摘要:

The effects of right vagus nerve stimulation on heart rate were examined in 16 dogs anesthetized with chloralose (60 mg/kg, iv) and urethane (600 mg/kg, iv) after a bilateral cervical vagotomy.Two protocols were followed. In the first, trains of 1, 3, or 5 stimuli, 2 msec each in duration, 10 to 15 v in magnitude, and separated by 10 msec were delivered at predetermined times after “P” wave onset as a single stimulation. In the second, the stimulation was carried out repetitively for 2 minutes at a predetermined frequency. Typically, in the first, the later in the cycle the stimulation occurred, the greater was the prolongation of the included cycle. With one stimulus in the stimulation, a typical P-P interval was 574 msec with a “P” to stimulation delay of 4 msec, and 620 msec when the “P” to stimulation delay was 200 msec. With five stimuli moving the stimulation through a range of 200 msec, the change in P-P interval was 150 msec. There was a functional dependence of the P-P cycle length on the time of arrival of the inhibitory pulse. The slope of this relationship is a function of the number of stimuli in the stimulation.With repetitive stimulation in the second protocol, there were zones wherein the heart rate synchronized to the vagal stimulation rate not only at the fundamental frequency but also at harmonics and subharmonics. This range of entrainment was also dependent upon the number of stimuli in the stimulation. The data suggest the possibility of phase shift as a mechanism for vagal regulation of heart rate.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

The anticholinesterase agents, physostigmine, neostigmine, and diisopropylfluorophosphonate were studied for their effect on the vasoconstrictor responses of perfused mesenteric arteries of rat produced by stimulation of their sympathetic postganglionic nerves. The experiments were performed at 30°C. All three anticholinesterase drugs greatly potentiated the vasoconstrictor response to nerve stimulation at a frequency of 1/sec, increased it less at a frequency of 2/sec, and still less at a frequency of 3/sec. At a frequency of 6/sec, there was practically no increase. The infusion of physostigmine potentiated slightly the response to injected norepinephrine, whereas the infusion of neostigmine or diisopropylfluorophosphonate did not alter the response to injected norepinephrine. The increase in response to adrenergic nerve stimulation produced by anticholinesterase agents was interpreted to be due to the inactivation of cholinesterase, thereby causing an increased accumulation of acetylcholine which in turn liberated more norepinephrine from the sympathetic postganglionic fibers.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

Repeated high-pressure injection of saline into the arterial system via carotid cannula in normal, ether-anesthetized rats has been previously shown to produce acute necrotizing lesions in the renal vasculature. In this study administration of the vasodilator aminophylline prior to high-pressure injections led to similar lesions, produced in dilated, hyperdistended vessels, at far lower pressures than in control animals, demonstrating that neither vasoconstriction nor the absolute height of blood pressure is a critical determinant in production of lesions. In the second part of the study previous treatment with desoxycorticosterone (DOCA)-saline for 12 to 18 days rendered the renal vasculature abnormally prone to lesions after high-pressure injections, compared with normal rats so injected or those receiving a DOCA-saline regimen only. Glomerular lesions were more severe than can be explained on the basis of simple addition of the lesions resulting from high-pressure injections to those arising from DOCA administration. This increased susceptibility of the vasculature to elevated pressure is probably a function of focal alteration of vascular smooth muscle. These observations support the proposal that hypertensive vascular lesions occur in dilated, hyperdistended vessels and the glomeruli distal to them, the dilatation probably resulting from focal smooth muscle alteration with partial or complete loss of contractility.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

The oxygen tension (Po2) on the external surface of arterioles between 8 and 100μ in diameter was measured with oxygen microcathodes (2 to 6μ diameter) in the suffused cheek pouch of hamsters and in the cremaster muscle of hamsters and rats anesthetized with pentobarbital and urethane. Intravascular Po2was measured in 10 vessels and compared with extravascular Po2. Good agreement was found, with a mean difference of 1.4 ± 0.8 (SE) mm Hg. Significant longitudinal gradients were observed in periarteriolar Po2. Oxygen tension fell from 35 ± 4 mm Hg on the small arteries (ca. 80μ diameter) to 20 ± 3 mm Hg at the end of the terminal arterioles. These measurements were obtained with a suffusion solution Po2of 39 ± 8 mm Hg, a tissue Po2of 8 ± 2 mm Hg and femoral arterial blood Po2of 69 mm Hg. When the suffusion solution Po2was raised to 79 mm Hg, the resultant measurements were 42 ± 3 on the small arteries and 21 ± 3 mm Hg at the end of the terminal arterioles. Similar experiments were carried out while animals were breathing 95% oxygen and the Po2of the cheek pouch suffusion solution was 39 mm Hg. Under these conditions, small artery Po2was 152 ± 13 mm Hg and terminal arteriolar Po2was 37 ± 9 mm Hg. Femoral artery blood Po2was 427 ± 12 mm Hg. These data are consistent with the hypothesis that oxygen diffuses from the precapillary vessels and that intravascular Po2falls progressively along the resistance vessels. This finding suggests a possible mechanism for the involvement of O2in local regulation of blood flow.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

The phenomenon of the “gap in atrioventricular conduction” was studied in eight human subjects, using a catheter technique for recording electrical activity of the His bundle. Premature atrial stimuli were applied throughout the basic atrial cycle, either during sinus rhythm or atrial pacing. As the coupling interval between the basic (A1) and premature (A2) atrial depolarizations was decreased, a point was reached where A2was no longer conducted to the ventricles. The region of conduction block was localized distal to the His bundle. The interval between basic and premature His bundle depolarizations at which block occurred provided a value for the effective refractory period of the His-Purkinje system. If A2was then made to occur earlier in the basic cycle, a point was reached where conduction of the premature response to the ventricles resumed. When this occurred, conduction delay of A2in the atrioventricular node had increased sufficiently to allow for recovery of excitability of the His-Purkinje system (the interval between successive His bundle depolarizations was greater than the effective refractory period of the His-Purkinje system). The gap phenomenon could be abolished by decreasing the basic cycle length or by beta-receptor blockade, both of which prevented conduction block of A2in the His-Purkinje system.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

Asynchrony of conduction may prove to be an important mechanism for reentrant arrhythmias. The purpose of these experiments was to explore asynchronous conduction in the distal branches of the canine Purkinje system. Microelectrodes were placed in Purkinje bundle preparations resembling a T configuration, thereby permitting assessment of differential conduction times induced by premature beats (S2).Equal conduction depression was observed in the post extrasystolic beat (S1at wide coupling intervals (S2-S1). Asynchrony of conduction was frequently observed in response to narrow coupling intervals. These differential conduction times induced disparities of activation times greater than 50 msec. In fibers exhibiting preferential depressed conduction, local block was observed with further decrease in the coupling interval. Disparities of activation times at very short S2-S1coupling times could be markedly increased by minimal decrease in coupling intervals (in the order of 1 to 5 msec). Conduction depression was not clearly dependent upon the level of “take-off” potential or action potential duration. Asynchronous conduction may thus be induced by narrow coupling of premature beats and could account for reentry.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

Chronic left ventricular overload and left heart failure were produced by an aortic-left atrial shunt and superimposed aortic constriction. With the shunt alone, plasma renin activity and sodium balance were normal. Superimposed aortic constriction produced a further elevation in left ventricular end diastolic pressure (LVEDP), increased plasma renin activity and sodium retention occurred. Seven dogs died in pulmonary edema within a week, but nine others recovered with a return in plasma renin activity and sodium excretion to normal. Five of these nine dogs that survived the acute effects of aortic stenosis developed pulmonary edema at least 7 days after aortic constriction; LVEDP was markedly elevated, plasma renin activity was high and sodium retention occurred. Six other dogs with chronic left ventricular overload, but not retaining sodium, were given deoxycorticosterone acetate (DOCA), 15 mg/day, to study the response in renal sodium excretion. In two of the dogs, LVEDP was below 35 mm Hg and the normal “escape” pattern, characterized by return of sodium excretion to the normal control level, was observed. However, in the other four animals, LVEDP was above 35 mm Hg, escape failed to occur and marked sodium retention resulted; a further elevation of LVEDP was observed and pulmonary edema occurred on four occasions. The failure of dogs with marked elevation of LVEDP to escape from DOCA indicates that other factors in addition to the renin-angiotensin-aldosterone system are involved in the sodium retention of left ventricular failure.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID