摘要:

Infusion into sheep of plasma containing zymosan-activated complement produces leukopenia, pulmonary leukostasis, and pulmonary artery hypertension. We previously demonstrated a close relationship between the pulmonary vascular response and elevations of plasma thromboxane. We have investigated the source of thromboxane synthesis in this model. Plasma containing zymosan-activated complement added to whole blood did not stimulate thromboxane synthesis. This observation suggested that leukocytes do not synthesize thromboxane directly in response to complement. Sheep rendered severely thrombocytopenic by the administration of antiplatelet serum responded to complement infusion in the usual way. Pretreatment with aspirin (10 mg/kg) protected sheep against the pulmonary vascular response and completely blocked thromboxane synthesis. Transfusion of functional platelets did not restore these responses. Twentyfour hours after aspirin treatment, in vivo thromboxane synthesis was significantly greater than platelet thromboxane synthesis in vitro. Thromboxane is synthesized by a tissue which recovers cyclooxygenase enzyme activity at a rate that is more rapid than platelet turnover. Sheep lung synthesizes thromboxane actively in vitro. It is postulated that leukocytes exposed to activated complement components damage pulmonary vascular endothelial cells and stimulate synthesis of thromboxane A2which causes pulmonary vasoconstriction.

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Studies on the nervous or humoral control of total peripheral resistance are often complicated by concomitant changes in cardiac output. We studied the influence of output on peripheral resistance in the absence of modulating reflexes. In barodenervated and vagotomized cats, cardiac output was varied by graded inferior caval vein occlusion or by arterial bleeding. Total peripheral resistance was obtained with an analogue device which continuously divided the pressure difference between aorta and caval vein by cardiac output (electromagnetic flowmeter). Cardiac output reduction caused a decrease of peripheral resistance, followed within 2 minutes by a slow increase. Resistance stabilized at preocclusion levels within 5.8 (range 4−9) minutes. The relative changes in resistance and cardiac output were linearly related, when cardiac output was reduced by less than 40%. With larger reductions, the relation became nonlinear, and with a drop of more than 65%, no further change was noticed. These changes in resistance could not be explained by variations in blood viscosity as measured by Hct. They were nonnervous in nature: when all reflexes were abolished by ganglionic blockade, a similar pattern was found. Humoral mechanisms like the vasopressin or the renin-angiotensin system, known to be activated by hypotension, probably played no role, since arterial osmolality remained stable and captopril did not influence the resistance response. The involvement of metabolic autoregulation could not be excluded, but was unlikely because O2consumption and serum lactate did not change.

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The effects of endogenous and of exogenous norepinephrine were studied in isolated rings of canine left circumflex coronary artery and its first ventricular branch. Norepinephrine was released from adrenergic nerve endings by transmural electrical stimulation and by tyramine. In rings contracted with prostaglandin F2atransmural electrical stimulation resulted in frequency dependent relaxations which were blocked by propranolol or tetrodotoxin; tyramine and exogenous norepinephrine caused concentration-dependent relaxations which were blocked by propranolol. The tyramine-induced relaxations also were inhibited by cocaine. The left circumflex artery was less sensitive than its branch to β-adrenergic activation; this difference was significant even between rings of the two vessels immediately adjacent to the branching point and was abolished by phentolamine. In the presence of propranolol, transmural electrical stimulation, tyramine and phenylephrine, produced contractions of the left circumflex artery, but not the branch; these contractions were prevented by phentolamine. Phentolamine, but not prazosin, augmented the β-adrenergic response of left circumflex artery to low frequency stimulation; in arteries preincubated with3H-norepinephrine, this was accompanied by an increased overflow of tritiated neurotransmitter. The prejunctional effect of phentolamine was also evident in branch coronary arteries which exhibit no postjunctional α-adrenergic responses. With high frequency stimulation, both α-adrenergic antagonists equally augmented the relaxation of left circumflex artery; the efflux of tritiated norepinephrine was not different from untreated arteries. These experiments demonstrate, in isolated coronary arteries, that the primary adrenergic response to released endogenous norepinephrine is β-adrenergic relaxation. The prejunctional effects of nonspecific α-adrenergic antagonists preclude their use in determining the importance of postjunctional coronary α-adrenergic receptor activation caused by sympathetic nerve stimulation.

