摘要:

In the controversy about the mechanisms determining the high zero flow pressures and the further interpretation of coronary diastolic pressure flow relations, this paper takes a stand in favor of intramyocardial compliance as the primary cause of the high zero flow pressures. An attempt has been made to estimate the compliance distribution within the coronary circulation and to show the specific effect of intramyocardial compliance on arterial and venous pressure-flow relations. Since no data are available on the distensibility of coronary arterioles and capillaries, these data were taken from studies on mesenteric vessels. Based on these data, it is shown that, depending on the transmural pressure, smooth muscle tone may either increase or decrease arteriolar compliance. A compliance distribution has been proposed based on assumed pressure, volume, and distensibility distributions. For all but the venous division of the circulation, experimental data on volume could be found in the literature. Based on this compartmental analysis, it is predicted that overall intramyocardial compliance may exceed epicardial arterial compliance by a factor 45. The literature presenting functional evidence for intramyocardial compliance effects has been reviewed. Experimental results on venous outflow during long diastoles have been analyzed. Pf=0 coronary pressure at zero flow, is higher when measured later in diastole. It is shown that this may be explained by charging of intramyocardial compliance in the period before flow ceases. The discrepancy between results on pressure-flow relations in the fully dilated bed and autoregulated bed are related to the differences in pressure, resistance, and compliance distributions.

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The immediate reduction of renal blood flow and glomerular filtration rate in response to intravenous infusion of leukotriene C4in the rat prompted an analysis of isolated rat renal glomeruli for the presence of specific receptors for leukotriene C4. Specific binding of [3H]leukotriene C4to glomeruli increased in a time-dependent manner, reached equilibrium after 60 minutes of incubation at 4±C, and was 80% reversible upon addition of excess unlabeled leukotriene C4at equilibrium. Specific binding of [3H]leukotriene C4to glomeruli increased in a dose-dependent manner, approaching saturation at concentrations of 40–60 nM. Inhibition of binding of [3H]leukotriene C4with increasing concentrations of unlabeled leukotriene C4was dose dependent. The equilibrium dissociation constant for [3H]leukotriene C4binding to glomeruli, calculated from saturation and competitive binding-inhibition studies, was 25 ± 7 nM and 35 ± 16 nM (mean ± sem), respectively, and glomerular leukotriene C4receptor density was 8.5 ± 1.5 and 9.0 ± 3.0 pmol/mg protein, respectively. The other natural vasoactive sulfidopeptide leukotrienes, leukotriene D4 and leukotriene E4, the chemotactic agent, leukotriene B4, and the sulfidopeptide leukotriene antagonist, FPL 55712, competed for the receptor at concentrations 2–3 orders of magnitude higher than the homoligand, leukotriene C4. The binding and specificity characteristics of the glomerular leukotriene C4receptor are similar to those previously reported for the DDT1 nonvascular smooth muscle cell line derived from hamster vas deferens, for guinea pig ileum smooth muscle, and for a subcellular fraction of rat lung homogenate, and represent the first characterization of such a receptor in a vascular tissue.

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Kinetics of sarcomere movement were studied in real-time by laser diffraction. Instantaneous sarcomere shortening was measured during afterloaded twitches simultaneously with instantaneous shortening and tension of the whole trabecula excised from rat right ventricle. Resting sarcomere length at optimal length was 2.20 ± 0.02 μm (mean ± sem). Maximum amplitude of sarcomere shortening was 0.30 ± 0.01 and 0.16 ± 0.01 μm, respectively, in twitches loaded with preload only, and in “isometric” twitches. When the isotonic load (expressed as a percentage of maximum isometric force TF) increased, the maximum velocity of sarcomere relaxation max Vr (μm/sec) decreased: max Vr = −4 exp (−2.5 ± 10–2 % TF);r= 0.95. The time course of sarcomere relaxation appeared to be progressively delayed when the total load increased from preload only up to “isometric” load. Sarcomere relaxation occurred in two successive exponential phases, a rapid phase [time constant (msec):r1] followed by a slower one (time constant.r2). When the total load increased,r1increased andr2decreased according to the linear relations: % TF = 0.2r1+ 4.8 (r= 0.83) and % TF = −0.1r2+ 157 (r= 0.95). The relative predominance of both the time course and the amplitude of these two phases depended upon the level of total load. The rapid process predominated at low load, the slow one at high load. The role of load and/or shortening in the time course of these two phases is discussed.

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

We established, for the isolated, isovolumically beating canine left ventricle, a comprehensive description of postextrasystolic contractile strength (dP/dtmax) as a function of extrasystolic and postextrasystolic stimulus intervals. In contrast to previous studies of postextrasystolic beats in in situ hearts, these isolated ventricles contracted isovolumically so that dP/dtmax was not affected by fluctuations in preload and afterload and was therefore considered to be a reliable index of intrinsic contractility. With the interval preceding extrasystoles constant, postextrasystolic contractile strength increased monoexponentially to a plateau as the interval preceding postextrasystoles lengthened, with a mean time constant (±sd) of 182 ± 44 msec (n= 53). The onset of this increase in postextrasystolic contractile strength coincided with repolarization of the extrasystolic action potential. With the interval preceding postextrasystoles held constant and long (1200 msec), postextrasystolic contractile strength decreased according to a monoexponential function as the interval preceding extrasystoles lengthened [mean time constant (±sd) of 176 ± 18 msec (n= 10)]. These phenomena could be quantitatively summarized by a single equation description of postextrasystolic contractile strength which involved monoexponential functions with one time constant. The mathematical form of this description led us to a simple interpretation of these phenomena in terms of currently proposed excitation-contraction coupling models of the heart.

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

To examine the interaction between normal and nonischemic areas of the left ventricle during acute ischemia, we implanted midwall ultrasonic segment length gauges in the ischemic zone and in nonischemic areas of the canine left ventricle. During acute ischemia, end- diastolic pressure and segment length in the nonischemic areas increased. There was no change from control in the segment length at the time of aortic valve opening and closure. Thus, in nonischemic areas, total segment shortening, as measured by the percent change in segment length from the time of end-diastole to aortic valve closure, increased. This was due to an increase in isovolumic shortening (end-diastole to aortic valve opening) with no change in ejection shortening (aortic valve opening to closure). The progressive increase in isovolumic shortening in nonischemic areas over time was directly paralleled by the progressive development of the isovolumic lengthening or bulge in the ischemic zone. Nonischemic areas, whether adjacent, on the opposite wall, or distant to the ischemic zone, all behaved similarly. Adrenergic blockade did not qualitatively alter these findings. We conclude that acute ischemia induces a mechanical disadvantage which is greater than just the loss of contractile function by the ischemic segment. Despite the apparent hyperfunction of nonischemic areas, the increased total segment shortening is expended in stretching the ischemic zone during isovolumic systole. As a result, there is no significant “compensatory” increase in ejection shortening in nonischemic areas. The results from the present study indicate that augmented total segment shortening in nonischemic areas is due to a combination of the Frank-Starling mechanism and regional intraventricular unloading of the nonischemic into the ischemic areas.

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

In urethane-anesthetized rats, electrophysiological recordings of spontaneously active neurons in the vasopressor area of the rostral ventrolateral medulla were analyzed for participation in cardiovascular regulation. A total of 138 units were found which were inhibited by transient increases in mean arterial pressure elicited by intravenous injection of norepinephrine, aortic occlusion, or electrical stimulation of the hypothalamus, with 100% inhibition occurring at 148 mm Hg. Histograms of postsystolic activity showed that these units had pulse-synchronous rhythms which grew more prominent as arterial pressure increased. Furthermore, electrical stimulation of the superior laryngeal nerve, which elicited a vasodepressor response, strongly inhibited these units. Thus, these neurons were termed negatively correlated cardiovascular units. At least half of these cells project to or through the thoracic spinal cord. In addition, arterial pressure sensitivity is conveyed through carotid sinus and aortic arch afferents. Approximately half of the cardiovascular units are also excited by hypothalamic stimulation. Finally, analysis of neighboring cells showed that it is possible to distinguish between cardiovascular and respiratory units. These data are consistent with the concept of a medullary center which supports tonic sympathetic vasomotor tone and which mediates baroreceptor reflexes, as well as vascular responses of the defense reaction.

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The kinetics of thallium exchange in cultured rat myocardial cells were studied and compared to those of potassium in the same tissue. Studies were carried out using low concentrations (10 nM to 5 μM) of thallium-204, approximating those likely to be encountered during clinical myocardial scintigraphy. Both thallium uptake and release could be described by a single exponential with a half-time of exchange which was approximately half that of potassium and which was largely independent of extracellular thallium concentration. Some 60% of thallium uptake occurred via an “active” or ouabain-inhibitable mechanism which, in the absence of extracellular potassium, could be activated by low concentrations (10 nM to 5 μM) of thallium. The apparent Km for thallium on this active transport mechanism was 2–7 μm. Increasing extracellular potassium from 0–10 mM caused significant, concentration-dependent decreases in both the total and the active component of the thallium influx. Similarly nonradioactive thallium (0.10 μM to 0.10 mM) caused a concentration-dependent decrease in active potassium influx. Analysis of these results by both Lineweaver-Burk plots and Dixon plots confirmed competitive inhibition, potassium on thallium influx and vice versa, for the active component of the fluxes, and noncompetitive in the remainder. These findings indicate that active transport accounts for the greater portion of the influx of thallium and potassium, and that this active transport occurs via a common mechanism. If, as the results suggest, the receptor for thallium and potassium is the same, then the analysis by Dixon plots would indicate that the affinity of the receptor for thallium is 260 to 900 times greater than for potassium. This would therefore explain the rapid accumulation of thallium-201 by the myocardium, in vivo, from the low circulating concentrations of the isotope.

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Volume densities of mitochondria, myofibrils, and unspecified cytoplasm were measured by ultrastructural morphometry in myocardium from dogs, rats, hamsters, mice, and in biopsied tissue from human hearts. Human myocardium was composed of 23% mitochondria, 59% myofibrils, and 18% cytoplasm. Volume densities for mitochondria were 22% for dogs, 28% for rats and hamsters, and 32% for mice. Myofibrillar volume densities were highest in dogs with 63%, 57% for rats and hamsters, and 49% for mice. Differences were significant between all except man and dog, and rat and hamster. In an extensive analysis of canine myocardium, it could be shown that the quantitative composition of tissue from the left ventricular free wall (anterior, lateral, posterior) and the papillary muscles was identical. There were also no differences between subepi- and subendocardium as well as the midmyocardium. Volume densities from longitudinal sections were identical to those from transversal sections. Fixation with glutaraldehyde by perfusion or immersion provided identical results. There were no differences between volume densities in samples from the left ventricular free wall (anterior, lateral, and posterior) in rats, hamsters, and mice. It is concluded that each mammalian species is characterized by a very typical quantitative composition of the myocardium. The increase in mitochondrial volume correlated well with the increase in heart rate and oxygen consumption in smaller animals. These quantitative data are regarded as the morphological correlate of the differing functional capacity of hearts from different species.

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Cells from the neural crest over occipital somites migrate to the heart, where they give rise to parasympathetic postganglionic neurons as well as ectomesenchymal elements which contribute to conotruncal septation. With a microcautery needle, the neural crest over occipital somites was ablated bilaterally in chicken embryos at an early stage of development. Histological examination on incubation day 15 revealed conotruncal malformations, involving malformation or absence of the conotruncal septum in all embryos. Two peaks of embryo mortality were observed. One peak (incubation days 6–8) occurred at the same time as conotruncal septal closure; the second peak (incubation days 11–13) was concurrent with the onset of functional parasympathetic innervation. A disruption of parasympathetic innervation was indicated by: (1) a decrease in acetylcholinesterase staining, (2) a decrease (27%) in the number of ganglion cells in the conotruncus, (3) decreases in the acetylcholine content of atrium (31%) and ventricle (39%), and (4) a decrease (21%) in muscarinic acetylcholine receptor density on incubation day 15. Radio-labeled ligand-binding studies revealed no change in the affinity of cardiac muscarinic receptors for [3H]methylscopolamine (KD = 0.17 − 0.21 nM). Agonist-binding affinity and sensitivity to guanine nucleotides were similarly unaffected. The reasons for the limited extent of the parasympathetic lesion are unclear, but may involve recruitment of precursor cells from other regions of the neural crest, partial regeneration of the neural crest following surgical removal, or an alteration in the contribution of incoming sympathetic or preganglionic parasympathetic elements. No such plasticity was associated with neural crest contributions to the structural development of the conotruncus. Malformations were observed in all lesioned embryos.

ISSN:0009-7330    

出版商:OVID    

年代:1985

数据来源: OVID