摘要:

Determination of regional ventricular wall stress would allow quantification of both regional contractile state and its interplay with global function. Current methods for quantifying regional stress include mathematical modelling and measurements with strain gauges. Both methods are difficult to validate. We hypothesized that transverse stiffness (i.e., the ratio of indentation stress to strain as the ventricular wall is indented in the direction perpendicular to the wall) would be proportional to the stresses in the plane of the wall and could be used to estimate the latter. To test this hypothesis, 6 arterially perfused canine ventricular septa were mounted in an apparatus that could exert biaxial load in the plane of the wall. A servo system maintained the central third of the septa isometric during active contractions while the septa were paced at 30-60 pulses/min. In the center of the isometric region, a probe of 7 mm diameter indented the septa while the transverse indentation stress and strain were measured. For values of peak systolic in-plane stress from 0.56 to 2.6 g/mm2, the transverse stiffness varied from 1.2 to 11.7 g/mm2and was linearly related to the in-plane wall stress in each septum (p<0.001, ANOVA). After cardioplegia, the transverse stiffness also correlated with passively applied wall stress for each dog (p<0.001). The slopes of the individual relations between transverse stiffness and wall stress from active contractions were similar to those from passively applied stress (mean ± SEM; 1.82 ± 0.36 versus 1.45 ± 0.31, NS). The intercepts with the transverse stiffness axis from active contractions, however, were greater than those from passively applied stress (2.23 ± 0.57 versus −0.16 ± 0.12 g/mm2, p<0.015). Moreover, at similar wall stresses, the transverse stiffness for active contractions was greater than that for passively applied stress (3.1 ± 0.7 versus 1.1 ± 0.2 g/mm2, p<0.005). Thus, regional transverse stiffness appears to allow quantitative estimation of regional in-plane stresses and can distinguish between actively generated and passively applied stress. This approach may allow one to accurately quantify the regional contractile state and to determine whether regional dysfunction is due to abnormal muscle that is not generating stress or to muscle capable of generating stress but which is abnormally loaded. (Circulation Research 1987;61:695-703)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

A model of electrically coupled sinus node cells was used to investigate pacemaker coordination and conduction. Individual cells were simulated using differential equations describing transmembrane ionic currents. Intrinsic cycle lengths (periods) were adjusted by applying constant depolarizing or hyperpolarizing bias current, and cells were coupled through ohmic resistances to form two- dimensional arrays. Activation maps of 81-225 coupled cells showed an apparent wavefront conducting from a leading pacemaker region to the rest of the matrix even though the pattern actually resulted from mutual entrainment of all spontaneously beating cells. Apparent conduction time increased with increasing intercellular resistance. Appropriate selection of pacemaker cycle lengths and intercellular resistances permitted the accurate simulation of the activation sequence seen experimentally for the rabbit sinus node. Furthermore, a simulated acetylcholine pulse applied to a randomly selected 20% of the cells in this model produced a pacemaker shift that lasted several beats. These results support the hypothesis that sinus node synchronization occurs through a "democratic" process resulting from the phase-dependent interactions of thousands of pacemakers. (Circulation Research 1987;61:704-714)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To clarify the immune mechanism in myocarditis, immunofluorescence techniques with laser flow cytometry were used to examine serial changes in lymphocyte subsets in the heart, spleen, and peripheral blood of DBA/2 and BALB/c mice inoculated with encephalomyocarditis virus (Experiment I). B cells were identified by staining with fluorescein isothiocyanate-labelled rabbit anti-mouse immunoglobulin. T-cell subsets were identified with rat anti-Thy 1.2, and nonpolymorphic Lyt 1 and Lyt 2 monoclonal antibodies plus fluorescein isothiocyanate-labelled anti-mouse immunoglobulin. On days 7 and 14 postinfection, the percentage of Thy 1.2+(pan T) cells in both strains had decreased in the peripheral blood; B cells showed no significant changes throughout the entire period. On the other hand, Thy 1.2+(pan T) and Lyt 1+, 23+(precursor and immature) T cells appeared to occupy the major portion of the myocardium on days 7 and 14 when congestive heart failure developed. To confirm this, serial immunohistologic studies (immunoperoxidase staining) of the hearts of DBA/2 and BALB/c mice with encephalomyocarditis virus-induced myocarditis were performed (Experiment II). In Experiment II, most of the stained cells in the hearts of both strains were Thy 1.2 positive and Lyt 1 and Lyt 2 positive on days 7 and 14. Thus, Experiments I and II demonstrated that lymphocytes at the site of inflammation in acute viral myocarditis carried antigenic markers that differed from those of peripheral lymphocytes and suggested that Thy 1.2+(pan T) cells, especially the Lyt 1+, 23+subset (immature T cells and T-cell subset precursors) were involved in the development of myocarditis in these animals. (Circulation Research 1987;61:715-725)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Mechanisms of energy deprivation contracture were investigated in cultured chick embryo ventricular cells. In the presence of zero-extracellular-Na+(choline chloride substitution)-nominal-zero-Ca2+([Ca2+] ˜ 5 μM), exposure of ventricular cells to 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG)-zero-glucose solution resulted in the development of a contracture (video motion detector) in 5.9 ± 0.5 minutes. Early after contracture development, the resupply of extracellular Na+, in the continued presence of CN + 2-DG, resulted in a rapid partial relaxation (tl/2= 1.9 ± 0.3 seconds), associated with an increase in45Ca efflux, presumably due to transsarcolemmal Ca2+extrusion due to Na+-Ca2+exchange. Ressupply of glucose and removal of CN + 2-DG, in the continued absence of Na+, resulted in an initially slower (t1/2= 11.6 ± 2.5 seconds), but more complete relaxation of contracture, which was not associated with increased Ca2+efflux. Pretreatment with 20 mM caffeine delayed the onset of contracture (9.2 ± 1.1 minutes) and resulted in a contracture that could not be relaxed by ressupply of external Na+only. Studies using the fluorescent Ca2+probe indol demonstrated that in zero-Na+-zero-Ca2+solutions, contracture due to CN + 2-DG was associated with an initial rise in [Ca2+]1but that this did not account for all of contracture force development. In cells exposed to CN + 2-DG in the presence of normal extracellular Na+and Ca2+concentrations, a small rise in [Ca2+]1was associated with initial contracture development, consistently preceding the development of a larger accelerated contracture presumably due to ATP depletion. We conclude that an early component of ATP depletion contracture is due to an increase in [Ca2+]1. The rate of this increase in [Ca2+]1depends to some extent on the loading of internal stores of Ca2+, particularly sarcoplasmic reticulum. Elevation of [Ca2+], may promote subsequent rigor by hastening ATP depletion by activation of Ca2+-ATPases. (Circulation Research 1987;61:726-734)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To elucidate the mechanisms responsible for the increase in α1-adrenergic receptors during ischemia in vivo, we developed a procedure for measuring α1-adrenergic receptors in isolated, calcium-tolerant adult canine myocytes. Specific [3H]prazosin binding was rapid, saturable, reversible, and demonstrated the expected order of potency and stereospecificity for the α1-adrenergic receptor. Myocytes exposed to 30 minutes of hypoxia at 25±C or only 10 minutes at 37±C exhibited a twofold to threefold increase in the number of α1-adrenergic receptors with no significant change in receptor affinity. This hypoxia-induced increase in receptor number was reversible by 10 minutes of reoxygenation at 37±C. In contrast, more prolonged hypoxia of 80 minutes or hypotonic shock actually decreased receptor number below normoxic, control values. The concentration of long-chain acylcarnitines in myocytes also increased threefold on exposure to 30 minutes of hypoxia. Sodium 2-[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate (POCA, 10 μM), a potent inhibitor of carnitine acyltransferase I, not only abolished the accumulation of long-chain acylcarnitines but also the increase in α1-adrenergic receptor number induced by 30 minutes of hypoxia. Likewise, incubation of normoxic cells with exogenous palmitoyl carnitine (1 μM) for 10 minutes also increased α1-adrenergic receptor number in the presence or absence of POCA. Thus, hypoxia results in an increase in α1-adrenergic receptors associated with an increase in endogenous long-chain acylcarnitines. Furthermore, inhibition of carnitine acyltransferase I prevents not only the sarcolemmal accumulation of long-chain acylcarnitines but also the exposure of the α1-adrenergic receptor, indicating that accumulation of endogenous long-chain acylcarnitines is critical to the hypoxia-induced increase in α1-adrenergic receptors on adult myocytes. (Circulation Research 1987;61:735-746)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Since the gradient between aortic pressure and left ventricular diastolic pressure is a major determinant of coronary blood flow, a change in left ventricular relaxation by its effect on early diastole could diminish early diastolic coronary flow. Two interventions that resulted in impaired left ventricular relaxation, hypothermia, and reperfusion following a left anterior descending coronary artery occlusion were studied to evaluate whether there were associated changes in coronary blood flow. With both interventions, there was a significant prolongation of left ventricular relaxation (p<0.01) accompanied by a significant decrease in early diastolic coronary blood flow (p<0.01). Verapamil did not have a significant effect on these hemodynamic changes during hypothermia. However, verapamil significantly blunted the effects of reperfusion following ischemia on ventricular relaxation (p<0.002) and early diastolic coronary blood flow (p<0.01). Thus, impaired left ventricular relaxation has an adverse impact on early diastolic coronary blood flow, which, under the condition of reperfusion following regional myocardial ischemia, can be alleviated with calcium channel blockade. (Circulation Research 1987;61:747-756)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The purpose of this study was to use a direct method, that of electron spin resonance (ESR) spectroscopy, to demonstrate that reperfusion after a period of ischemia results in a sudden increase in the production of free radicals in the myocardium. The isolated buffer-perfused rat heart was used with N-tert-butyl-α-phenylnitrone (PBN) as a spin-trapping agent. Samples of coronary effluent were taken and extracted into toluene for detection of radical adducts by ESR spectroscopy. After 15 minutes of total, global ischemia, aerobic reperfusion resulted in a sudden burst of radical formation that peaked at 4 minutes. When hearts were reperfused with anoxic buffer, no dramatic increase in radical production was observed. Subsequent reintroduction of oxygen, however, resulted in an immediate burst of radical production of a similar magnitude to that seen in the wholly aerobic reperfusion experiments. The ESR signals obtained (aN= 13.60 G, aH= 1.56 G) are consistent with the spin-trapping by PBN of either a carbon-centered species or an alkoxyl radical, both of which could be formed by secondary reactions of initially-formed oxygen radicals with membrane lipid components. (Circulation Research 1987;61:757-760)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID