摘要:

Isolated canine interventricular septa were studied with standard microelectrode tech-niques. Focal automaticity was induced by applying depolarizing current through an extracellular pipet in contact with the right bundle branch (RBB) of the ventricular specialized conducting system. Automaticity appeared with depolarization to transmembrane potentials of −50 mV or less. The spontaneous activity was neither depressed nor accelerated when overdrive suppression was at-tempted. Activity originating within the focus propagated into fully polarized surrounding tissue. However, entrance block, phasically related to the spontaneous cycle length, was an intrinsic property of these foci. Early premature beats initiated outside the focus failed to enter the focus, but the resulting electrotonus delayed the next automatic beat. Late premature beats captured and thereby accelerated the focus. Thus, the automatic foci could be entrained by extrafocal activity. Consequently, continuous pacing at various rates precipitated complex rhythms with fixed coupling. Similar foci with exit conduction, entrance block, and electrotonic modulation also were demonstrated in focally depolarized papillary muscles in feline septal preparations. The unique properties of focally depolarized areas in which spontaneous activity is generated at low membrane potentials provide a mechanism capable of generating a wide array of arrhythmias.Circ Res 47: 238-248, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

To quantify the interaction between epinephrine infusion and carotid sinus baroreceptor reflex control of vascular capacity and resistance, we have simultaneously measured total systemic compliance, Ct, arterial compliance, Ca, changes in “unstressed vascular volume”, ΔV0, and resistance, R, in nine dogs whose carotid sinuses were isolated and cardiac output fixed by a perfusion pump. In response to intrasinus pressures (ISP) of 50, 125, and 200 mm Hg without epinephrine infusion, total systemic compliance (Ct) was 1.00, and 1.10, and 1.22 ml/mm Hg per kg, whereas arterial compliance showed no change and averaged 0.0984 ml/mm Hg per kg for all ISP's. Resistance was 1.45, 0.88, and 0.57 nun Hg/(ml per min per kg) for intrasinus pressure of 50, 125, and 200 mm Hg. The change in unstressed vascular volume from ISP of 50 to 125 was 7.32 ml/kg and 5.03 ml/kg for an ISP change from 125 to 200 mm Hg. When epinephrine was infused at a constant rate of 1.2 μg/min per kg at a fixed ISP of 125 mm Hg, arterial pressure rose by 69.1 mm Hg, the change in unstressed vascular volume was 8.02 ml/kg, and resistance increased from 0.89 to 1.54 mm Hg/(ml per min per kg), an increase of 73% of control. At the same infusion rate and at each ISP of 50, 125, and 200 mm Hg, compliances, Ctand C, and resistance were measured. In contrast to the control data, Ctshowed no increase with changes in ISP (0.92, 0.94, and 0.92 ml/mm Hg per kg), whereas C, measured 0.081 ml/ mm Hg per kg. Resistance was 1.71, 1.46, and 1.19 mm Hg/min per kg for intrasinus pressures of 50, 125, and 200 mm Hg. The change in unstressed vascular volume caused by an ISP change of 50-125 mm Hg was 1.78 ml/kg and for an ISP change of 125-200 mm Hg was 1.30 ml/kg. The data indicate that epinephrine greatly attenuates the reflex control of the vascular properties by mechanisms other than the modification of the carotid sinus receptor characteristics.Circ Res 47: 249-257, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Computations of compliance of the left ventricle (LV) during diastole assume passive tissue characteristics. To evaluate this assumption, we measured diastolic LV intramyocardial pressure simultaneously in the subepicardium and subendocardium in 18 open-chest dogs, using 1-mm in diameter micromanometers. Subepicardial pressure, 26 ± 1 mm Hg (mean ± SKM) exceeded subendo-cardial pressure, 14 ± 1 mm Hg (P< 0.001), and it exceeded left ventricular end-diastolic pressure (LVEDP) (9 ± 1 mm Hg) (P <0.001). After an infusion of dextran-40 (10 dogs), subepicardial diastolic pressure increased to 42 ± 4 mm Hg which was higher than diastolic subendocardial pressure, 26 ± 2 mm Hg (P< 0.001) and LVEDP, 24 ± 2 mm Hg (P< 0.001). Following cardiac arrest (12 dogs) with the intramyocardial probes unchanged in position, LV intracavitary pressure, 9 ± 1 mm Hg, and suben-docardial pressure, 13 ± 3 mm Hg, did not differ significantly from the pressures in the beating heart. Subepicardial pressure, 9 ± 1 mm Hg, was lower than in the beating heart (P< 0.001). Following distension of the arrested LV (12 dogs), subepicardial pressure, 31 ± 7 mm Hg, was lower than both subendocardial pressure, 58 ± 12 mm Hg (P< 0.001) and LV intracavitary pressure, 54 ± 11 mm Hg (P< 0.001). These observations indicate that tone is maintained by the subepicardium during diastole. Furthermore, the LV wall does not appear to behave as a passive shell during ventricular filling.Circ Res 47: 258-267, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We used standard microelectrode techniques to study Tyrode's-superfused human atrial fibers obtained at cardiac surgery. Two types of sustained rhythmic activity occurred. One resulted from slow phase 4 depolarization and had a spontaneous rate = 20-26 beats/min. Epinephrine increased and the slow channel blockers, AHR-2666 (AHR) and verapamil decreased both phase 4 slope and spontaneous rate. Acetylcholine (ACh) and lidocaine decreased the slope of phase 4, but the slowing of rate was less than that induced by AHR and verapamil. Tetrodotoxin (TTX) also decreased the slope of phase 4 and spontaneous rate, to an extent that was intermediate between the actions of AHR-verapamil and ACh-lidocaine. A second type of sustained rhythmic activity was triggered by delayed afterdepolarizations (DAD). DAD amplitude increased as stimulus cycle length decreased and, at critical cycle lengths, DAD initiated trains of spontaneous action potentials at rates > 70 beats/min. Spontaneously occurring DAD were suppressed by AHR and were transiently diminished by ACh. This effect of ACh was accompanied by hyperpolarization of the fibers. DAD also were induced by epineph-rine. These DAD were unaffected by TTX, lidocaine, or ACh and were suppressed by AHR and verapamil. In summary, the slow inward current contributes to the sustained rhythmic activity that occurs with automaticity or DAD in human atrium. A TTX-sensitive current also contributes to automaticity. DAD that occur spontaneously are largely insensitive to the effects of agents that increase K conductance (although ACh has a transient effect) and those that are induced in the presence of epinephrine do not respond to agents which increase K conductance (ACh, lidocaine) or TTX.Circ Res 47: 267-277, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

To study the physiology of the high affinity vascular smooth muscle receptor for angio-tensin II, we have characterized125I-angiotensin II binding sites in a participate fraction prepared from rat mesenteric arteries.1251-Angiotensin II binding was saturable at physiological concentrations of hormone, and was of high affinity. Scatchard analysis indicated a single class of binding sites with an equilibrium dissociation constant (Kd) of 0.91 ± 0.11 (SD) nM, and a total binding capacity of 53.7 ± 3.0 fmol/mg protein. Parallel studies with3H-angiotensin II yielded a similar Kj (1.18 ± 0.48 nM) and total binding capacity (56.8 ± 9.2 fmol/mg protein).mI-Angiotensin II associated with binding sites rapidly (t1/2for association = 4 minutes at 37°C), and reversibly. Kinetic analysis of binding at 22°C by two independent methods yielded comparable values for both the association rate (4.0 and 6.8 x 105/M per sec) and dissociation rate (3.2 and 3.8 x 10−4sec) constants. Equilibrium dissociation constants calculated from kinetic analysis (0.56 and 0.80 nM) were in close agreement with that obtained from steady state Scatchard analysis. Analogues and antagonists of angiotensin II competed for binding in a potency series which exactly paralleled that observed for bioassay systems utilizing pressor response in vivo and vascular smooth muscle contraction in vitro.125I-Angiotensin II binding was stimulated 2-to 3-fold in the presence of 1 nun divalent cations (Mn2+> Mg2+> Ca2+) and reversibly inhibited by EDTA and EGTA. Dithiothreitol (5 mil), a sulfhydryl-reducing agent that has been reported to block vasoconstrictor response to angiotensin II, inhibited125I-angiotensin II binding by 45%. The present study defines specific angiotensin II binding sites in a muscular artery representative of the resistance vasculature. We conclude that these binding sites, unlike those previously described in conductance-type vessels (aorta), have a sufficiently high affinity to interact with physiological levels of hormone.Circ Res 47; 278-286 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Intravenous infusions of angiotensin II were given to conscious sheep. During these infusions, the pressor action of angiotensin was antagonized by concomitant infusion of sodium nitroprusside. Under these conditions, angiotensin produced a dose-dependent tachycardia. This dose-dependent tachycardia was not affected by propranolol and therefore it was not due to an action of angiotensin on sympathoadrenal mechanisms. The dose-dependent tachycardia was reduced by atro-pine, and abolished by increases in systolic pressure. We conclude that iv infusions of angiotensin cause a central, dose-dependent reduction in vagal tone. This action is normally antagonized by the barore-ceptor reflex response to the hypertensive action of angiotensin. Therefore, in those conditions in which endogenous angiotensin production is increased and blood pressure is not elevated (e.g., sodium deficiency and pregnancy), angiotensin may influence heart rate.Circ Res 47: 286-292, 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