摘要:

Plasmalemmal folds and caveolae were investigated by qualitative and quantitative analysis of electron micrographs obtained by freeze fracture and transmission electron microscopy (TEM) of rabbit right ventricular papillary muscles whose mean sarcomere lengths ranged from 1.64 to 2.28 fun. In passively extended muscles, folds were observed at sarcomere lengths of 2.3 /an and could be shown by extrapolation to become completely extended at a maximum sarcomere length of 2.8 μn. It was concluded that the plasmalemma does not contribute to resting tension in the physiological range of sarcomere lengths. Caveolae are present in both the external plasmalemmal envelope and T-tubular plasmalemma. They show no preferential distribution with respect to underlying myofibrillar striations or membrane folds and are nearly devoid of membrane particles in freeze-fractured material. The surface density of caveolar necks (4.0/pm:apparent plasmalemmal area) is only 16-20% of that reported for frog skeletal muscle. Caveolae augment plasmalemmal area by 21-32%, assuming two or three caveolae per neck, respectively. Caveolar membrane does not serve as a reservoir of membrane to be recruited into external plasmalemma, at least over the physiological range of sarcomere lengths. In heart muscle they do not account for the T-tubular access resistance, and their function in this tissue remains unknown. Circ Res 46: 244-255, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Instantaneous pressure (P) in the canine left ventricle is determined predominantly by the simultaneous volume (V) of the ventricular lumen; that is, the instantaneous P-V relation is reasonably well approximated by a regression line of isochronous pressures from different beats on the simultaneous volume values. Strictly speaking, however, the P-V data points from differently loaded contractions slightly scatter around the regression line, indicating that V is not the sole determinant of P. To identify the secondary determinants of P at a given V, we forced the ventricle to have a fixed V at a specified time in the cardiac cycle while changing the end-diastolic volume and the velocity of ejection over a wide range under a constant inotropic background. We found that, at any specified time and V, P decreased with increases in the simultaneous velocity of ejection (-dV/dt, ml/sec), the peak velocity of ejection (peak-dV/dt, ml/sec), and the volume ejected by the specified time (/−dV, ml). Multiple regression analysis of the data yielded a formula: %P = 100-0.14 (-dV/dt)-0.07 (peak -dV/dt)-0.54 (J-dV), in which %P denotes P of an ejecting beat in percent of the isovolumic P at the same time and V. All those partial regression coefficients are statistically significant (P< 0.005). The results indicate that the instantaneous ventricular pressure can be reduced from isovolumic pressure by 10-20% if the magnitude of those ejection parameters are near physiological maxima. Circ Res 46: 256-263, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The local intra-arterial infusion of histamine, in doses which produce maximal increases in protein efflux, failed to increase lymph total protein concentration in canine forelimbs perfused at constant inflow with autologous blood from dogs subjected to severe hemorrhagic hypotension. Norepinephrine and isoproterenol in low concentrations were less effective in antagonizing protein efflux produced by high doses of histamine than by low doses of this agent. This suggests that other vasoactive substances released in response to a hemorrhagic stimulus may also be physiological antagonists of the direct actions of histamine on the microvascular membrane. The simultaneous infusion of vasopressin or serotonin, or pretreatment with high doses of glucocorticoids, antagonizes the protein efflux produced by local intra-arterial infusions of histamine into forelimbs perfused at constant inflow. Angiotensin II, acetylcholine, low doses of glucocorticoids, and papaverine all failed to alter measurably the protein efflux produced by histamine under similar conditions. We conclude that a variety of hormones and other vasoactive agents may function as antagonists of the direct action of histamine on the microvascular membrane, and that the antagonism of histamine-induced protein efflux is independent of changes in histamine receptor blockade, blood flow, microvascular pressure, and perfused surface area. Moreover, in experiments employing adrenergic blocking agents, the antagonism of histamine-induced protein efflux by catecholamines was due to stimulation of β-adrenergic receptors.Circ Res 46: 264-275, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Hypotension after left ventriculography (LVG) is believed to result from direct myocardial toxicity, peripheral vasodilation, or a combination of both. The contribution of each has not been established. Thus, LVG was performed in anesthetized dogs under conditions in which peripheral vascular reactivity (PVR) was altered pathophysiologically (aortic coarctation) or pharmacologically (acetylcholine infusion). Ventricular pressure (LVP), its first derivative (dP/dt), aortic pressure (AoP), and carotid and femoral flows were monitored. When PVR was normal, LVG was associated with significant hemodynamic changes which reached a maximum 25-35 seconds after injection. Left ventricular and aortic diastolic pressures were decreased by 22 and 48%, whereas carotid and femoral systolic flows were increased by 41 and 59%. During acetylcholine infusion, LVG did not cause systolic hypotension and peripheral flows were maintained strikingly constant. Similarly, LVG also was associated with insignificant changes in systolic pressures and carotid flow in the presence of aortic coarctation. These results demonstrate that the hypotension attendant with LVG is directly related to the augmentation in peripheral flow, suggesting that the response is mediated almost exclusively by peripheral vasodilation. Circ Res 46: 276-282, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Using an analytical mathematical model, we studied and contrasted the effects of variations in geometry and volume conductor properties of the torso on epicardial and body surface potentials. The model consists of a spherical heart (blood cavity bounded by a spherical muscle shell that includes a double layer source, and pericardium) eccentrically placed in a spherical torso flung region bounded by muscle and fat layers). The effects of the following parameters on body surface and epicardial potentials were studied: (1) separation of the cardiac sources; (2) location of the heart within the torso; (3) combined effects of all torso inhomogeneities, (4) "internal" inhomogeneities (intracavitary blood, pericardium); (5) "external" inhomogeneities flung region, skeletal muscle, subcutaneous fat), and (6) hypertrophy and dilation. It was determined that, although internal inhomogeneities affect both epicardial and surface potentials similarly, the effect of external inhomogeneities on body surface potentials is different from their effect on epicardial potentials. The effects of hypertrophy and dilation are seen to depend on specific details regarding alterations in size and shape of blood cavity, heart, and activation surface. The most important conclusion of the study is that epicardial potential maps accurately reflect the underlying source configuration, are free of the effects of body shape and size, and are affected significantly by only one extracardiac inhomogeneity-namely, the lung region. Such maps, therefore, can enhance our capability to interpret and diagnose electrophysiological events within the heart. Ore Res 46: 283-291, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Cardiac hypertrophy is a characteristic change that occurs in senescence. Muscles from senescent as compared to mature hearts also demonstrate functional alterations that are similar to the alterations found in muscles from experimentally hypertrophied hearts. Thus, an attractive hypothesis is that functional alterations in senescent muscles are related to the underlying hypertrophy. To test this hypothesis, we used a rat model of aging in which experimental hypertrophy was produced by aortic banding. The time course and extent of cardiac hypertrophy, as well as isometric twitch and viscoelasticity parameters, as a function of age, first were determined in muscles from the rat hearts. Aortic banding then was performed on middle-aged rats to produce the same extent of hypertrophy as seen in the senescent hearts. The resulting functional alterations in muscles from the banded (B) hearts were compared to the senescent (S) and middle-aged (M) muscles. Using tibia] length as a reference, we found 14% LV hypertrophy in senescent compared to both young and middle-aged rats, indicating that the hypertrophy occurred during the last quarter of life. The S muscles demonstrated a 25% prolongation in contraction duration (CD) and a 30% increase in slope of the active stiffness-tension line (oA) compared to both young adult and middle-aged muscles. Compared to middle-aged muscles, the B muscles demonstrated a similar spectrum of change in mechanical properties as the S muscles (8% increase in CD and 15% increase in aA), but the quantitative differences between the B and S muscles were significant. Over the functional range of developed tensions, the B muscles demonstrated the lowest and the S muscles the highest values of stiffness. The findings suggest that a portion of the mechanical property alterations seen in the senescent heart are due to the underlying hypertrophy. However, the hypertrophy produced by mechanical loading of the LV cannot explain all of the senescent changes. Circ Res 46: 292-300, 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

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