased calcium binding and calcium uptake as a function of time and of calcium concentration. Sarcoplasmic reticulum ATPase activities were not altered by hypertrophy. These findings in physiologic hypertrophy contrast with those of pathologic hypertrophy in which ATPase activity of contractile proteins and calcium binding and uptake of sarcoplasmic reticulum have generally been found to be depressed.

Actomyosin↗
PubMed1981

Cardiac responses to exercise training in male and female rats.

The purpose of the present study was to determine if contractile function adapts to physical training in the same way in hearts of male and female rats. Male and female rats were trained with a running program sufficient to cause equal increases in cytochrome oxidase activity in gastrocnemius muscles in both groups. Hearts were then studied in an isolated perfused working rat heart apparatus with varying preloads and fixed afterloads. Five groups were studied: 1) free-eating sedentary males (MS-FE); 2) running males (MR); 3) sedentary females (FS); 4) running females (FR); and 5) food-restricted sedentary; males (MS-FR). Heart weights were similar in MS-FE and MR and in FS, FR, and MS-Fr. Stroke work, stroke volume, coronary flow, and myocardial oxygen consumption were significantly higher in MR than in MS-FE but were almost identical in FR and FS. MS-FR showed stroke work, stroke volume, and ejection fractions that were similar to MR but higher than MS-FE and both female groups. Thus when hearts of equal weights were compared, a training effect was only seen in males. These results suggest that despite similar skeletal muscle adaptations, hearts of male rats adapt to physical training by running with improved intrinsic performance, whereas hearts of female rats do not.

Animals↗
PubMed1981

Cardiac function in hypertrophied hearts from chronically exercised female rats.

Physiological cardiac hypertrophy was produced in female rats by subjecting them to a swimming program for 8 wk. Conditioned rats (C) had body weights similar to sedentary control rats (S), but hearts from C weighed 33% more than hearts from S. Heart function was assessed in an isolated working-heart apparatus at similar heart rates and aortic diastolic pressures and over a range of 5-20 cmH2O left atrial filling pressure (LAP). At any given LAP, absolute values for cardiac output and coronary flow were greater (p less than 0.001) in C than S, but when these values were normalized for dry left ventricular (LV) weight, no differences were observed. Peak LV systolic pressure and ejection fraction were greater (p less than 0.01) in C than S at all LAP. Derived measures of contractility calculated at the midwall demonstrated greater (p less than 0.01) velocity and extent of circumferential fiber shortening in C compared with S. Therefore, chronic swimming in female rats leads to enhanced contractile performance of the left ventricle despite a marked degree of hypertrophy. These results contrast with our earlier observations in female rats trained by running where neither hypertrophy nor enhanced function were observed.

Animals↗
PubMed1981

The effect of streptozotocin-induced diabetes in rats on cardiac contractile proteins.

In order to determine whether diabetic cardiomyopathy in rats is associated with altered contractile proteins, male and female rats were made diabetic with intravenous streptozotocin (STZ). Calcium ATPase activity of cardiac actomyosin was significantly decreased after 1 week of diabetes and was depressed by 60% by 2 weeks. Rats pretreated with 3-O-methyl glucose to prevent the hyperglycemia caused by STZ had normal Ca2+-actomyosin ATPase activities, and non-diabetic rats whose food was restricted to keep their body and heart weights similar to those found in diabetic animals had only a slight fall in actomyosin ATPase activity. Ca2+-ATPase and actin-activated ATPase activities of pure myosin were similarly depressed in preparations from hearts of diabetic animals. Sodium dodecylsulfate gel electrophoresis and isoelectric focusing failed to reveal differences in the patterns of contractile proteins or light subunits between diabetics and controls, but pyrophosphate gels showed a shift in the myosin pattern. Because of depressed circulating thyroid hormone levels in diabetic animals, cardiac contractile proteins were also studied in preparations from thyroidectomized rats. Calcium activities of actomyosin and myosin ATPase were lower than values found in hearts of diabetic rats. When diabetic animals were kept euthyroid with thyroid replacement, actomyosin ATPase activity was still depressed. Thus STZ diabetes causes a significant decrease in cardiac contractile protein ATPase activity. This may be related to altered proportions of myosin isoenzymes.

Adenosine Triphosphatases↗
PubMed1981

Reversibility of diabetic cardiomyopathy with insulin in rats.

Diabetes appears to cause a cardiomyopathy independent of atherosclerotic coronary artery disease and hypertension. Left ventricular papillary muscle function studies in rats made severely diabetic with streptozotocin have shown a slowing of relaxation and a depression of shortening velocity. However, the effects of insulin therapy on the myocardial mechanics of diabetic rats have not been studied. Therefore, rats diabetic for 6-10 weeks were treated with PZI insulin for 2, 6, 10, or 28 days and the mechanical performance of their left ventricular papillary muscles was compared to that of untreated diabetics and age-matched controls; cardiac contractile protein enzymatic activity was also measured. Neither 2 nor 6 days of therapy had any effects on the depressed cardiac muscle performance of diabetic animals, although plasma glucose concentration was restored to normal. By 10 days of therapy, recovery of mechanical performance was nearly complete, and by 28 days of therapy, complete reversal of the altered myocardial mechanics was observed. Crystalline insulin added to the bath (9 mU/ml) had no effect on myocardial mechanics in either diabetics or controls. A gradual recovery of actomyosin and myosin ATPase activity in the hearts of insulin-treated diabetic animals was also found, complementing the mechanical studies. In addition to demonstrating a gradual but complete reversibility of the abnormalities in papillary muscle function in diabetic rats (although control of hyperglycemia was less than ideal), this study confirms that this model of a cardiomyopathy is not a result of streptozotocin-induced cardiac toxicity. Additional data are provided indicating that depressed thyroid hormone levels in diabetic rats are not responsible for the mechanical changes observed.

Animals↗
PubMed1980

The evaluation of ischemic heart disease thallium-210 with comments on radionuclide angiography.

Coronary artery disease causing myocardial ischemia and infarction is the leading cause of death in America. Methods that can be used to diagnose and follow the response to therapy of coronary artery disease or its effect on myocardial ischemia should help control the morbidity and mortality of ischemic heart disease. The use of ECG monitoring is less sensitive and specific for ischemia than thallium (TI) imaging or the use of radionuclide angiography (RNA). In large patient populations, the findings of a positive ECG and TI or RNA study will be highly predictive for the presence of coronary artery disease, while negative test results make the disease unlikely. A combined approach to the patient with possible ischemic heart disease is presented.

Cardiac Catheterization↗
PubMed1980

Cardiac contractile proteins and sarcoplasmic reticulum in hearts of rats trained by running.

Rats were trained with two running protocols previously demonstrated to result in enhanced cardiac performance. Control groups included free-eating sedentary animals and food-restricted animals in which the body weights were the same as the runners. Calcium binding by isolated sarcoplasmic reticulum (SR) was slightly but significantly increased in SR from runners at low but not high calcium concentrations at 15 s and 1 min. Calcium uptake in the presence of 1 mM oxalate was increased in SR from runners. Actomyosin ATPase activity was increased by 10% (P less than 0.001) with one running protocol but not with the other. Myosin Ca2+ ATPase activity and actin-activated ATPase activity were also slightly increased in hearts of runners. In food-restricted cardiac actomyosin ATPase was significantly decreased. Actomyosin ATPase activity was found to be normal in hearts of sedentary animals subjected to water immersion without exercise. Therefore, physical training of rats by running, which produces a cardiac mechanical advantage similar to training by swimming, is not accompanied by cardiac biochemical changes of the same magnitude as in the hearts of swimmers.

Absorption↗
PubMed1980

The effect of diabetes on performance and metabolism of rat hearts.

To explore the effects of diabetes on myocardial function and metabolism we injected male rats with streptozotocin and studied their hearts 8 weeks later. Blood sugar levels in the treated rats were about 600 mg/100 ml. Body and heart growth rates were diminished. When studied in an isolated working rat heart apparatus using 5.5 mM glucose, hearts of diabetic animals showed diminished cardiac output and stroke work at high filling pressures. There also were significant depressions in peak left ventricular systolic pressure, peak aortic flow rate, maximum negative dP/dt, myocardial oxygen extraction, myocardial lactate production, and effluent lactate:pyruvate ratios. Myocardial glycogen stores, calculated glycogen utilization, and pyruvate production were increased in hearts of diabetics, and myocardial oxygen consumption was the same as in control hearts. The end-diastolic pressure-volume relationship was shifted to the right in hearts of diabetics. Most of the abnormalities observed in hearts of diabetic rats persisted when insulin and 15 mM glucose were included in the perfusion medium. Hearts from young rats or from age-matched food-restricted rats with heart weights similar to those of diabetics did not show depressed function or a pressure-volume shift. Our findings indicate that streptozotocin diabetes in rats results in abnormal myocardial performance. This is not due to restrictions in coronary flow or myocardial oxygenation and is not correctable by the provision of high glucose plus insulin in the perfusion medium.

Animals↗