摘要:

Consideration of muscle energetics suggests that the ventricle has a very definite optimum range of operating wall tensions, and that clinical advantage can be gained by maintaining the tension within this range. Circ Res 46:161-166, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

In man, therapeutic doses of imipramine suppress ventricular arrhythmias, and toxic doses can cause severe intraventricular conduction disturbances and cardiac arrest. To determine the cellular mechanisms responsible for these actions, we studied the effects of imipramine hydrochloride at concentrations from 3 x 1<T8to 3 x 10~6g/ml on the transmembrane potentials of sheep and calf Purkinje and ventricular muscle fibers using standard microelectrode techniques. All imipramine-induced changes in transmembrane potentials became more marked with increasing concentration. At 1 x 10"' g/ml (a low therapeutic concentration in man), imipramine shortened the Purkinje fiber action potential (18%) and reduced upstroke velocity slightly (6%). At 1 x 10"6g/ml (a high therapeutic or toxic concentration in man), imipramine reduced the upstroke velocity of Purkinje fiber action potential by 23% and of ventricular muscle by 53%; conduction velocity fell by 26%. In Purkinje fibers, imipramine at 1 x 10~6g/ml suppressed spontaneous firing elicited by isoproterenol and hypokalemia, due to a +7.9-mV shift in threshold voltage with little or no effect on spontaneous phase 4 depolarization. Depression of action potential phase 0 and action potential shortening may play a role in the antiar-rhythmic effect of imipramine at therapeutic concentrations. At toxic imipramine concentrations, depression of phase 0 is marked and can account for the potentially fatal conduction defects and arrhythmias seen during imipramine toxicity in man. Circ Res 46:167-175, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Pulmonary leukostasis, as a result of complement activation, has been invoked as a cause of pulmonary dysfunction. To investigate this phenomenon, we studied the pulmonary response to infusion of autologous complement-activated plasma in sheep and rabbits. Complement activation was produced by plasma incubation with zymosan. Leukopenia, with selective loss of polymorphonuclear leukocytes into the lungs, occurred in all animals immediately after the onset of plasma infusion. Complement-activated plasma infusion in sheep produced a significant fall in the arterial Po2and a marked rise in pulmonary vascular resistance, whereas no such effects were observed in rabbits. Pretreatment of the sheep with sulfinpyrazone eliminated the pulmonary response to complement-activated plasma without altering the leukopenic response. Pulmonary histology in rabbits and sheep confirmed the presence of intracapillary leukostasis after the plasma infusions, whether or not sulfin-pyrazone had been administered previously. The pulmonary response to complement activation is associated with pulmonary capillary leukostasis, but leukostasis alone is not an adequate explanation of the phenomenon. Circ Res 46:175-180, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Splanchnic nerve stimulation (SNS) mobilizes up to 25% of the total blood volume from the splanchnic venous bed, constricts the splanchnic arterioles, and releases catecholamines and renin. This study examines the effects of these changes on cardiac preload, afterload, and output in cats anesthetized with chloralose. Before adrenalectomy, SNS caused increases in right atrial and arterial pressures and cardiac output, but total peripheral resistance did not change. After adrenalectomy, SNS increased right atrial pressure, arterial pressure, and peripheral resistance, but cardiac output did not change. It is concluded that adrenal catecholamines are necessary for an increased cardiac output during SNS. After adrenalectomy and elimination of the baroreceptor reflexes, SNS still caused no increase in cardiac output. When the increases in arterial pressure were prevented by nitroprusside infusions or by opening an arteriovenous (A-V) shunt, SNS caused an increase in cardiac output even though the increase in right atrial pressure was much smaller than before. The results are quantitatively described by the Frank-Starling relationship between stroke work and right atrial pressure and are interpreted as follows. Venoconstriction alone causes an increase in cardiac output with a minimal rise in cardiac preload (right atrial pressure). However, if afterload (systemic and pulmonary arterial pressures) increases, this reduces the increase in cardiac output causing a further rise in preload. The rise in preload tends to restore cardiac output but is limited by pooling of blood elsewhere in the venous system (about 4 ml/kg for each 1-mm rise in right atrial pressure). A new equilibrium is then reached between preload, afterload, and cardiac output. Thus, this study demonstrates the interaction between preload and afterload in the control of cardiac output. Circ Res 46:181-189, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

In 10 dogs, we placed a Doppler flow probe, an ameroid constrictor, and a hydraulic cuff occluder around the left circumflex coronary artery (CA). Ultrasonic dimension gauges were implanted in control segments (CS) and ischemic segments (IS) of the left ventricle (LV). A microtransducer was used to measure LV pressure (LVP). Sixteen to 35 days later, when CA occlusion was nearly complete and collaterals had developed, the dogs were studied by telemetry during exercise, while running behind a van (8-11 mph for 3.5 minutes). Control exercise and exercise after propranolol (P) (average dose 0.5 mg/kg, iv) were conducted on the same day 2 hours apart. During control exercise, significant increases occurred in heart rate (HR) (116-249 beats/min), LVP (124-163 mm Hg), end-diastolic pressure (EDP) (8.1-25.9 mm Hg), peak (+)dP/dt (3618-7348 mm Hg/sec), and percent shortening (%AL) of CS (19.7-28.8) (allP< 0.01), but percent systolic wall thickening (%AW) and %AL of IS decreased greatly [22.2 ± 3.8 to 5.1 ± 1.3% (P< 0.01) and 12.6 ± 2.1 to 7.1 ± 2.4% (P< 0.01), respectively]. During matched exercise periods after P, significantly less marked increases occurred in HR (101-182 beats /min), LVP (123-139 mm Hg), EDP (9.4-20.9 mm Hg), peak (+)dP/dt (2801-4312 mm Hg/sec), and %AL of CS (17.1-22.4%) (allP< 0.01). However, %AW and %AL of IS did not deteriorate [19.0 ± 3.6 to 14.3 ± 3.2% (NS) and 11.3 ± 3.1 to 11.5 ± 3.9% (NS)]; both were significantly different from control exercise (P< 0.01). It is concluded that amelioration by propranolol of an exercise-induced myocardial oxygen demand-supply imbalance in a collateral-dependent zone can markedly reduce regional ischemia and dysfunction at the same exercise level. Circ Res 46:190-200, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied the effects of hypoxia on the electrical activity and ultrastructure of pacemaker cells of sinoatrial nodal tissue excised from rabbit heart. The slope of slow diastolic depolarization was markedly reduced within 15-20 minutes after gassing Tyrode's solution with nitrogen, whereas other action potential parameters were not much affected. At 60-90 minutes in the hypoxic solution, the maximum diastolic potential decreased by 13 mV, and the peak potential decreased to −5 mV, but abbreviated action potentials continued to occur for another 30-60 minutes. After 60-90 minutes of hypoxia, reoxygenation did not produce complete recovery of the action potential. In glucose-free solution, action potentials ceased within 40 minutes of hypoxia, but reoxygenation restored electrical activity. A good correlation was found between the duration of hypoxia and the extent of ultrastructural change in sinoatrial nodal cells. After 15-20 minutes of hypoxia, mitochondria showed decreased electron density of their matrix and loss of intramitochondrial particles. The glycogen content was reduced. After 60-90 minutes of hypoxia, further changes in the mitochondria occurred: clearing of the matrix, fragmentation of cristae, rupture of the outer membrane, and formation of myelin figures. Glycogen had almost completely depleted after reoxygenation. These changes were partly reversible except for the glycogen content. Our results provide electrophysiological evidence that cells in the sinoatrial nodal tissue can withstand long exposure to hypoxia, using energy produced by the anaerobic glycolytic pathway. Circ Res 46: 201-213, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Collateral blood flow was studied in chronically instrumented awake dogs 11-12 weeks after implantation of ameroid constrictors on the right and left circumflex coronary arteries. Using 7-10 fim radionuclide-labeled microspheres, transmural myocardial blood flow was measured during resting conditions and at similar heart rates during ventricular pacing and treadmill exercise. The absence of significant myocardial fibrosis was verified histologically. Control transmural flow was distributed normally in all dogs. In five dogs a marked maldistribution of flow occurred in the collateral region during pacing and exercise. During pacing, flow to the epicardial layers increased while flow to the endocardial layers was unchanged, resulting in a marked endocardial perfusion deficit. During exercise, flow increased substantially to all transmural layers, but the endocardial perfusion deficit remained. Mean transmural blood flow increased similarly in the collateral and noncoUateral regions during pacing; however, during exercise, mean flow in the collateral region was significantly lower than in the noncollateral region. These data demonstrate that the collateral vessels became flow limiting and functioned inadequately during tachycardia produced by pacing and exercise; i.e., a marked perfusion deficit occurred in the endocardial layer. Blood flow to all layers in the collateral-dependent region was higher during exercise than during pacing, possibly due to exercise-induced vasodilation of the collateral channels. Circ Res 46: 214-220, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied the effect of acute hypoxia on pulmonary conversion of angiotensin I to II in anesthetized dogs. When arterial Poswas decreased from 86 ± 14 (SD) to 33 ± 8 mm Hg without changing pH or Pco2, the single passage conversion of intravenous boluses of radiolabeled angiotensin I in tracer doses fell significantly (P< 0.005) from 72 ± 4 to 67 ± 6%. The effect of comparable levels of hypoxemia on the conversion of continuous intravenous infusions of pharmacological doses (1000 times physiological) of angiotensin I was greater: from 55 ± 14 to 33 ± 13% (P< 0.025). There was prompt return of percent conversion ratios to control levels when hypoxemia was reversed. We conclude that acute hypoxia is associated with a reversible decrease in pulmonary angiotensin converting enzyme availability. Circ Res 46: 221-226, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We used intracellular microelectrodes to study the effect of changes in extracellular calcium ion concentration [Ca2+]oon the transmembrane potentials of canine cardiac Purkinje fibers in control Tyrode's solution and in the presence of agents thought to modify membrane permeability to potassium. In Tyrode's solution, decreasing [Ca2+]ofrom 2.7 to 0.9 mM increased action potential duration measured at 60 mv (APD «,) and at full repolarization (APDioo) but did not significantly modify the normal linear relationship between cycle length and APD between cycle lengths of 500 to 4000 msec. We used 9-aminoacridine (9-AA) to decrease potassium permeability. At concentrations between 0.01 and 1.5 x 10"5M, 9-AA caused a concentration-dependent increase in APD-Mand APD1Oo and a significant increase in the slope of the line relating APD to cycle length. The usual effects of changes in [Caz+]oon APD were potentiated by 9-AA. We then used lidocaine (L) to increase potassium permeability. At concentrations between 0.75 and 1.5 x 10~5M, L significantly increased the slope of the line relating APD and cycle length. In the presence of L an increase in [Ca2+]oincreased both APD_eo and APD,oo, and a decrease in [Ca2+]odecreased both parameters. 9-AA thus potentiated and L reversed the effects of changing [Ca2+]oon APD. The results suggest that changes in [Ca2+]omodify repolarization by modifying both slow inward current and potassium permeability and that the extent to which the latter changes can determine the effect of [Ca2+]oon APD. Ore Res 46: 227-236, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We administered a high cholesterol diet to racing greyhounds and studied its effects on the characteristics of carotid sinus reflex control of arterial pressure-flow relations. Dogs were anesthetized with halothane, and pressure and flow were simultaneously measured in the ascending aorta and the celiac, mesenteric, renal, and iliac arteries. The carotid sinuses were isolated bilaterally and perfused with a physiological salt solution under controlled conditions. The variation of regional pressure-flow relations and regional vascular resistance was assessed as a function of mean carotid sinus pressure (MCSP) with the vagi bilaterally sectioned to eliminate aortic arch afferents. Some differences were found in set point (i.e., MCSP = mean arterial pressure) values of hemodynamic variables; cardiac output and renal and iliac flows were significantly lower. Control and set point values of mean arterial pressure were not significantly different between the two groups. The variation of every hemodynamic variable with the exception of heart rate with carotid sinus pressure was attenuated markedly in the diet-treated dogs. Substantial lesions were found involving the entire carotid sinus region of every diet-fed animal. These results suggest that pathological alterations in the carotid sinus region are at least in part responsible for a reduction in the sensitivity of carotid sinus baroreflexes associated with atherosclerosis. Circ Res 46: 237-244, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID