ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

In isolated right atria of the rabbit heart, we studied the activation pattern within the sinus node, using the microelectrode technique. After the electrophysiological experiments, the prep-arations were subjected to a correlative morphological investigation, using light or electron microscopy. Different criteria for defining the dominant pacemaker were compared. A group of at least 5000 cells, located within the central part of the node where the most characteristic tissue architecture was found, was considered to be responsible for generation of the impulse. At the ultrastructural level, this leading cell group appeared to be part of a larger uniform cell group. The number of gap junctions observed suggests that all nodal cells are coupled by these structures. Toward the periphery, the excitation wave was propagated preferentially in an oblique cranial direction toward the crista terminalis. Neither morphologically nor electrophysiologically specific pathways were found for the conduction, but the preferential direction could be explained by the tissue architecture. Circ Res: 46:11-22, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The contraction elicited by norepinephrine (NE) and histamine (H) in the rabbit aortic strip occurs after a shorter latency and increases at a higher initial velocity to a greater steady state level when drug entry is limited to the intimal compared with the adventitial surface. Differences in the steady state contraction, but not in latency or initial velocity, disappear when intramural disposition pathways of the two agonists are blocked pharmacologically by deoxycorticosterone and a combination of iproniazid and 17-β-estradiol, respectively. These and other observations are consistent with the hypothesis that inner vascular smooth muscle cells respond more than outer cells to submaximal concentrations of NE and H, an explanation that accounts for the persistence of differences in latency and initial velocity of response after disposition blockade. Although the effectiveness of disposition mechanisms in reducing agonist concentration may be uniform through the aortic medial thickness, because of differences in muscle sensitivity, the consequence of disposition on the contractile response to agonists entering through the adventitia would be greater than that through the intima. Thus, disposition mechanisms in the outer smooth muscle lamellae provide a functional barrier to susceptible agonists entering through the outside vessel wall surface. Circ Res 46: 22-28, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Coronary vessels have β2-adrenergic receptors, but their role in distributing flow across the ventricular wall independently of cardiac metabolic and mechanical factors that influence coronary resistance is unknown. We studied the working heart of open-chest dogs and measured blood flow with radioactive microspheres in four layers across the left ventricular wall before and during β2-receptor activation by intracoronary infusions of salbutamol or isoproterenol. Myocardial β1, receptors were blocked with practolol, and aortic pressure, heart rate, and myocardial oxygen consumption were prevented from changing significantly. β2activation produced a progressively greater increase in flow from the subendocardiumtothe subepicardium with a decrease in the subendocardial:subepicardial (I:O) ratio from 1.40 to 1.00. Coronary resistance decreased progressively from the subendocardium to the subepicardium. To assess the influence on the above results of the transmural redistribution of flow that normally is developed by myocardial contraction in the working heart, similar experiments were conducted in the empty beating heart. A two-step vasodilation with salbutamol decreased the I:O flow ratio from 1.76 to 1.40 and then to 1.27. Coronary resistance decreased from the subendocardium to the subepicardium during both steps of vasodilation. For comparable increments of flow, the decrease in the I:O flow ratio in the empty beating heart was smaller than that in the working heart. These results indicate that the activation of coronary β2receptors redistributes flow toward the subepicardium by producing a larger vasodilation in this region independently of the metabolic and mechanical influences of heart contraction on coronary resistance. This effect is enhanced in the intact heart by the transmural gradient of resistance to flow produced by cardiac contraction.Circ Res 46: 29-36, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We induced experimental concussive brain injury by a fluid percussion device in anesthetized cats equipped with a cranial window for the observation of the pial microcirculation of the parietal cortex. Brain injury resulted in transient but pronounced increases in arterial blood pressure and in sustained arteriolar vasodilation associated with reduced or absent responsiveness to the vasoconstrictor effect of arterial hypocapnia and with reduced or absent ability of the vessels to undergo autoregulatory vasodilation in response to reductions in arterial blood pressure. Such vessels had reduced resting oxygen consumption in vitro. Electron microscopic examination of the same vessels that were studied physiologically disclosed the presence of discrete endothelial lesions consisting of either vacuolization or crater formation. Occasionally there was extensive destruction and necrosis of the endothelial cells. There was little or no morphological evidence of vascular smooth muscle damage. There was a close association between the presence of endothelial lesions and vessel dilation and unresponsiveness, suggesting a causal relationship. In cats in which the transient posttraumatic hypertensive episode was prevented, the vessels retained their normal caliber, remained normally responsive, and had no endothelial lesions. The results show that the vascular lesions in the pial microcirculation following this type of brain injury are due to the rise in arterial pressure. Circ Res 46: 37-47, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied the effects on sinus rate and atrioventricular (AV) conduction of electrical stimulation from a 12-polar electrode catheter advanced into the right pulmonary artery of 21 anesthetized dogs. In each experiment, the distal tip of the electrode catheter was positioned at a standard fluoroscopic site, and a sequence of bipolar electrograms was recorded during sinus rhythm from the 11 adjacent catheter electrode pairs using a standardized technique. Within each sequence of electrograms, a characteristic change in the polarity of the atrial complexes was identified at a site in the proximal right pulmonary artery. This recording site was labeled the site of initial polarity transition. Stimulus-strength response testing was performed from each catheter electrode pair during spontaneous sinus rhythm and during atrial fibrillation sustained by rapid atrial pacing. The least stimulus strengths required to slow sinus rate or to depress AV conduction were obtained using an electrode pair at a proximal right pulmonary artery site identified as the optimal stimulation site. This stimulation site was at, or immediately proximal to, the recording site of initial polarity transition. Stimulation distal to the site of initial polarity transition precipitated atrial fibrillation using stimulus strengths which were very low compared to stimulus strengths required to precipitate atrial fibrillation at more proximal sites. Negative chronotropic and negative dromotropic effects persisted throughout 5-minute periods of stimulation from the optimal stimulation site and could be modulated by varying stimulus parameters. Using neurophysiological and neuropharmacological techniques, we demonstrated that these effects were produced by stimulation of preganglionic parasympathetic efferent nerve fibers. Circ Res 46: 48-57, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We determined quantitatively the importance of vasopressin (AVP) release in the regulation of arterial pressure during hemorrhagic hypotension in dogs. The recovery of arterial pressure after rapid hemorrhage was studied in 10 dogs with spinal cord destruction below the level of C-l to remove efferent sympathetic nerve activity. Bilateral nephrectomy was used to remove the reninangiotensin system. Results for this group were compared to those for another group of dogs in which the entire central nervous system, including the pituitary gland, were removed surgically. In all groups, arterial pressure was lowered rapidly from an average control value of 106 ± 2 (mean ± SE) to 51 ± 1 mm Hg by hemorrhage. In dogs with spinal cord destruction and bilateral nephrectomy, arterial pressure rose from 51 mm Hg to 89 ± 3 mm Hg in 3 minutes and stabilized at that level over the next 30 minutes, representing a 71% compensation of arterial pressure. Left atrial pressure fell from 3.3 to 0.8 mm Hg during hemorrhage and subsequently rose only 12% during the hemorrhage. Plasma AVP rose during hemorrhage from 19 ± 2 to 75 ± 10 μU/ml. Injection of the competitive AVP inhibitors, [1-deaminopenicillamine, 4-valine]-8-D-arginine-vasopressin (dPVDAVP), completely reversed the effects and returned the compensated pressure to 50 mm Hg. In the complete absence of the central nervous system, arterial pressure compensation averaged only 10 ± 3%. Plasma osmolality, sodium and potassium concentrations, hematocrit, and heart rate were unchanged in all experimental groups. The relationships involved in the AVP-arterial pressure control system were determined quantitatively and analyzed. A systems analysis using experimentally determined values for AVP secretion and metabolism, plasma AVP, and changes in arterial pressure closely predicted the changes observed during hemorrhage. It appears from this study that AVP has potent systemic vasoconstrictor actions enabling it to make a significant contribution in the restoration of arterial pressure during hemorrhage. Circ Res 46: 58-67, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied the effects of preload on transmural myocardial perfusion and coronary pressure-flow relationships in mongrel dogs. The left circumflex (LC) artery was cannulated and perfused through an external circuit of rigid tubing originating in the left subclavian artery and containing an electromagnetic flowmeter (EMF), a solenoid, and a short segment of soft tubing which could be occluded. The solenoid, triggered by the R-wave of the ECG, was adjusted so that perfusion occurred only during diastole. Autoregulation was abolished by maximal vasodilation with carbocromen. In 16 dogs, overall radioactive microsphere flow in the perfused LC segment was 1.67 ± 0.17 (SKM) ml/min per g at normal preload and 1.54 ± 0.19 ml/min per g at elevated preload. The endocardial: epicardial flow ratio decreased from 0.76 ± 0.03 at normal preload to 0.55 ± 0.04 at elevated preload (P< 0.01). EMF pressure-flow curves, determined by stepwise constriction of the perfusion circuit in the same dogs, showed a rightward shift with increased preload and an increase in PZF, the pressure at which inflow became zero (12 ± 0.9 nun Hg at normal preload vs. 19 ± 1.0 mm Hg at elevated preload,P< 0.01). Microsphere pressure-flow curves in eight additional dogs suggested that a small endocardial: epicardial difference in diastolic PZF at normal preload is accentuated at elevated preload. We conclude that effects of increased preload produced by volume expansion are 2-fold: (1) a selective reduction of flow in the inner layers of the heart, and (2) a shift to the right of the diastolic pressure-flow relationship. The former seems reasonably related to direct effects of preload on intramyocardial tissue pressure, whereas the latter suggests additional effects of local reflex, myogenic or mechanical phenomena. Circ Res 46: 68-77, 1979

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We stimulated the aortic chemoreceptors in dogs that were anesthetized with chloralose and artificially ventilated by perfusing the isolated aortic arch with venous blood. Inotropic responses were determined by measuring the maximum rate of change of left ventricular pressure (dP/dt max) with aortic pressure and heart rate held constant. Stimulation of the aortic chemoreceptors resulted in an average increase in heart rate of 14 ± 2.0 beats/min (mean ± SE) from 166 ± 7.7 beats/min and an increase in dP/dt max of 501 ± 85 mm Hg/sec from 3508 ± 154 mm Hg/sec. These changes were statistically significant (P< 0.001). The afferent pathway of the reflex was shown to be in the vagus nerves and the efferent pathway in the cardiac sympathetic nerves. In some of the dogs, the carotid chemoreceptors were also stimulated. This resulted in decreases in heart rate and dP/dt max of 48 ± 24 beats/min and 795 ± 142 mm Hg/sec. Thus we have shown that stimulation of aortic chemoreceptors evokes chronotropic and inotropic responses opposite to those evoked from stimulation of carotid chemoreceptors. Circ Res 46: 77-83, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The thromboresistance of 13 potentially blood-compatible polymers was assessed in sheep by determining survival of5lCr-labeled platelets. Polymer tubing (120-150 cm x 2.0-2.3 mm i.d.) coiled around the neck was incorporated into the circulation through silicone rubber connectors as a carotid artery-external jugular vein shunt. The mean platelet half-life in control animals ("shunt control") was 78.2 ± 2.8 (SEM) hours. Eleven of the 13 polymers tested significantly shortened platelet half-life. Polyvinyl chloride (T½= 45.4 ± 3.0 hours), polyperfluoro ethylene (T½= 47.0 ± 1.6 hours), and a polymethyl acrylate (PMA)/acrilonitrile copolymer (T½= 50.7 ± 7.0 hours) produced the greatest shortening. Only silica-free polydimethyl siloxane (T½= 74.7 ± 4.9 hours) and PMA (T½= 81.5 ± 3.4 hours) were indistinguishable from shunt controls. Pretreatment of PMA tubing with autologous plasma in a paired trial significantly increased platelet half-life (P< 0.05 vs. untreated PMA). This system offers an economical, reproducible, sensitive, and biologically relevant method for assessment of the reactivity of artificial surfaces with platelets. Circ Res 46: 84-90, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID