摘要:

We studied the mechanism of post-overdrive suppression in superfused rabbit sinus node pacemaker cells. Small specimens of sinus node tissue isolated from rabbit hearts were driven at a fast rate (overdrive) for 10-120 seconds using single sucrose gap methods. During the control perfusion (35 °C Tyrode's solution), overdrive caused a progressive decrease in maximum diastolic potential (MDP), overshoot (OS), and maximum rate of depolarization at phase 0 [dV/dt)max]. After cessation of the overdrive, the rate of diastolic depolarization decreased, and the spontaneous activity was suppressed temporarily (post-overdrive suppression). MDP, OS, (dV/dt)m.«, and the spontaneous activity returned within a few seconds to the level observed before overdrive. Atropine (2 x 10−6g/ml) did not influence the effects of overdrive. After ouabain administration (3 x 10−7g/ml) or in low temperature perfusate (25°C), the effects of overdrive were accentuated, and a marked suppression of spontaneous activity with a long pause of over several seconds was seen following the overdrive. These results suggest that the post-overdrive suppression of sinus node is attributable, at least in part, to ionic shifts following overdrive, and may be potentiated by metabolic dysfunction of pacemaker cells. Circ Res 46: 90-99, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The purpose of this study was to determine if autonomic nerve interventions exerted quantitatively dissimilar effects on recovery properties of endocardium compared with epicardium. Effective refractory periods (ERP) were measured by the extrastimulus technique in the endocardium and epicardium of the canine left ventricular anterior wall. The basic train and premature stimuli were administered to the endocardium and overlying epicardium via different poles on the same multipolar needle electrode, using cathodal stimuli. Sympathetic augmentation produced via bilateral carotid arterial occlusion or electrical stimulation of right, left, and both sympathetic nerves shortened ERP. Bilateral sympathetic denervation prolonged ERP. The changes in ERP of the endocardium were no different than were changes in the ERP of overlying epicardium. In separate studies, electrical stimulation of the cervical vagi prolonged ERP similarly in epicardium and endocardium. Pacing at slower rates or physostigmine administration potentiated the ERP prolongation in endocardium similar to epicardium. Augmented sympathetic tone produced by carotid occlusion also potentiated prolongation of ERP by vagal stimulation. The percent change in endocardial sites was slightly but significantly less than in epicardial sites. ERP prolongation due to vagal stimulation was attenuated markedly after sympathectomy and abolished with both propranolol and atropine. We conclude that, in the normal anterior left ventricular myocardium of the dog, sympathetic augmentation shortens ERP in epicardial sites equivalent to that in the underlying endocardial sites, that vagal nerve stimulation prolongs ERP in epicardial sites equal to or slightly greater than in the underlying endocardial sites, and that vagal stimulation antagonizes background sympathetic activity. Circ Res 46: 100-110, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied the pulmonary vascular response to hypoxia and associated transvascular flux of fluid into the lungs of newborn lambs. After a 2-hour baseline period, 14 unanesthetized lambs, 1-3 weeks old, breathed 10-12% oxygen in nitrogen for 3-6 hours. We measured steady state lung lymph flow, pulmonary arterial and left atrial pressures, blood flow to the lungs, and the concentration of protein in lymph and plasma. As Pao2decreased from 81 ± 3 torr to 32 ± 1 torr, pressure in the pulmonary artery almost doubled, left atrial pressure was unchanged, and pulmonary blood flow increased by 14%. Calculated pulmonary vascular resistance increased by 69%. Contrary to results of previous experiments performed with mature sheep, lymph flow increased by 80%, and the concentration of protein in lymph decreased during hypoxia. These results suggest that hypoxia increased the pulmonary transvascular gradient of hydraulic pressure in the lambs, increasing filtration of fluid into the lungs. Possible explanations are that pulmonary vasconstriction during hypoxia (1) occurred distal to the sites of transvascular fluid flux or (2) redistributed the increased blood flow to fewer lung vessels, thereby increasing intravascular pressure at the sites of fluid exchange. Postmortem lung blood content was significantly less than that of control lambs, but there was no difference in extravascular lung water content or lung histology, suggesting that pulmonary lymph flow kept pace with transvascular filtration of fluid and prevented pulmonary edema. The concentration of protein in lymph relative to that in plasma decreased with hypoxia, and the ratio of [albumin] to [globulin] in lymph was unchanged, indicating that sustained alveolar hypoxia of this magnitude had no demonstrable effect on the sieving characteristics of the pulmonary endothelium of the lambs.

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We used standard microelectrode techniques to record delayed afterdepolarizations (DAD) induced by ouabain (2 x 10−7M) in isolated canine Purkinje fibers (PF) and studied the response of DAD to the fast Na+channel blocker, tetrodotoxin (TTX, 1 mg/liter); the slow channel blocker, verapamil (verap, 1 mg/liter); the putative Ca2+blocker, AHR-2666 (AHR, 45 mg/liter); and lidocaine (lido, 4 mg/liter), which increases steady state outward current and decreases background inward current. PF were driven at cycle lengths of 1000-200 msec. Ouabain superfusion for 30 minutes induced DAD with amplitudes of 17.0 ± 1.5 (mean ± SE) mV at a cycle length of 200 msec. TTX, verap, AHR, and lido all depressed DAD amplitude (P< 0.05). To intercompare the effects of the drugs, graphs were constructed relating DAD amplitude to basic cycle length, and the relative magnitude of effects of the drugs on DAD amplitude at all cycle lengths was tested using a nested analysis of variance. The effects of verap and AHR were equivalent, and both decreased DAD amplitude more at short (to 37% of ouabain control) than at long (to 76%) cycle lengths (P< 0.05). Lido had a different effect and decreased DAD nearly equivalently at short (to 64%) and long (to 75%) cycle lengths. The actions of TTX were intermediate between-and significantly different from-those of the other drugs (P< 0.05). AHR and verap appear to act similarly, by modifying the current responsible for DAD, whereas lido appears to act by a different mechanism, perhaps by increasing steady state outward current. The actions of TTX may be a result of its effect on the transient inward current or on a background current carried by Na+. CircRes 46: 117-124, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We investigated the mechanism(s) responsible for the decreased cardiac output during continuous positive-pressure ventilation (CPPV). Seven dogs were anesthetized with chloralose-urethane, intubated, and ventilated using a volume ventilator. We measured heart rate, stroke volume, and the determinants of stroke volume: left and right ventricular end-diastolic volumes, isovolumic and ejection phase indices of myocardial contractility, and pulmonary and systemic arterial pressures. Myocardial blood flow was estimated using radioactive microspheres. Variables were measured during a control period of intermittent positive-pressure ventilation (IPPV), 8-20 minutes after the initiation of CPPV using 12 cm H2O positive end-expiratory pressure (PEEP), and 8-20 minutes after the removal of PEEP. CPPV decreased cardiac output but did not affect total or regional myocardial blood flow or the ratio of subendocardial to subepicardial blood flow. Isovolumic and ejection phase indices of myocardial contractility, heart rate, and systemic arterial pressure did not change during CPPV. Right and left ventricular end-diastolic and end-systolic volumes decreased markedly during CPPV. We conclude that CPPV decreases cardiac output in accordance with Starling's law by decreasing preload. Circ Res 46: 125-132, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Dobutamine, a recently synthesized catecholamine, was developed as an agent which would produce increased inotropy in low cardiac output states without major changes in heart rate, cardiac rhythm, or peripheral vascular resistance. However, the effect of dobutamine on the capacitance vasculature is unknown. Since alterations of systemic vascular capacity influence venous return and hence cardiac output, we performed the present study. The muscular capsules of the canine spleen make them representative of the capacitance vasculature. We weighed exteriorized canine spleens continuously in 26 anesthetized dogs. Dobutamine infused for 15 minutes at 4 and 16 μg/kg per min was associated with decreases in splenic weight of 15 ± 2% (SEM) (P< 0.0005) and 33 ± 2% (P< 0.0001) from controls of 249 ± 27 g and 313 ± 42 g. Dobutamine-induced splenic contraction was abolished by phenoxybenzamine but not by propranolol. Injections of dobutamine into the splenic artery produced significant decreases in splenic weight without any change in systemic hemodynamics. In six additional dogs with ganglionic blockade and supported by total cardiopulmonary bypass, decreases or increases in vascular volume were recorded as changes in oxygenator volume. Dobutamine infusion at 30 μg/kg per min for 10 to 24 minutes in these dogs was associated with decreases in vascular volume of 259 ± 28 ml (P< 0.0001). Selective blockade revealed the dobutamine effect to be mediated by α-adrenergic receptor stimulation alone. Thus, in the intact animal, the administration of dobutamine should increase venous return and hence cardiac output through an α-adrenergic-mediated decrease in systemic vascular capacity. Circ Res 46:133-138, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Moderate and severe levels of experimental valvular aortic stenosis (VAS) were produced in anesthetized, open-chest dogs to determine the effects of VAS on subepicardial (EPI) and subendo-cardial (ENDO) blood flow, O2extraction, and O2consumption (MVO2). Regional flow was determined by microspheres, and O2saturation and extraction were analyzed by a three-wavelength absorbance microspectrophotometric method. Left ventricular pressure-volume work increased by 49% in moderate and 135% in severe VAS. The ENDO:EPI flow ratio averaged 1.21 ± 0.09 in controls and decreased to 0.90 ± 0.16 in moderate and 0.89 ± 0.09 in severe VAS, and coronary flow increased by 40% and 58%, respectively. O2 extraction increased with both moderate and severe VAS, with extraction being higher in the ENDO than the EPI. MVO2increased more in severe VAS than in moderate VAS. The ENDO: EPI MVO2 ratios fell to 1.10 (moderate) and to 0.84 (severe) from 1.44 in controls. We conclude that the O2supply and consequently the MVO2became limited in the ENDO relative to that in the EPI by simultaneous limitation of the O2extraction reserve and the blood flow to this region during the increased O2requirements imposed by experimentally induced VAS. Circ Res 46: 139-145, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Angiotensin II is more potent as a vasopressor than angiotensin III when given intravenously. We tested the hypothesis that differential changes in mesenteric blood flow contribute to this difference in potency. The effects of angiotensin II and angiotensin III on mesenteric blood flow were compared in 31 dogs anesthetized with pentobarbital. These agonists were administered either as bolus injections (10-160 pmol) or as constant infusions (30 pmol/min per kg) directly into the vasculature supplied by the superior mesenteric artery. Approximately equipressor doses of angiotensin II (40 pmol/min per kg) and angiotensin III (80 pmol/min per kg) also were given intravenously. On the basis of duration and graphic integration of the response in mesenteric blood flow, but not on the basis of absolute change in amplitude, angiotensin II was consistently more potent than angiotensin III as a mesenteric vasoconstrictor. The intra-arterial and intravenous constant infusion doses were repeated after the administration of meclofenamate (4 mg/kg, iv). Meclofenamate did not alter any of the responses to angiotensin II or angiotensin III. We conclude that the differential constrictor properties of these compounds in the mesenteric vasculature contribute to the greater potency of intravenously administered angiotensin II on arterial pressure. The results provide no evidence for an interaction between prostaglandins and the vasoconstrictor properties of angiotensin II or III in the intact mesenteric vasculature of the anesthetized dog. Circ Res 46:146-151, 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