摘要:

ABSTRACTWe have tested the widely accepted hypothesis that digitalis, in nontoxic concentration, can act directly on cells of the sinoatrial pacemaker to cause slowing. The effect of autonomic nerves on sinoatrial cells was eliminated either by chronic cardiac denervation or by use of autonomic blocking agents such as atropine, 0.5 mg/kg, and propranolol, 2 mg/kg, or MJ‐1999, 3 mg/kg. When the effects of autonomic nerves were eliminated, acetylstrophanthidin, 0.120 mg/kg, failed to cause slowing of sinus rate in the anesthetized cat and the anesthetized dog. Similarly, ouabain, 5 × 10−7m, and acetylstrophanthidin, 1.5 &mgr;g/ml, after prior administration of autonomic blocking agents failed to cause slowing of the isolated rabbit right atrium perfused with Tyrode's solution. These results indicate that the sinus slowing caused by cardiac glycosides may be mediated entirely by alteration of the neural control of the heart and that the drug, in nontoxic concentration, does not have a direct negative chronotropic action on the mammalian sinoatrial node.

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

ABSTRACTThe quantitative importance of total systemic autoregulation in the whole body was studied in dogs in which the cardiovascular control loops of the central nervous system were eliminated by decapitation and alcohol destruction of the spinal cord. Transient changes in cardiac output, right atrial pressure, oxygen consumption, arteriovenous oxygen difference, and hematocrit that occurred immediately after single‐step changes of 25 to 50 mm Hg in arterial pressure were followed by gradual return of the variables toward control values. The time required to reach a new steady state ranged from 13 to 75 minutes with an average of 35 minutes. The calculated open‐loop gain of the autoregulation control system ranged from 0.93 to 9.5 with an average gain of 3.32 ± 0.7 (se) indicating more than 75% compensation. In a second group of animals the arterial pressure was increased from 50 mm Hg to as high as 150 mm Hg in small steps of 10 to 15 mm Hg allowing 5 to 20 minutes on each step for the autoregulation response to occur. The pressure‐flow curves showed significant total systemic autoregulation. The return of arteriovenous oxygen difference and oxygen consumption toward control values is consistent with a metabolic mechanism of autoregulation. The absence of significant transcapillary fluid flux in autoregulating preparations indicates (a) that the locus of autoregulatory resistance changes is completely or almost completely in the precapillary vessels of the circulatory system and (b) that autoregulation is important in maintaining capillary pressure at a normal level as well as in maintaining blood flow at the level required by the tissues.

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

ABSTRACTHighly flexible model red cells were molded of acrylamide gel and suspended in a mixture of castor oil and diiodomethane to produce a neutrally buoyant fluid suspension in which the particles behaved mechanically very much like living erythrocytes. The various suspensions were permitted to flow down long cylindrical tubes while measurements of flow rate and pressure drop were made for various concentrations. The fluid suspensions were found to exhibit non‐Newtonian viscous behavior which agrees very well with that of whole blood under comparable conditions. The fluid suspensions also exhibited a yield stress below which particle motion ceases. The yield stress was found to depend strongly on particle concentration, as is the case for whole blood.

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

ABSTRACTIncorporation of tritiated leucine into myocardial proteins was inhibited at low concentration by quinidine, procaine amide, and diphenylhydantoin, but not by lidocaine or propranolol. This inhibition could be demonstrated in vitro and when the animals were treated with these agents. The relationship between this finding and myocardial depression produced by these antiarrhythmic agents is not known but may reside in general depression of cellular metabolism and protein synthesis or in inhibition of synthesis of a specific membrane carrier protein.

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

ABSTRACTThe evidence supporting the hypothesis that adenosine is the mediator of metabolic regulation of coronary blood flow was obtained from experiments characterized by myocardial hypoxia. If adenosine serves the role of physiological regulator of coronary blood flow, it must also be released by the normal heart. Experiments designed to study this question were performed on 15 open‐chest dogs in which adenosine was sought in perfusates of the epicardial surface of the well‐oxygenated heart. The pericardial space was perfused with warm (37°C) Tyrode's or Krebs‐Henseleit solutions (400 to 1200 ml over 1 to 3 hours), and the perfusates were analyzed for adenosine. With a normal myocardial oxygen supply, adenosine was present in the perfusates in a concentration of 3.1 ± 0.5 × 10−8m. Partial asphyxia, induced by reducing pulmonary ventilation, significantly (P≤ 0.02) increased the adenosine concentration of the perfusates to 5.4 ± 0.8 × 10−8m. In four dogs the normal pericardial fluid was found to contain adenosine in a concentration of 10.9 ± 2.9 × 10−7m, which probably represents the basal extracellular adenosine concentration in the myocardium. The results indicate that the normal myocardial cells release adenosine continuously into the surrounding interstitial fluid, and it is suggested that the level of the interstitial fluid concentration of adenosine probably regulates coronary blood flow to maintain the oxygen balance of the myocardium.

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

ABSTRACTCardiac responses to supramaximal electrical stimulation of postganglionic sympathetic nerve fibers were studied in 17 lambs, 10 hours to 3 days of age. In all lambs left ventricular contractility increased within 3 seconds and was unaltered by atropine, ganglionic blockade, or nerve sectioning proximal to the stimulating electrodes but was abolished by beta‐receptor blockade. The responses were repeatedly demonstrated in two lambs subjected to bilateral adrenalectomy. Acidemia (pH 6.9) produced by lactic acid infusion failed to diminish the inotropic responses. Intravenous or left atrial injections of tyramine produced chronotropic and inotropic responses comparable to sympathetic nerve stimulation. Glucagon, 50 to 200 &mgr;g/kg, failed to elicit cardiac responses in lambs from 1 to 60 days of age. It is concluded that sympathetic neural mechanisms may strongly influence myocardial contractility in the newborn lamb and that these responses are independent of adrenal medullary release of catecholamines. These findings further suggest that the lamb possesses a myocardial adenyl cyclase system that responds only to catecholamines and may be blocked with propranolol.

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

ABSTRACTThe mechanisms by which the catecholamines and glucagon increase myocardial contractility were investigated by studying the effects of cyclic 3′;, 5′;‐AMP, epinephrine, and glucagon on calcium accumulation by a microsomal fraction of canine myocardium thought to represent sarcoplasmic reticulum, and by assaying the microsomal fraction for adenyl cyclase activity. Each agent produced a concentration‐dependent increase in calcium accumulation. Moreover, adenyl cyclase, an enzyme activated by epinephrine and glucagon and responsible for the production of cyclic 3′;, 5′;‐AMP, was present in the microsomal fraction. Its specific activity and responsiveness to epinephrine and glucagon were similar to that previously found in sarcolemmic fractions. The beta‐receptor blocking agent propranolol abolished the activation of adenyl cyclase and increase in microsomal calcium accumulation produced by epinephrine, but was without effect when these same changes were produced by glucagon. These findings are consistent with the hypotheses that: (1) the positive inotropic effects of epinephrine and glucagon may occur as a result of an augmentation of the sarcotubular calcium pool(s); and (2) this effect is mediated, at least in part, by an elevation of cyclic 3′;, 5′;‐AMP levels produced by activation of an adenyl cyclase localized to the sarcoplasmic reticulum.

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID

摘要:

ABSTRACTTransmembrane potentials of A‐V nodal cells in isolated rabbit hearts were recorded while the route of entry of atrial activity into the A‐V node was changed by stimulating the atrium at a high, constant rate on either the crista terminalis or the interatrial septum. Atrial activity arising from the interatrial septum provided a less effective input to the A‐V node, as shown by the occurrence of 2:1 A‐V conduction block, compared to 1: 1 during driving on the crista terminalis at the same rate. The amplitude and rate of rise of the action potentials of most A‐V nodal cells was smaller during driving on the interatrial septum, and many cells developed a larger or smaller “hump” in the repolarization phase, which was absent during stimulation on the crista terminalis. The pattern of A‐V nodal excitation during stimulation on the crista terminalis was similar to that during spontaneous sinus rhythm, but was profoundly altered during stimulation on the interatrial septum. The results can be explained by assuming that an atrial wave front coming from the interatrial septum excites the atrial margin of the A‐V node asynchronously, resulting in inhomogeneous conduction within the node, causing longitudinal dissociation. The results show that successful propagation through the A‐V node is at least partly determined by the direction of the atrial wave front. This factor may play an important role during atrial fibrillation.

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1969

数据来源: OVID