ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

I made a detailed comparative examination of five mathematical models of left ventricular (LV) mechanics: the Laplace model, Lame model, Valanis-Landel model, Rivlin-Saunders model, and a nonhomogeneous version of the Valanis-Landel model. All five models are used to predict LV pressure- volume (P-V) and pressure-wall stress (P-S) behavior using the same geometric and stress-strain data (rat data is used as an example). These predictions are presented in graphical form for comparison with each other and observed LV P-V behavior. The first model, based on the Law of Laplace, uses the thin wall approximation in three distinct ways, and this approximation is not consistent with LV mechanics. The small deformation and linear stress-strain assumptions of the Lame model also are inconsistent with LV mechanics. Two more homogeneous models (Valanis-Landel and Rivlin-Saunders) avoid the errors of the first two. The discrepancy in the predictions of these two models demonstrates that uniaxial stress-strain data of papillary muscle are insufficient to characterize the multiaxial stress- strain behavior of myocardial tissue. Finally, a nonhomogeneous version of the Valanis-Landel model which explores the variation of myocardial stress-strain behavior needed to achieve constant wall stress is presented. Circ Res 46: 321-331, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

To test the hypothesis that ryanodine inhibits the release of contractile Ca2+from intracellular stores, we compared the contractile responses by rabbit, cat, dog, and rat papillary muscles to ryanodine. Results of cumulative ryanodine concentration (10−9to 10−4M) response studies indicate the following order of sensitivity to ryanodine: rat > dog = cat > rabbit which mimics the relative dependence of these species on intracellular Ca2+for force development. In the presence of 2.5 mM [Ca2+]$, cumulative additions of ryanodine or a single exposure to 10−4M concentration produced biphasic contractile responses in rabbit, cat, and dog, but not rat ventricular muscle. The elevation of [Ca2+]oto 5 RIM either antagonized the expression of ryanodine's negative inotropic effect or promoted the positive effect of this agent in all species tested. Ryanodine did produce a biphasic change in contractility in the presence of 2.5 mM [Ca2+]oin K+-depolarized, isoproterenol-restored rat papillary muscles. In addition, prior exposure of rat myocardium to ryanodine (2.5 mM [Ca2+]o) was similar to a decreased [Ca2+]oin that it permitted inotropic agents, such as increased stimulation rates, hyperos- molality, and ouabain to produce positive contractile responses from this tissue. In contrast, the positive response by rat cardiac muscle to paired electrical stimulation is prevented by ryanodine. Ryanodine also accelerated the rest-decay of force development in rat myocardium, suggesting that it increased the rate of loss of calcium from contractile-dependent Ca2+stores. The results are consistent with ryanodine effecting a decreased availability of intracellular contractile Ca2+, perhaps through a diminishment of its release. Circ Res 46: 332-343, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Cardiacβ-ladrenoceptors respond to sympathetic nerve stimulation (SNS), but it is not clear that SNS evokesβ-2adrenoceptor-mediated vasodilation. Sensitivity ofβadrenoceptors to catecholamines and to SNS was evaluated in dogs. Norepinephrine (NE) and epinephrine (E) were equipotent vasoconstrictors (femoral artery blood flow or gracilis autoperfusion pressure) beforeα-adrenoceptor blockade with dibozane (DIB). After DIB, NE was 1/100 as potent a vasodilator as E, which was equipotent with isoproterenol (ISO). SNS evoked gracilis muscle vasoconstriction before DIB and vasodilation after. Dilation induced by SNS or acetylcholine (ACH) after DIB was blocked by atropine (AT), but that caused by NE was not. Dilation evoked by NE, E, or I after DIB and AT was blocked by propranolol (PROP). Vasoconstrictor responses to NE, E, or SNS in dogs without DIB were not augmented by PROP at a dose that blocked the dilator effect of ISO. NE and E were equipotent and both 1/10 as potent as ISO as positive inotropic and chronotropic agents. Cardiac responses to NE, E, ISO, and SNS were antagonized by PROP. Subclassification of adrenoceptors that subserve cardiac stimulation asβ-1and that subserve vasodilation asβ-2was substantiated. Cardiacβ-1adrenoceptors responded to SNS and to circulating E and NE. Vascularβ-2adrenoceptors responded to circulating E, to ISO, and to high doses of NE, but not to SNS.β-2Adrenoceptors in blood vessels appear not to be innervated and may function as hormone receptors sensitive primarily to E released from the adrenal medulla, rather than to NE released from adrenergic nerves.Circ Res 46: 344-352, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Acetylcholine (ACh) and carbamylcholine (Carb) inhibited Ca-dependent action poten- tials and contractions in ventricular muscle from the avian heart. The inhibition by choUnergic drugs was antagonized by atropine (muscarinic) and occurred by two pathways, "indirect" and "direct." Before hatching, ACh had no effect per se, but it inhibited Ca-dependent action potentials that had been augmented by isoproterenol (ISO). This "indirect" pathway for inhibition was detected as early as the 7th incubation day. Acetylcholine had no effect on basal cyclic AMP content, but it reduced cyclic AMP when the nucleotide had been increased by ISO. After hatching, ACh inhibited Ca-dependent action potentials and contractions not only "indirectly" but also "directly." "Direct" inhibition by ACh occurred in preparations treated with 6-hydroxydopamine (or reserpine) and propranolol, so that endogenous cardiac catecholamines probably were not involved. Further, basal levels of cyclic AMP increased after hatching and "direct" inhibition by ACh was associated with a reduction of cyclic AMP. These results are interpreted in a model in which cyclic AMP modulates the permeability of the membrane to Ca2+and in which GTP regulates the β-adrenergic receptor and adenylate cyclase. It is speculated that "indirect" muscarinic inhibition results from interference with GTP-dependent regu- lation of β-adrenergic receptor/adenylate cyclase interaction and "direct" muscarinic inhibition results from interference with GTP-dependent regulation of adenylate cyclase.Circ Res 46: 353-362, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

This study seeks to explain mechanisms responsible for the contour of pressure and flow waves and the pattern of vascular impedance in human systemic arteries. Pulsatile pressure and flow were recorded from the ascending aorta of seven patients undergoing open heart surgery and from the ascending aorta and other arteries of 17 patients at diagnostic catheterization. Ascending aortic pressure/flow relationships in the seven surgical patients were expressed as input impedance to the systemic circulation. Pressure and flow wave contour and impedance results were interpreted with the aid of a multibranched model of the systemic arterial tree, whose parameters could be manipulated to simulate different physiological and pathological conditions. Our data and data previously published on pressure and flow waves and their relationship in human subjects could be explained on the basis of two reflecting sites in the systemic circulation-one representing the resultant of all arterial terminations in the upper part of the body, and the other, some 1.5 times further away, the resultant of all arterial terminations in the lower body. The concept of the arterial system as an asymmetric T tube with two discrete ends has been advanced previously to explain the main features of pressure and flow waves and their relationship in different experimental animals. This concept appears equally applicable to human subjects. Circ Res 46: 363-372, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

This study was undertaken to determine some of the electrophysiological effects of histamine on the coronary arterial vascular smooth muscle of the dog. Transmembrane potentials were recorded from small (<500 μm o.d.) isolated canine coronary arteries with glass microelectrodes filled with 3 M KC1. Histamine (10−6M) increased the resting membrane potential (Em) from -55 to -64 mV and reduced input resistance from 9.8 to 4.0 mO. These effects of histamine were abolished when Mn2+(1 mM) was added to block Ca2+influx.The amplitude, maximal rate of rise, and frequency of the Ca2+-dependent action potential induced by tetraethylammonium ion (TEA) increased in the presence of histamine in a dose-dependent manner (10−7to 10−6M). Also, the effect of histamine on the TEA-induced action potential was inhibited by the H1antagonist pyrilamine maleate (10−7M). When tension was recorded from helically cut strips of coronary arteries, variable results were obtained upon addition of histamine; i.e., some preparations showed no change in tension and others, a small increase. When histamine was added to this preparation in the presence of TEA, tension increased to 60% of the maximum contraction induced by K+. These findings suggest that histamine increases the Ca2+inward current in coronary arterial smooth muscle. The hyperpolarization induced by histamine may be due to an increased K+conductance that is mediated by an increased Ca2+influx, since inhibition of Ca2+influx by Mn2+prevented the hyperpolarization. Circ Res 46: 372-377, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We examined the reflex change in refractory period (RP) of the left ventricle produced by stimulation of the central end of the caudovagal nerve (CVS). RP was recorded in the region of distribution of the left anterior descending coronary artery. During the determination of RP, hearts were paced at cycle lengths between 244 and 315 msec. Initially, the tonic effects of removing vagal and sympathetic influences were determined. Neither right nor left vagotomy nor cardiac sympathectomy (symx) affected RP; however, bilateral vagal block decreased RP by 3 msec, whereas bilateral symx increased RP by 7 msec. Atropine increased RP by 2 msec, probably via inhibition of muscarinic receptors in ganglia. After determination of each of the tonic influences, CVS was performed with pulses of 35-50 Hz, 0.6-1.0 msec in duration, and 1.6-4.0 V. CVS increased RP by 8 msec. Right vagal cold block abolished the response, but left vagal block had no effect. Left symx had no effect on the response, but right symx limited it to 6 msec. Bilateral symx was similar to right symx alone. Subsequent atropine administration blocked 4 msec of the remaining response. Atropine given before symx limited the increase in RP due to CVS to 4 msec. After subsequent right symx, the increase in RP was only 1 msec. Left symx after atropine decreased the response only 1 msec. Total symx after atropine abolished the response. The degree of initial sympathetic activity had no effect on the RP response. We conclude that: (1) the afferent limb of the reflex lies in the right vagus; (2) the dominant efferent reflex path lies in the vagi; (3) the sympathetics have a significant role only when the vagi are blocked; (4) when active, the efferent sympathetic paths course mostly through the right side; (5) the vagi do not require existing sympathetic activity to exert an effect.Circ Res 46: 378-386, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied the structural alterations that follow the application of currents similar to those used in clinical electric countershock procedures in cultured chick myocardial cells. Myocardial cells 48 hours in culture were subjected to electric field stimulation. The cells then were fixed for electron-microscope examination 30 seconds postshock. The ultrastructural alterations that appeared after an 80 V/cm shock included the appearance of >25% of the mitochondria per cell in the "condensed" configuration and mitochondria with swirled or tubular cristae. Large-amplitude swelling of the mitochondria and swollen endoplasmic reticulum also were observed in a few cells. The alterations that appeared after a 200 V/cm shock included contracture and disorganization of the myofibrils, large-amplitude swelling and loss of cristae in the mitochondria, swollen endoplasmic reticulum and nuclear envelope, and intracellular edema. The degree of ultrastructural change was dependent on the intensity of the shock. These structural alterations are consistent with an osmotic imbalance which occurs during a shock-induced prolonged depolarization of the cell membrane (Jones et al., 1978a), possibly due to a transient dielectric breakdown during the shock, and may underlie the arrhythmias and necrosis which often occur after high-intensity clinical and experimental eountershock procedures in vivo. Circ Res 46: 387-394, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Two major groups of renal chemosensory neural elements have been identified in the rat: one specifically activated by renal ischemia, the previously described "R" chemoreceptors, and the other by backflow of nondiuretic urine into the renal pelvis. The latter group is the object of the present investigation. In anesthetized, male Sprague-Dawley rats, single-unit recordings were obtained by dissection of the centrally cut nerves of the right kidney. The responses of single units to backflow into the renal pelvis of nondiuretic urine, diuretic urine, and solutions containing urea, mannitol, or inorganic ions were compared. The excitatory effect of the backflow of nondiuretic urine was due to its chemical composition rather than to changes in pelvic pressure and pelvic distension. The same units were activated markedly by renal ischemia. The resting discharge rate of the units was very high in nondiuretic conditions, and it declined progressively when diuresis was induced by expansion of the extracellular fluid volume. It is concluded that this group of sensory elements responds to the chemical environment in the renal interstitium as modified by ions crossing the pelvic epithelium, by leakage of ions out of ischemic cells, and by alterations in the excretory function of the kidney and renal blood flow. This group of renal sensory nerve endings has been termed "R2" chemoceptive receptors, to distinguish them from the previously described group of renal "R" chemoreceptors. Circ Res 46: 395-405, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID