Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Myocardial Contraction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1998

Myocardial contraction band necrosis in stranded cetaceans.

The term contraction band necrosis describes focal hypercontraction and lysis of small groups of myocardial cells. Contraction band necrosis of the myocardium was identified in 100% of 52 whales and dolphins (cetaceans) stranded along the western coast of the Gulf of Mexico between April 1991 and November 1996. The myocardial lesions in the cetaceans were identical, both grossly and histologically, to those previously described in man and other animals. Such lesions may contribute to the high mortality rate in stranded cetaceans.

Animals↗
PubMed1998

[Myocardial contraction and intensive therapy in phthisiosurgical patients].

The changes in myocardial contractility were studied in 88 patients operated on for pulmonary tuberculosis in pre- and postoperative periods using echocardiography. It was found that among patients operated on for acute and common forms of pulmonary tuberculosis tahere was a considerable proportion of those with hypo- and hyperkinetic types of central hemodynamics which were characterized by unstable hemodynamic parameters and needed corrective therapy both in pre- and postoperative periods. Strategy of preoperative preparation and postoperative management of patients was elaborated by the status of the central hemodynamics.

Adolescent↗
PubMed2006

Modeling ischemia-induced dyssynchronous myocardial contraction.

Left ventricular (LV) contraction dyssynchrony is not easily quantified. We previously described a model for quantifying LV dyssynchrony that referenced regional amplitude and phase angles to global LV systole using esmolol-induced regional dyskinesis. We tested the hypothesis that our sine wave model and phase angle analysis of regional dyssynchrony in a canine model could also assess dyssynchrony of contraction during regional ischemia. Hence we compared intracoronary esmolol and matched regional ischemia in 10 anesthetized open-chest dogs. Regional and total LV volumes (conductance catheter), piezoelectric crystal shortening, and LV pressures were measured before, during, and after esmolol-induced apical dyskinesis and matched regional ischemia. We defined regional phase angle of contraction (alpha) as the relative distance, measured in degrees, that regional minimal volume differed from global end-systole. We also compared maximal stroke volume (SV), observed effective SV (that portion of regional SV contributing to total SV for each treatment), and calculated effective SV (total regional SV x cosine alpha). Dobutamine infusion increased homogeneity of regional alpha relative to baseline. Both esmolol and ischemia significantly delayed (P < 0.05) apical contraction as quantified by increased alpha (12.4 degrees +/- 28.1 degrees to 27.4 degrees +/- 30.4 degrees and 54.2 degrees +/- 32.6 degrees , respectively) (mean +/- sd) and decreased regional effective SV (4.7 +/- 2.5 mL to 3.6 +/- 2.2 mL and 4 +/- 2.5 mL, respectively) relative to baseline. Our study indicates that intracoronary esmolol and ischemia induced qualitatively similar mechanical effects on myocardial function and that a sine wave model to estimate regional effective SV is a sensitive method to detect and quantify regional dyssynchrony induced by ischemia. Potentially, phase angle and regional amplitude analyses may prove to be effective measures to identify and quantify the beneficial effects of resynchronization therapies on myocardial function.

Animals↗
PubMed1994

Changes in myocardial contraction pattern during initial reperfusion.

The characteristics of hypercontraction during initial reperfusion were studied in 10 pentobarbitone-anesthetized cats. The left anterior descending coronary artery was occluded for 10 min followed by 1 h of reperfusion, and regional function was assessed by two cross-oriented pairs of sonomicrometers placed in the left ventricular anterior wall. At 1 min of reperfusion (hyperfunctional phase) there was an uniform contraction pattern with 90% recovery of ejection shortening in both circumferential and longitudinal segments. During initial hypercontraction, end-diastolic segment lengths remained unchanged, whereas end-systolic segment lengths decreased transiently. Inotropic stimulation during reperfusion in four additional animals also affected end-systolic lengths more than end-diastolic lengths. This suggests that the initial hyperfunctional phase is due to an inotropic stimulation of the stunned myocardium, most probably caused by intracellular Ca2+ overload. At 5 min of reperfusion a nonuniform contraction pattern had developed with 68% recovery of shortening in circumferential segments vs. 25% in longitudinal segments. The decreased performance in longitudinal segments was paralleled by a delayed start of contraction as well as a decreased velocity of contraction. Because longitudinal segment shortening is a sensitive parameter of subendocardial performance, our results indicate a brief transmural hypercontraction followed by increasing dysfunction (stunning) in the subendocardial layer.

Animals↗
PubMed1984

Effects of myocardial contraction on ultrasonic backscatter before and after ischemia.

To determine whether contraction and relaxation influence quantitative myocardial ultrasonic backscatter we measured systolic and diastolic integrated backscatter separately in 10 pentobarbital-anesthetized dogs with defined, paced heart rates, before and after coronary occlusion. Data were acquired from intramural sites by coupling a broadband 5-MHz transducer to the left ventricular epicardium. Integrated backscatter was obtained from seven sequential ECG gated intervals throughout the cardiac cycle over the frequencies of 2.5-7.5 MHz and referenced to values obtained with a steel reflector. Before coronary occlusion myocardium in all dogs exhibited a decrease in integrated backscatter from end diastole to end systole (P less than 0.05) in control zones and in zones destined to become ischemic (P less than 0.05). Thirty minutes after occlusion integrated backscatter did not change in control zones but was elevated in ischemic zones with blunting of the diastolic-to-systolic variation. Thus myocardium undergoing contraction exhibits a decrease in integrated backscatter, and measurement of integrated backscatter at end systole differentiates ischemic from normal myocardium.

Analysis of Variance↗
PubMed1979

[Various characteristics of lipid metabolism in experimental myocardial infarct and their effect on myocardial contraction].

It was established in rabbit experiments that in acute focal myocardial ischemia induced by ligation of the descending branch of the left coronary artery, diminution of the force of cardiac contractions and an increase in the content of free fatty acids in blood plasma are observed. Progressing intramyocardial lipolysis is noted for 6 days. Lipolysis blockade with large doses of nicotinic acid leads to an extremely sharp drop in the contractile force of the heart in experimental animals with acute focal myocardial ischemia and to drastic damage of the myocardial ultrastructures as well as to disorders of the metabolism of intracellular lipids.

Acute Disease↗
PubMedDate not supplied

[Modifying effect of incorporated 137Cs on the mechanism of adrenergic control of myocardial contraction].

Incorporated 137Cs (absorbed dose of 0.26 Gy) causes decrease of myocardial's contractile function and inotropic response to beta-adrenagonists effect, isoproterenol-stimulated adenylate cyclase activity and beta-adrenoreceptors affinity. Adrenergic effects, mediated by alpha-adrenergic structures on heart contractile function, on the contrary, become stronger, that is due to the increase of the receptors' density on sarcolemma surface.

Adenylyl Cyclases↗
PubMed1998

[Reversible dysfunction of myocardial contraction].

It has been known for more than 20 years that in some patients after revascularization partial or complete improvement of previous left ventricular dysfunction occurs. The condition for this improvement is viable myocardium, i.e. contractile reserve. Chronic reversible contractile dysfunction, also called hibernating myocardium heart muscle is along with the presence of acute reversible dysfunction--a stunned myocardium the prerequisite for this improvement. In the submitted review the authors try to present at least some contemporary views on the pathophysiological mechanism of the development of a hibernated myocardium. The normal blood flow through the heart muscle at rest in the majority of reversibly dysfunctional segments is a change as compared with the formerly accepted definition. The authors mention histological changes of the hibernating myocardium, in particular so-called dedifferentiation. Attention is paid to a review and comparison of methods used at present to detect a viable myocardium. From the aspect of clinical practice it appears that unless revascularization occurs, the presence of a viable heart muscle is a factor which causes a poorer prognosis of the patients.

Humans↗
PubMed1997

Sympathetic modulation of the effect of nifedipine on myocardial contraction and Ca current in the rat.

The regulation of cardiac L-type Ca2- current (Ica) and contraction by dihydropyridine antagonists and beta-adrenergic receptor agonists has been the subject of numerous studies over the last decade. However, little is known on the crosstalk between these two regulatory pathways. For instance, a fundamental question that remains unanswered is: does activation of the beta-adrenergic receptors modify the sensitivity of the myocardium to dihydropyridine agonists? To answer this question, we examined in the present study how activation of the beta-adrenergic receptors modifies the effects of nifedipine on the mechanical and energetic parameters of the isolated perfused rat heart. Activation of the beta-adrenergic receptors was achieved by perfusing the hearts with isoprenaline, a non-selective beta-adrenergic receptor agonist, and could be reduced by atenolol, a beta-adrenergic receptor antagonist. To examine possible alterations during hypertension in the sensitivity of the hearts to the drug, tested, the study was performed in both normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive animals (SHR). While 0.1 microM nifedipine reduced left ventricular pressure (LVP) by 36% and 34% in WKY and SHR rats, respectively, under basal conditions, its effects became negligible in both groups of rats after stimulation of the hearts with 0.1 microM isoprenaline. Addition of 1 microM atenolol in the presence of isoprenaline restored the inhibitory effect of nifedipine to control values in both WKY and SHR rats. Additional experiments were performed in isolated ventricular myocytes from WKY rats using the whole-cell patch-clamp technique. The inhibitory effects of 0.1 to 1 microM nifedipine were significantly larger on basal Ica than after the current had been previously elevated by 0.1 microM isoprenaline. Addition of 1 microM atenolol in the presence of isoprenaline partially restored the inhibitory effect of nifedipine on Ica. Our results demonstrate a reduced sensitivity of the heart muscle to nifedipine during activation of beta 1-adrenergic receptors. This effect is partly explained by a reduced inhibitory effect of nifedipine on Ic during activation of cAMP-dependent phosphorylation.

Adrenergic beta-Agonists↗
PubMed1997

Usefulness of myocardial velocity gradient derived from two-dimensional tissue Doppler imaging as an indicator of regional myocardial contraction independent of translational motion assessed in atrial septal defect.

Independence of myocardial velocity gradient from translational motion of the heart was tested by comparing normal subjects and patients with atrial septal defect. Myocardial velocity gradient obtained from patients fit within the normal range, even though the translation of the left ventricle was exaggerated in patients, demonstrating the translation independence of myocardial velocity gradient in clinical settings.

Adolescent↗