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

We have studied the cardiovascular responses which can be evoked when the gallbladder is stimulated pharmacologically or mechanically. To determine the potential for reflex cardiovascular activation, we applied capsaicin, a selective thin-fiber agonist, to the serosal surface of the gallbladder. This algesic substance evoked cardiovascular responses which included increases in mean arterial pressure (MAP) by 14%, heart rate (HR) by 3%, left ventricular dP/dt at 40 mm Hg developed pressure (dP/dt DP40) by 14%, and systemic vascular resistance (SVR) by 19%. There were no demonstrable effects on the cardiovascular system when this same substance was applied to the surface of the liver. Bilateral vagotomy at the level of the diaphragm did not alter the responses to capsaicin. Right atrial overdrive pacing did not reduce the positive inotropic effect elicited when the gallbladder was stimulated. Removal of the celiac and superior mesenteric ganglia, or selective denervation of the gallbladder, abolished the cardiovascular responses which were evoked previously. β-Adrenergic blockade, however, abolished only the reflex chronotropic and inotropic responses. Thus, the potential for eliciting reflex cardiovascular alterations by stimulating gallbladder afferents with capsaicin was established. In subsequent studies, stimulating the gallbladder with bradykinin, an endogenous polypeptide, evoked a reflex activation of the cardiovascular system similar to that seen with capsaicin (MAP = 14%; HR = 4%; dP/dt DP40 = 18%; SVR = 14%). These reflex responses were dose dependent, were produced by mucosal as well as serosal application of this substance, and were eliminated by bilateral splanchnic nerve section. In contrast to capsaicin and bradykinin, distension of the gallbladder did not cause any cardiovascular alterations. We conclude that stimulation of gallbladder afferents by the algesic substance capsaicin or by bradykinin, an endogenous substance that under certain conditions may be formed in bile, can induce significant reflex activation of the cardiovascular system.

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

We hypothesized that acute myocardial infarction could be detected in standard two-dimensional echocardiograms of closed-chest dogs by evaluating regional echo amplitude distribu-tions using computerized image analysis. We tested this hypothesis by performing standard, 2.4 MHz two-dimensional echoes before and 2 days after circumflex coronary occlusion in seven closed-chest dogs. Control and infarcted regions of interest were studied in digitized stop-frame images. Average gray level was calculated for each region of interest, and the shape of the gray-level distribution was analyzed by calculation of skewness and kurtosis and by qualitative features of shape. Average gray level increased significantly from the pre-to postocclusion images in the infarcted regions (16.7 ± 4.2 vs. 32.4 ± 4.4 units,P< 0.01), but not in the control regions (17.4 ± 4 vs. 22.3 ± 5.5.,P= NS). Average gray level could not distinguish between infarcted and normal regions within the postocclusion images (36 ± 5.2 vs. 33.6 ± 5.8,P= NS). Three independent observers qualitatively evaluated histogram shape and correctly identified7/7MI regions (100% sensitivity) and 14/20 normal regions (70%specificity). Quantitatively, infarct regions exhibited a significant decrease in kurtosis (2.8 ± 0.9 to 0.44 ± 0.5,P< 0.01); the normal regions showed no significant change in kurtosis from pre-to postocclusion images (7.1 ± 4.0 vs. 5.2 ± 2.9,P= NS). Within postocclusion images, infarcted regions displayed a significantly lower kurtosis than did normal regions (0.27 ± .47 vs. 2.5 ± 1.0,P< .01).

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The effects of torso inhomogeneities on electrocardiographic potentials were investi-gated via computer simulation, using a 23-dipole heart model placed within a realistically shaped human torso model. The transfer coefficients relating the individual dipoles to the torso surface potentials, as well as the body surface potential maps, the vectorcardiogram, and the 12-lead electrocardiogram resulting due to normal activation of the heart model, were calculated for each of the following torso conditions: homogeneous, homogeneous + skeletal muscle layer, homogeneous + muscle layer + lungs, and homogeneous + muscle layer + lungs + intraventricular blood masses. The effects of each inhomogeneity were deduced by comparing results before and after its inclusion. For individual dipole transfer coefficients we confirm the validity of the “Brody effect,” whereby the high conductivity blood masses augment radially oriented dipoles and diminish tangentially oriented ones. With regard to the vectorcardiogram, the electrocardiogram, and the body surface potential maps, the major qualitative effects were an augmentation of the head-to-foot component of the vectorcardiogram due to the lungs, and a smoothening of notches in the electrocardiogram (temporal filtering) and of isopotential contours in the body surface potential maps (spatial filtering) with a consequent loss of information, due to the blood masses, muscle layer, and, to a lesser extent, the lungs. Besides the above qualitative effects of the inhomogeneities, there were also large quantitative effects on the surface potentials, namely, magnitude increases due to the blood masses and magnitude decreases due to the muscle layer, that—if unaccounted for—could compromise the inverse solution of these potentials for the cardiac dipole sources.

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

In our morphometric study of the effects of exercise on the heart, male Wistar-Kyoto rats at 5 weeks of age were subjected daily to a moderate treadmill running program that lasted for7weeks. The heart responded to physical conditioning by different magnitudes of tissue growth of the right (22%) and left (7%) ventricular myocardium, the latter change not statistically significant. The increase in right ventricular volume was associated with a 25% enlargement of ventricular area, a 26% average lengthening of the myocytes, and no change in sarcomere length and in ventricular midwall thickness. Exercise produced significant alterations in the quantitative parameters of the microvasculature of the right ventricle, but no appreciable changes in the left ventricle. Right ventricular hypertrophy was characterized by an absolute 44% growth of the endothelial luminal surface brought about through a 16% increase in capillary numerical density, and a 41% augmentation of the total length of the capillary network. Maximum diffusion distance from the capillary wall to the mitochondria of myocytes decreased 10% as a result of capillary proliferation and the lack of lateral expansion of myocyte cross-sectional area. Evaluation of the subcellular constituents of myocytes showed no change in the mitochondria: myofibrils volume ratio, indicating a growth of these components proportional to each other and to the growth of the myocyte population as a whole. It was concluded that, as a result of running exercise, right ventricular growth is analogous to eccentric hypertrophy in which the structural adaptations of the capillary bed can be expected to improve the diffusion and transport of oxygen within the tissue.

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Biphasic contractions were produced in dog trabeculae by replacing 90–95% of the calcium in the bathing solution with strontium. These conditions produced prolonged action potentials accompanied by contractions with two distinct phasic components. The early component disappeared slowly when the remaining Ca++was removed, whereas the late component was eliminated quickly when Sr++was removed. Manganese ion (0.25 ITIM) preferentially decreased the late component without changing the action potential, whereas caffeine and ryanodine decreased or eliminated the early component. Ryanodine did not alter the action potential. Isoproterenol rapidly increased the early component and, more slowly and to a lesser degree, increased the late component. The results suggest that the early component is caused by intracellular release of activator cation, probably from the sarcoplasmic reticulum, whereas the late component is the result of Sr++entry across the sarcolemma, possibly by way of the slow inward current.

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Since heart failure may occur in the setting of lung dysfunction and CO2retention with only modest increases in cardiac work load, we questioned whether myocardial function is impaired by hypercapnic acidosis. To determine the influence of hypercapnic acidosis on right ventricular function, we measured the effects of acute (2 hours) and chronic (2 weeks) hypercapnic acidosis on right ventricular performance during normal and increased right ventricular afterload in five conscious dogs. Systemic hemodynamic and right ventricular functions were unaltered during normal right ventricular afterload by acute hypercapnic acidosis (Paco2= 49 ± 3 mm Hg, pH = 7.27 ± 0.003). As right ventricular afterload was increased by progressive balloon occlusion of the right ventricular outflow tract during acute hypercapnic acidosis, the rise (slope) in right ventricular end- diastolic pressure was increased 4-fold (P< 0.01) over that observed in normocapnic control. Maximum isovolumic right ventricular dP/dt rose (P< 0.05) comparably with increasing right ventricular afterload during normocapnic control and acute hypercapnic acidosis. Chronic hyper- capnic acidosis (Paco2= 55 ± 2 mm Hg, pH = 7.28 ± 0.01) resulted in systemic vasodilation and increased (P< 0.05) heart rate and cardiac output during normal right ventricular after load. As right ventricular afterload was increased during chronic hypercapnic acidosis, the rate of rise in right ventricular end-diastolic pressure was 2-fold (P< 0.01) above normocapnic control but maximum isovolumic right ventricular dP/dt was unchanged in contrast to normocapnic control and acute hypercapnic acidosis. Moreover, cardiac output fell and stroke work was unchanged with increasing afterload during chronic hypercapnic acidosis. β-Adrenergic blockade resulted in an increased (P< 0.01) rate of rise in right ventricular end-diastolic pressure with afterload during normocapnic control and chronic hypercapnic acidosis. We conclude that hypercapnic acidosis results in dimin-ished right ventricular performance during increased right ventricular afterload, evidenced by accentuated rise in right ventricular end-diastolic pressure, and may contribute to the congestive heart failure and edema observed in patients with pulmonary hypertension and CO22retention.

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

In nine conscious, chronically instrumented dogs, ultrasonic dimension transducers measured left ventricular anterior-posterior and septal-free wall minor axis and major axis diameters. Matched micromanometers measured right and left ventricular transmural and transeptal pressures. Ventricular pressures and volumes were varied by inflation of implanted vena caval and pulmonary artery occluders, and the functional significance of the two types of ventricular interaction, i.e., direct and series, was determined. The left ventricle was represented by a modified ellipsoidal geometry. Left ventricular stroke volume calculated from the dimension data correlated well with that measured directly from ascending aortic electromagnetic flow probes during all interventions (r ⩾ 0.96). Partial pulmonary artery occlusion significantly increased right ventricular diastolic and systolic pressures as compared to values obtained during control and venal caval occlusion. During pulmonary artery occlusion, latitudinal septal eccentricity was increased throughout the cardiac cycle compared to control and vena caval occlusion (P< 0.05), indicating leftward interventricular septal shifting and significant alteration of left ventricular shape. The normalized diastolic pressure-volume curve was shifted to the left with pulmonary artery occlusion compared to control and indicated a decrease in left ventricular chamber compliance. However, when selected cardiac cycles with similar end- diastolic volumes from vena caval and pulmonary artery occlusions were compared, parameters of left ventricular systolic function (stroke volume, percent systolic shortening, peak aortic blood flow, peak left ventricular pressure, and its first derivative) remained relatively constant. These data suggest that mean myocardial fiber length is the major preload determinant of left ventricular systolic function independent of chamber pressure and shape, and that direct ventricular interaction mediated by interventricular septal shifting has minimal effects on systolic myocardial performance in this model. Thus, series ventricular interaction during acute imbalances in biventricular loading, where the output of the right ventricle determines the input of the left, seems to be far more important than direct interaction to the regulation of overall cardiac function.

ISSN:0009-7330    

出版商:OVID    

年代:1983

数据来源: OVID