ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

Intracellular microelectrodes and small unipolar leads applied to the endocardial surface of the right atrium in vitro were used to study the complex extracellular wave patterns recorded from the neighborhood of the cardiac pacemaker during spontaneous activity. Sinus activity propagated slowly toward the site of atrial invasion on the venous border of the crista terminalis. Atrial activation was marked by a primary negative wave that appeared 20–40 msec after pacemaker firing. Two sources of complex multiphasic waves were found. First, potentials from transitional sinus tissue propagated toward the atrium and caused low-voltage waves that preceded and slurred the onset of the atrial initial negativity. Second, bundles and layers of the crista terminalis muscle were excited asynchronously around the invasion region, as if cross-connections were infrequent. Waves originating from this source occurred after the firing of the invasion site. No extracellular wave could be associated with the firing of the true pacemaker cells. The sinoatrial ring bundle (SARB) yielded a discrete biphasic deflection along most of its way toward the coronary sinus. This potential appeared most frequently after that of the adjoining crystal muscle, raising questions about the functional role of the SARB as an internodal preferential pathway.

ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

The goal of this study was to determine if physiological levels of cardiopulmonary vagal afferent activity modulate carotid chemoreceptor and baroreceptor reflexes. In anesthetized, ventilated dogs, the aortic nerves and the cervical sympathetic trunks were cut, and atropine was administered so that vagotomy would interrupt only cardiopulmonary afferent impulses. Reflex vascular responses were observed in perfused gracilis muscle and hindpaw. Carotid chemoreceptors were activated with nicotine or hypoxic, hypercapnic blood; carotid baroreceptors were stimulated by changes in carotid pressure. Interruption of vagal afferents augmented reflex vascular responses during changes in carotid pressure from 75 to 125 mm Hg. Interruption of cardiopulmonary vagal afferents potentiated reflex vasoconstrictor (muscle), vasodilator (paw), and vasopressor responses to activation of the carotid chemoreceptors. The potentiation of the chemoreceptor reflex frequently occurred in the absence of increases in base-line vascular resistance. Vagotomy also potentiated ventilatory responses to stimulation of the carotid chemoreceptors in spontaneously breathing dogs. The results indicate that interruption of cardiopulmonary afferents potentiates the vascular and ventilatory responses to activation of the carotid chemoreceptors and augments the gain of the carotid baroreceptor reflex at low carotid pressures. These findings suggest that physiological levels of cardiopulmonary vagal afferent impulses suppress carotid baroreceptor and chemoreceptor reflexes through an interaction in the central nervous system. The suppressive effect on the chemoreceptor reflex may be distinct from tonic restraint of the vasomotor center by vagal afferents, since it involves sympathetic vasodilator as well as vasoconstrictor responses and may occur without suppression of base-line adrenergic constrictor tone.

ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

Recent reports have indicated that vascular responsiveness can be altered by exogenously administered or endogenously released prostaglandin. Furthermore, in certain tissues inhibitors of prostaglandin synthesis have been shown to limit the increase in blood flow in response to bradykinin and to enhance the reduction in blood flow in response to angiotensin and norepinephrine. These findings suggest an important local circulatory role for prostaglandins. We attempted to implicate further prostaglandins in local blood flow regulation by examining the effects of indomethacin (IND) and 5,8,11,14-eicosatetraynoic acid (ETA), inhibitors of prostaglandin synthesis, on microvascular arteriolar responses to bradykinin, prostaglandin E, (PGE,), prostaglandin E2 (PGE2), histamine, norepinephrine, and angiotensin. Male Wistar rats were anesthetized with sodium pentobarbital, and their cremaster muscle was exteriorized and prepared for in vivo microscopic observation of microvessels. Changes in arteriolar luminal diameters in response to topical administration of vasoactive agents were quantified with an imageshearing measüring eyepiece in conjunction with a television microscope and recorder. Local administration of IND or ETA significantly reduced the arteriolar dilation elicited by bradykinin, whereas the responses to PGE, and PGE2 remained unaltered. Responses to histamine, although somewhat reduced, were not significantly different from control. Vasoconstrictor responses of arterioles elicited by norepinephrine and angiotensin were potentiated by IND or ETA administration. These results indicate that prostaglandins synthetized in skeletal muscle microcirculation in situ (1) mediate, in part, vasodilator responses to bradykinin and (2) modulate vasoconstrictor responses to angiotensin and norepinephrine. Thus, these findings support the hypothesis that prostaglandins are local regulators of microvascular responsiveness.

ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

To determine whether transmural metabolite gradients develop in the contracting, ischemic left ventricle due to factors other than a nonuniform distribution of myocardial blood flow, right and left coronary artery inflow was completely stopped with vessel occluders in open-chest dogs for 15 or 30 seconds before a transmural myocardial tissue sample was obtained for regional analysis of creatine phosphate, adenosine triphosphate (ATP), and lactate. Heart rate was controlled, and the decline in left ventricular systolic pressure during the period in which coronary blood flow was stopped was attenuated by aortic constriction. Studies were also performed in dogs that were (1) pretreated with propranolol, (2) subjected to ventricular fibrillation, and (3) volume loaded. Control studies revealed no transmural metabolite gradients in the normally perfused ventricle, but creatine phosphate was slightly lower in the inner region than it was in the outer and middle ventricular wall regions. With coronary blood flow stopped for 30 seconds, a significant lactate gradient, increasing from the outer to the inner region, was present. Propranolol-treated dogs with their coronary blood flow stopped for 30 seconds also exhibited a lactate gradient, but dogs with ventricular fibrillation and their coronary blood flow stopped for 30 seconds did not. Volume-loaded dogs with their coronary blood flow stopped for only 15 seconds had a significant lactate gradient. Reciprocal gradients occurred in creatine phosphate but not in ATP. The findings suggest that the contracting ventricle uses energy unevenly and that in myocardial ischemia one of the factors causing greater subendocardial vulnerability is a greater energy need in this region.

ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

The effect of spatially varying shear on transport to the wall of a two-dimensional branch was examined, using oxygen as the test solute and the results of earlier fluid mechanical calculations to provide the shear profiles in a region characterizing the aortic bifurcation. The numerical technique employed allowed both blood-phase and mural resistances to solute uptake to be treated simultaneously and self-consistently. The calculated profiles of wall concentration and mural flux were significantly different from those which would have obtained if the shear had been uniform. The calculations suggest that, even when solute is rapidly taken up from the blood, the occasional high-shear and flow-development sites encountered along the arterial tree prevent the diffusion boundary layer adjacent to the wall from thickening to the point at which nutrition is compromised. The indirect effect of arterial geometry on transport, consequent to its direct effect on the magnitude and the distribution of the relevant hemodynamic variables, was illustrated using the branch area ratio as the geometric parameter. The shapes of the flux and interfacial concentration profiles along the branch wall were markedly dependent on the extent to which wall shear affected intimal permeability.

ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

This study was designed to evaluate the sensitivity of changes in myocardial carbon dioxide and oxygen tensions as indicators of regional myocardial ischemia and also to determine to what extent these changes can be related to changes in intramyocardial ST segment voltage. Changes in ST segment voltage recorded in unipolar epicardial electrodes proved to be a less-sensitive indicator of underlying myocardial ischemia than were changes in ST segment voltage recorded in unipolar intramyocardial electrodes. In 9 dogs, regional ischemia was produced by placing a variable constrictor on the left circumflex coronary artery; circumflex flow was monitored. Myocardial carbon dioxide and oxygen tensions were measured using a mass spectrometer. Unipolar electrograms were recorded using a multicontact plunge electrode. With progressive degrees of proximal stenosis, ranging from a critical stenosis, which is associated with a decrease in mean flow of less than 15%, tö a severe stenosis associated with an 80% decrease, ST voltage increased 21 mv and carbon dioxide tension increased 84 mm Hg, but oxygen tension decreased only 7 mm Hg. The study suggests that increases in intramyocardial ST segment voltage, an index of myocardial ischemia, are associated with parallel increases in myocardial carbon dioxide tension, each providing a more sensitive quantitative correlate of regional myocardial ischemia than do decreases in oxygen tension. The local accumulation of carbon dioxide may be an important pathophysiological mechanism in myocardial ischemia.

ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

Experiments were undertaken to investigate further the effect of furosemide on rennin secretion in the anesthetized dog. To separate the effects of the macula densa and the baroreceptor mechanisms, experiments were conducted in kidneys made nonfiltering by combining 2.5 hours of renal ischemia with ureteral ligation. Furosemide, in a dose of 5 mg/kg, increased renin secretion and decreased renal resistance in dogs with a nonfiltering kidney. Prior dilation of the nonfiltering kidney with either acetylcholine or papaverine prevented changes in both resistance and renin secretion. However, following dilation of the intact filtering kidney with acetylcholine, furosemide caused an increase in rennin secretion. Infusion of d,l-propranolol decreased renin secretion in both the filtering and the nonfiltering kidneys. Following propranolol treatment, furosemide increased rennin secretion in the filtering kidney but had no effect on renal resistance. These experiments indicate that furosemide stimulates renin secretion by both the macula densa and the baroreceptor mechanisms. The data suggest that stimulation of the sympathetic nervous system may alter renin secretion by modulating the renal baroreceptor, but sympathetic innervation does not appear to be involved in the macula densa mechanism.

ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

The solid angle theorem was used to analyze the relationships between TQ and ST segment deflections recorded from precordial and epicardial locations and the time course, size, shape, and transmural location of the ischemic process in the ventricular myocardium. Mathematical predictions were compared with experimental data from the intact heart. Precordial electrograms obtained in anesthetized close-chest pigs were compared with epicardial electrograms recorded directly from the heart's surface. Various areas of ischemia were produced by occluding large and small coronary artery branches, and the resultant changes in ischemic shape were delineated with Thioflavin S injections and postmortem ultraviolet photography. Formally derived equations and cumulative experimental data were in close agreement, suggesting that in the ischemic ventricle (1) TQ depression always accompanies ST elevation, (2) TQ and ST segment changes in magnitude and polarity are complex functions of ischemic size, shape, and transmural location; (3) precordial electrocardiogram (ECG) ST segment elevation is directly related to ischemic size; and (4) epicardial ECG ST segment elevation is inversely related to ischemic size. It is thus concluded that precordial and epicardial ECG TQ and ST segment deflections are complex functions of ischemic geometry and that their accurate interpretation with respect to ischemic size and shape and in the presence of pharmacological interventions is often difficult and may be misleading.

ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

The lung parenchyma as a tissue has a rather unusual stress-strain relationship. A theoretical derivation of this relationship is presented which connects the surface tension and the tissue elastic stress in the alveolar septa with the alveolar geometry. The mathematical expression contains a few meaningful physical constants which can be determined by in vitro and in vivo experiments. With this stress-strain relationship, the general equations of lung mechanics are formulated, and solutions to some simpler problems are presented. First, the equilibrium of a lung subjected to a uniform inflation pressure (definition: alveolar air pressure - intrapleural pressure - pleural tension x mean curvature of pleura) is analyzed, and the stability of the equilibrium states with respect to small perturbations is examined. Second, an exact solution for a lung in a chest under the influence of gravity is presented; the solution is “exact,” of course, for only a particular lung, but it can serve as a standard to check numerical procedures being developed in many laboratories. Finally, three types of possible atelectasis-planar, axial, and focal-are analyzed. The planar type can exist in a normally inflated lung, provided the layers of alveoli are forced to collapse toward a plane by some external agent. But axial atelectasis (alveoli collapse into a cylinder) can occur only if the dimension of all alveoli in the direction perpendicular to the axis is smaller than the resting dimension (at which the elastic tension in the alveolar septa vanishes). Similarly, focal atelectasis can occur only if the entire lung is smaller than the resting volume.

ISSN:0009-7330    

出版商:OVID    

年代:1975

数据来源: OVID