摘要:

We induced atrioventricular dissociation and initiated ventricular pacing in intact dogs and isolated cat hearts. Left ventricular pressure, its time derivative (dP/dt), and action potentials were recorded. When a test pulse was introduced at varying intervals after a period of steady pacing, an optimum contractile response was obtained at an average interval of 720 msec. A similar optimum interval was obtained after pacing at various frequencies and after paired pulse stimulation but was shortened to 560 msec after infusion of epinephrine. The magnitude of the optimum contractile response increased with an increase in the frequency of prior pacing which was accompanied by an increase in the time the cell membrane was depolarized. The optimum contractile response following paired pulse stimulation was greater than that following regular pacing, with the same number of stimuli per minute and the same time of membrane depolarization. The results are explicable in terms of intracellular calcium ion recirculation with separate compartments for release to and uptake from the contractile proteins. A negative feedback control of Ca2+inflow to the cell by intracellular Ca2+content is postulated to explain the effect of paired pulse stimulation and shortening of action potential duration following an increase in regular pacing frequency.Circ Res 47: 559-567, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We analyzed brain tissue in 139 rats for adenosine and its metabolites, inosine and hypoxanthine, during the initial 120 seconds of seizures induced by bicuculline. We also measured ATP, ADP, AMP, phosphocreatine (PCr), and lactate. We divided the rats into four groups by adjustment of their preictal arterial oxygen tension: group I, PaO2> 200 mm Hg), adenosine increased within ten seconds of the onset seizures and remained elevated even after 120 seconds. Elevations in inosine and hypoxanthine were delayed compared to the increases in adenosine. A reduction PaO2(50 mm Hg) or systemic blood pressure during seizures caused a further augmentation in the increase brain adenosine levels. During the seizure period, transient changes in adenine nucleotides and energy charge were observed, but PCr remained de-pressed and lactate continued to rise. The rapid sustained increase in cerebral adenosine levels, temporally paralleling the changes in cerebral blood flow, supports role for adenosine the regulation of cerebral blood flow.CircRes 47: 568-577, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied in vitro the effects of heparin on the growth of rat aortic smooth muscle cells. Measurements of growth were monitored by [3H]thymidine uptake and changes in cell number over a period of 3 days. Our results show that heparin—highly anticoagulant or nonanticoagulant—signifi-cantly inhibits growth of smooth muscle cells. We also show that this is a highly specific interaction with regard to molecule and cell type: i.e., other polyanions, except for a low molecular weight dextran sulfate, do not have the same effect on growth, and not all cells are inhibited by heparin; e.g., endothelial cell growth actually is enhanced. After removing antithrombin from our media, we carried out experiments which show that heparin is effective even though thrombin, a potent mitogenic agent, is still present and active. We also found that passing the platelet extract over a heparin column did not remove all of the mitogenic activity of the platelet preparation. Both experiments indicate an inhibitory role for the heparin molecule, per se. Our results support the findines of a recent paper (Guyton et al., 1980) showing that heparin can limit the size of myointimal plaques in rats after carotid injuries by inhibiting smooth muscle cell proliferation.Circ Res 47: 578-583, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The intravenous infusion of high doses of histamine (400 fig base/min) produced only small increases in weight (=+30 g) and lymph total protein concentration (+0.9 g/100 ml) in canine forelimbs perfused at constant inflow. The weight gain was associated with profound decreases in aortic pressure (112 to 30 mm Hg) and in forelimb perfusion pressure (105 to 75 mm Hg) and marked increases in forelimb skin small-vein pressure (from 12 to 25 mm Hg). After treatment with phentol-amine, the intravenous infusion of these doses of histamine under the same conditions produced marked decreases in forelimb perfusion pressure (120 to 60 mm Hg) and failed to increase forelimb skin small-vein pressure, yet still produced only minimal increases in weight (+12 g) and lymph total protein concentration (+0.8 g/100 ml). Following treatment with both phentolamine and propranolol, the intravenous infusion of histamine caused very marked increases in forelimb weight (⋍+75 g) and lymph total protein concentration (+2.9 g/100 ml). These marked increases in forelimb weight and lymph formation were associated with profound decreases in perfusion pressure (112 to 60 mm Hg) but no change in skin small-vein pressure relative to control. These same increases in weight and lymph total protein concentration were observed after treatment with propranolol alone. Thus, treatment with propranolol markedly increased net fluid filtration and protein efflux during intravenous infusions of massive doses of histamine, indicating that this edemogenic agent causes an endogenous release of catecholamines which tend to antagonize the direct actions of histamine on the microvascular mem-brane via stimulation of β-adrenergic receptors.Circ Res 47: 584-591, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The present study evaluated potential mechanisms for the slow length-dependent change in myocardial contractile state. Using 40 isolated right ventricular cat papillary muscles, we found that 10 mM caffeine reversed the subsequent slow change in myocardial performance following a change in muscle length. Since caffeine acts both at the sarcolemma and the sarcoplasmic reticulum, we atten-uated the sarcolemmal influx of calcium with verapamil, manganese, and low external calcium concen-tration. None of these interventions altered the caffeine reversal of the length-dependent effect. It thus appears that the length-dependent alteration of contractile state is of intracellular origin, and probably related to altered calcium handling by the sarcoplasmic reticulum.Circ Res 47: 592-598, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We assessed transmurally the coronary autoregulatory response to elevated perfusion pressure in 85 anesthetized, open-chest dogs. Steady state and transient flow distributions were measured with 9 ± 1 /im radioactive microspheres. Steady state distributions of myocardial blood flow were uniform transmurally(P >0.05) at perfusion pressures of 103 ± 1 (n= 81) and 146 ± 2 (n= 34) mm Hg, whereas Endo:Epi ratios of 1.26 ± 0.05 and 1.51 ± 0.07 at perfusion pressures of 194 ± 1(n= 60) and 221 ± 3 (n= 14) mm Hg, respectively, indicated progressive redistribution(P <0.05) of flow toward subendocardium. As perfusion pressure was increased, autoregulation failed first in subendo-cardium. At high perfusion pressures, subendocardial flow exceeded subepicardial flow (P< 0.05) whether or not subepicardial flow was autoregulated. The initial, transient response to elevation of coronary perfusion pressure from 99 ± 1 to 145 ± 2 (n= 5) mm Hg was an increase (P< 0.05) in Endo: Epi ratio from 1.05 ± 0.06 to 1.30 ± 0.06. By 2 minutes this ratio had returned to near control. In contrast, the initial Endo:Epi ratio of 1.32 ± 0.05 caused by elevation of perfusion pressure to 190 ± 5 (n= 6) mm Hg did not wane (P> 0.05). A selective increase in subendocardial oxygen demand could not explain greater subendocardial flow since (1) elevated perfusion pressure had no effect on aortic and left ventricular pressures, cardiac output, and heart rate, (2) left ventricular oxygen consumption was constant in the presence of preferential subendocardial perfusion, (3) regional myocardial oxygen tension increased in parallel with blood flow to subepicardium and subendocardium. Also, elevated perfusion pressure caused a greater steady state increase in subendocardial flow in four empty, nonworking hearts. The results demonstrate transmural variation in coronary autoregulatory poten-tial; the subepicardial vasculature appears better adapted to autoregulate blood flow at elevated perfusion pressures.Circ Res 47: 599-609, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The objective of these experiments was to better understand the factors responsible for the decline in tension at short sarcomere lengths in cardiac muscle. We measured the effects of variation of extracellular calcium concentration on the sarcomere length-tension relation in thin trabeculae and papillary muscles excised from right ventricles of rats. Sarcomere lengths were measured by optical diffraction. Experiments were carried out using two protocols. In the primary protocol, the muscle was allowed to contract isometrically. The sarcomeres in the central region, shortened and stretched the end regions adjacent to the clips. The sarcomere length was measured at the time of peak tension and plotted against the active tension. In a secondary protocol, the sarcomere length and tension were measured during contractions in which sarcomere length in the central region was held approximately constant. Both protocols were carried out at extracellular Ca2+concentrations ranging from 0.3 to 5.0 IDM. The height of the length-tension curves was progressively depressed as extracellular Ca2+was reduced from 2.5 to 0.3 min; the variation of the shape of the curve was modest. On the other hand, when Ca2+was increased to 5 DM, there was less upward shift of the sarcomere length-tension relation, indicating a tendency toward saturation. The results obtained using the sarcomere isometric protocol were similar to those obtained with the muscle isometric protocol. Extracellular Ca2+appears to act principally as a modulator of the height of the length-tension curve, though it has a modest effect on the shape as well. On the basis of these results, we deduce that several of the factors previously cited as possible explanations of the decline in tension at short sarcomere length are not likely candidates.Circ Res 47: 610-619, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The effect of diabetic metabolism on the human vascular wall was studied, using the fetal cardiovascular system at birth as an experimental model. The ultrastructure of umbilical arteries from nine newborn children of nonsmoking diabetic mothers (White group D) was compared with that of 30 healthy nonsmokers. Intimal cushions, thickening of the basement membrane often with a multilaminal appearance, and glycogen accumulations, both in the cells of the intima and the media, were found. The cells of the intima were very rich in fibrillas, identical to the underlying media myocytes. Endothelial cell death with formation of a pseudoendothelium due to migrating myocytes might be the explanation.Circ Res 47: 620-626, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID