摘要:

We have shown that systolic pressure - volume area (PVA), which is equivalent to the total mechanical energy generated by ventricular contraction, correlates linearly with myocardial oxygen consumption, Vo2, in canine left ventricle. Systolic force -time integral, FTI, also correlates with Vo2. In this study, stroke volume was increased from 0 (isovolumic) in isolated cross -circulated canine left ventricle in a stable contractile state while keeping PVA constant with a servo pump. Ventricular total force was calculated from ventricular pressure and volume by the force -equilibrium equation and was integrated from the end of diastole to the end of systole as identified with the time of Emax to yield FTI. Under the conditions of constant PVA, FTI significantly (p < 0.001) decreased by 10 ± 7% and 25 ± 8% with increases in stroke volume from 0 to 8 ± 4 ml and 17 ± 3 ml and in ejection fraction from 0 to 0.24 ± 0.10 and 0.61 ± 0.05, respectively, while Vo2and Emax remained constant. Therefore, we conclude that in a stable contractile state, it is possible to keep PVA constant even when stroke volume and ejection fraction are varied and that under such conditions, FTI no longer predicts Vo2. PVA remains a reliable predictor of Vo2regardless of ventricular loading conditions.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Sarcomeric myosin heavy chain (MHC), the main component of the sarcomere, contains the ATPase activity that generates the contractile force of cardiac and skeletal muscles. The different MHC isoforms are encoded by a closely related multigene family. Most members (seven) of this gene family have been isolated and characterized in the rat, including the α- and β-cardiac, skeletal embryonic, neonatal, fast IIA, fast IIB, and extraocular specific MHC. The slow type I skeletal MHC is encoded by the same gene that codes for the cardiac β-MHC. Each MHC gene studied displays a pattern of expression that is tissue and developmental stage specific, both in cardiac and skeletal muscles. Furthermore, more than one MHC gene is expressed in each muscle while each gene is expressed in more than one tissue. The expression of each MHC gene in cardiac and skeletal muscles is modulated by thyroid hormone. Surprisingly, however, the same MHC gene can be regulated by the hormone in a significantly different manner, even in opposite directions, depending on the muscle in which it is expressed. Moreover, the skeletal embryonic and neonatal MHC genes, so far considered specific to these 2 developmental stages, are normally expressed in certain adult muscles and can be reinduced by hypothyroidism in specific muscles. This complex pattern of expression and regulation of the MHC gene family in cardiac and skeletal muscle sheds new light on the mechanisms involved in determining the biochemical basis of the contractile state. It also indicates that the cardiac contractile system needs to be examined in a broader context, including skeletal muscles, in order to understand fully its developmental and physiologic regulation.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The effects of changing loading conditions and inotropic state on maximum isotonic lengthening rate (+ dL/dt, muscle lengths/sec) were examined in isolated rat myocardium. Physiologically sequenced contractions were studied in 18 left ventricular papillary muscle preparations (stimulation rate, 12/min). To study the effects of changing loading conditions, only one loading variable (preload, total load, or late load) was changed during each contraction, while the others were held constant. To study the effects of isoproterenol (10−6M) and temperature (28 vs. 33 ± C) on maximum isotonic lengthening rate, preload and late load were held constant and +dL/dt was examined at a common total load. When preload was increased from 0.7 ± 0.1 to 1.4 ± 0.1 g/mm2, muscle length increased from 0.98 ± 0.003 to 1.01 ± 0.002 muscle lengths, the extent of shortening increased from 0.05 ± 0.003 to 0.08 ± 0.003 muscle lengths, but minimum length (0.93 ± 0.01 muscle lengths) and + dL/dt (1.1 ± 0.1 muscle lengths/sec) were unchanged. When total load was increased from 1.5 to 4.5 g/mm2, minimum length increased from 0.91 ± 0.05 to 0.97 ± 0.05 muscle lengths and + dL/dt fell from 1.4 ± 0.1 to 0.5 ± 0.1 muscle lengths/sec. Late load (the load borne by or applied to the muscle during isotonic lengthening) was altered by changing its magnitude (g/mm2) or time (milliseconds after stimulation) of application. As late load was increased from 1.4 ± 0.02 to 2.1 ± 0.3 g/mm2, + dL/dt increased from 1.3 ± 0.2 to 2.1 ± 0.3 muscle lengths/sec. As the time of late load applications increased from 230 ± 9 to 289 ± 12 msec after stimulation, + dL/dt increased from 1.3 ± 0.2 to 2.5 ± 0.4 muscle lengths/sec. At constant preload and late load and for a given value of total load and minimum length, + dL/dt was faster at a higher temperature (28 vs. 33 ± C) and with the addition of isoproterenol, 10−6M. At a common total load (2.5 g/mm2), +dL/dt rose from 1.6 ± 0.1 muscle lengths/sec at 28 ± C to 2.4 ± 0.2 muscle lengths/sec at 33 ± C and 2.05 ± 0.1 muscle lengths/sec with isoproterenol. Thus, the load against which the muscle shortens (and/or the length to which it shortens), the magnitude of the late load, and the time at which the late load is applied are independent determinants of maximum isotonic lengthening rate. Under any constant set of loading conditions, both isoproterenol and increased temperature increase the maximum isotonic lengthening rate.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The role of thyroid hormone on the heart in terms of contractility, induction of growth, and selective synthesis of cardiac isomyosins was studied. After transplanting rat hearts from inbred hypothyroid donors into the abdomen of hypothyroid recipients of the same strain, two hearts were obtained in the same animal, both having reduced heart rate (200–250 bpm), decreased maximum rate of force, and high predominance of V3isomyosin. The heart in situ carried a full load, while the transplant was denervated, beat isovolumically with minimum external work. After surgery, the recipient rats were put either on normal diet only (controls) or injected with a daily dose of T3(average 200 μg/kg), which increased the heart rate to 340 bpm in 3 days (euthyroid level) and to 450 bpm in 7 days (hyperthyroid level). In T3-treated rats, the contractility of both hearts normalized in 7 days and showed hyperthyroid pattern in 14 days, while the mass of the in situ hearts increased to normal values in 7 days (+130 mg) and hypertrophied in 14 days (+ 340 mg), in contrast to the transplanted heart, which underwent atrophy (−90 mg and −210 mg) similar to that of control group (−225 mg). The predominant V3isomyosin was completely reversed to V1in two weeks in both hearts. Thus, T3can neither stimulate cardiac growth nor can it attenuate the rate of atrophy in the denervated ``nonworking'' heart in spite of its direct effect on contractility and synthesis of isomyosins, which was similar to that observed in the in situ heart.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The purpose of this study was to examine the electrical and mechanical responses of cat middle cerebral arteries to electrical stimulation of the adventitial vs. intimal surface of the vessels and to determine the responses as a function of transmural pressure. Middle cerebral arteries were cannulated at both ends. Within each cannula was a stimulating electrode. Electrical stimulation (0.5-msec square current pulses at 0.5 Hz yielding 160 μA of current between electrodes) resulted in significant reduction in diameter that was greater at both 40 and 80 mm Hg vs. 100 or 140 mm Hg. Conversely, adventitial stimulation of perivascular nerves with transmural platinum stimulating electrodes resulted in significant vasodilation. The constrictor response to intimal stimulation, as well as the dilatory response to adventitial stimulation, was blocked by tetrodotoxin. The constrictor response to luminal stimulation was enhanced by scorpion toxin demonstrating a functional role for tissues containing fast Na+channels. Perfusion with collagenase to disrupt the endothelium also abolished the constrictor response to luminal stimulation. The divergence of responses between adventitial and luminal surface stimulation may suggest that different cell layers within a blood vessel serve different functions, one to increase resistance and another to decrease resistance. For example, in cat middle cerebral arteries, the adventitial nerves (i.e., via reflexes) may increase flow, while blood-borne substances may mediate release of agents that reduce flow.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Characteristics of the bindings of [3H](−)dihydroalprenolol, [I25I](−) iodocyanopindolol, [3H]prazosin, [3H]yohimbine, and [3H]nitrendipine to porcine coronary membranes were investigated and the results compared with studies of porcine aortic membranes. In the equilibrium binding study carried out in sarcolemma-enriched fractions, there were no major differences in the Kdvalues of these radioligands between coronary artery and aorta. However, the densities of/β-, α1, and α2-adrenocetors and [3H]nitrendipine receptors of coronary artery were 258, 12, 12, and 561 fmol/mg protein, respectively, while those of aorta were 37,525,1,000, and 215 fmol/mg protein. β-Adrenergic agonists competed with [3H](−)dihydroalprenolol binding sites in coronary artery, the order of potency being (−)isoproterenol > (−)norepinephrine > (−)epinephrine > (+)isoproterenol. In case of aorta, the order was (−)isoproterenol > (−)epinephrine > (−)norepinephrine. The competition by (±)bisoprolol β,-selective antagonist) and ICI 118,5510β2-selective antagonist) for [125I](–)iodocyanopindolol binding sites in coronary artery resulted in nonlinear Hofstee plots (β1: β2= 90%: 10%). In case of aorta, linear Hofstee plots were obtained. From these results, we conclude that (1) coronary β- receptors in pigs are predominately of β1-type, while those of aorta are of %bT2-type; (2) regarding the relative population of adrenoceptors, coronary artery is β-dominant(β/α =11), while aorta is α- dominant (β/α = 0.02); (3) compared withα-adrenoceptors, coronary artery has a greater number of [3H]nitrendipine binding sites (nitrendipine/α-adrenoceptor = 23) than aorta (nitrendipine/α-adrenoceptor = 0.14).

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

We tested the hypothesis that coronary artery blood flow is sufficient to meet myocardial requirements throughout cardiac tamponade in a conscious euvolemic canine model recovered from surgery. Seven mongrel dogs were chronically instrumented to measure ascending aortic blood flow (electromagnetic flowmeter); intrapericardial, right atrial, and aortic blood pressures; regional myocardial blood flow (radionuclide labelled microspheres); and myocardial consumption of lactate, pyruvate, and oxygen. Data were collected during progressive cardiac tamponade induced by intrapericardial saline infusion to the point of hemodynamic decompensation. Decompensated cardiac tamponade (DCT) was defined as a decline in mean aortic blood pressure to 70% of the level present when the pericardia! space was drained of fluid (baseline) and was produced in all animals within 25 minutes. Cardiac tamponade caused a continuous decline in coronary artery blood flow from 1.26 ± 0.35 (baseline, mean ± SD) to 0.53 ± 0.15 ml/min/g (DCT,p<0.01), which was associated with a decrease in myocardial oxygen consumption from 1.26 ± 0.35 (baseline) to 0.74 ± 0.27 ml/min/g (DCT,p< 0.05) and a slight increase in myocardial oxygen extraction from 71 ± 3 (baseline) to 81 ± 4% (DCT,p<0.05). This change in oxygen extraction occurred because of both an increase in arterial and a decrease in coronary venous oxygen content. At all degrees of cardiac tamponade, the lactate-pyruvate ratio did not change significantly from baseline (7.56 ± 2.31), there was no evidence of lactate production, and the normal endocardial to eplcardial blood flow ratio present at baseline (1.41 ± 0.23) was preserved. Although aortic blood pressure was initially well maintained, aortic blood flow declined, and right atrial blood pressure increased continuously as intrapericardial pressure increased. A second group of 2 chronically instrumented animals was prepared to determine whether an adequate coronary vasodilatory reserve was present throughout cardiac tamponade. The reactive hyperemic response to brief coronary artery occlusion (hydraulic occluder) of a large epicardial vessel was measured (Doppler flow probe) in the conscious animal during progressive cardiac tamponade. Although a normal reactive hyperemic response was found at all stages of cardiac tamponade, the peak coronary artery blood flow obtained during reactive hyperemia decreased as intrapericardial pressure increased. Thus, in this conscious canine model of acute progressive cardiac tamponade, despite a continuous decline coronary artery blood flow was always adequate to support aerobic metabolism, and a normal coronary artery vasodilatory reserve was present, even at the time of hemodynamic decompensation. In this euvolemic animal model, myocardial ischemia did not contribute to the deterioration in cardiac function that occurred during acute cardiac tamponade.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Although prolonged functional abnormalities after transient myocardial ischemia have been well described, the interrelationship between postischemic systolic and diastolic alterations remains controversial. Therefore, 24 chronically instrumented conscious dogs were studied with left ventricular and pleural micromanometers, ultrasonic dimension transducers in the left anterior descending (LAD) coronary distribution, and vena caval and coronary artery occluders. The LAD was occluded for 15 minutes and reperfused for 24 hours while vena caval occlusions were performed at intervals to measure myocardial segment length at 0 mm Hg transmural diastolic left ventricular pressure (L0). Coronary occlusion produced an immediate fall in systolic function as assessed by ejection shortening and stroke work and also induced a 16 ± 4% increase in L0, which was termed diastolic creep. Throughout reperfusion, reversal of diastolic abnormalities correlated strongly with recovery of segmental shortening and stroke work(p< 0.001). Correlation between systolic dysfunction and diastolic creep was also observed during alteration of inotropic state by dopamine, during initial reperfusion hyperfunction, and during pharmacologic manipulation of afterload. In 5 additional dog hearts fixed in diastole by rapid glutaraldehyde infusion after coronary occlusion, myocardial creep measured by the segment length transducers paralleled sarcomere elongation measured by electron microscopy. Thus, the direct correlation between diastolic creep and systolic dysfunction throughout reperfusion and during hemodynamic alterations suggests that diastolic properties of postischemic myocardium may not be entirely passive and that systolic and diastolic dysfunction induced by ischemia may have a common basis at the cellular level.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Microvascular reactions to increases in intravascular pressure were studied in the cremaster muscle of the anesthetized rat by enclosing the animal in an airtight box with the muscle exteriorized for observation of the microcirculation. Since the cremaster was exposed to atmospheric pressure, increasing pressure within the box produced equal increases in arterial and venous pressures. Thus, intravascular pressure was altered without affecting the pressure gradient for blood flow. Raising box pressure had no effect on respiration or heart rate and did not change the systemic activity of the sympathetic system, angiotensin II, or vasopressin. Diameters and flows were measured for first (107 ± 3 μm, mean ± SEM), second (87 ± 5), third (29 ± 2), and fourth (15 ± 2) order arterioles during increases in intravascular pressure of +10, + 20, and + 30 mm Hg. No significant changes in the diameters of first or second order arterioles were elicited when pressure was increased. However, when box pressure was increased to +10, + 20, or + 30 mm Hg, a sustained constriction occurred in third (29%, 45%, and 63%, respectively) and fourth (5%, 38%, and 57%, respectively) order arterioles. Blood flow was significantly reduced in all arterioles, and perivascular Po2was decreased adjacent to third and fourth order arterioles. Furthermore, the third order arteriole constrictor response was not abolished by local α-receptor blockade (phentolamine), indicating that it was not mediated by a local sympathetic axon reflex. Collectively, these data indicate that a potent, nonneural, pressure-dependent mechanism for vasoregulation is present in small arterioles of the cremaster. The sustained constriction in the presence of reduced blood flow and reduced periarteriolar oxygen tension indicates that the vascular response is independent of and capable of overriding flow -dependent (i.e., metabolic) control in resting skeletal muscle. The observations are compatible with the operation of a powerful myogenic mechanism in small arterioles.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Cardiac failure appears rapidly during severe hypoxia and precedes a substantial reduction in adenosine triphosphate content. Reduced adenosine triphosphate turnover, in the presence of nearly normal content, may be the metabolic basis for contractile failure during hypoxia. To measure both the myocardial content and the turnover rates of high-energy phosphate compounds during hypoxia, we performed31P-nuclear magnetic resonance studies by placing a surface coil directly over the left ventricle in intubated rats that were instrumented for hemodynamic measurements and ventilated with either 21, 10, or 8% O2. Normoxia produced a hemodynamic and metabolic steady state for 4 hours and hypoxia for at least 60 minutes. Under normoxic ventilation (n= 10, mean ± SD), the arterial Poi was % ± 14, pH 7.38 ± 0.11, and systolic blood pressure 96 ± 8 mm Hg; under hypoxic ventilation with 10% O2(n =5), the arterial Po2was 57 ± 10, pH 7.39 ± 0.09, and systolic pressure 68 ± 10; and under hypoxic ventilation with 8% O2(n= 5), the Po2was 52 ± 7, pH 7.37 ± 0.04, and systolic pressure 51 ± 4. Hypoxic ventilation with 10 or 8% O2decreased the creatine phosphate content from 51.4 ± 5.4 μmol/g dry wt to 39.3 ± 5.4 and 45.6 ± 4.1 and depressed adenosine triphosphate slightly from 25.0 μmol/g dry wt to 21.8 ± 2.1 and 21.9 ± 1.0, respectively. High-energy phosphate turnover, measured as flux through the creatine kinase reaction, decreased from 22.7 ± 6.7 μmol/g dry wt/sec during normoxic ventilation to 13.7 ± 3.6 and 15.9 ± 2.6 during ventilation with 10 and 8% O2, respectively. Thus, the decreased turnover of high-energy phosphate compounds, not their tissue contents, may be the metabolic basis for contractile failure during hypoxia.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID