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 145 records · Page 8Linked to original sources
PubMed1983

[Changes in the hemodynamics and myocardial contraction in ventricular extrasystole].

On the basis of electrokymographic and echocardiographic findings, the authors elucidated a sharp fall in myocardial hemodynamics and contractility during extrasystole contractions arising from the ventricles which was directly dependent on the severity of blood circulation insufficiency. Post-extrasystole contractions occurring after a full compensatory pause tended to compensate the worsened hemodynamics only partially; the degree of compensation being the higher, the better the functional state of the myocardium.

Adult↗
PubMed1997

[Pulmonary hypertension and myocardial contraction in disseminated types of pulmonary tuberculosis].

To elucidate the influence of hemodynamic factors on the development of right ventricular failure, hemodynamic parameters of the lesser and greater circulations and those characterizing myocardial contractility were studied in 36 patients. Despite profuse lung damage, pulmonary failure, and marked external respiration dysfunction that accompanied disseminated pulmonary tuberculosis, pulmonary hypertension was moderate and failed to be followed by hemodynamic overload, right cardiac hypertrophy and dilatation. Significant reductions in myocardial contractility both of the right and left cavities with a rise in the intensity of an inflammatory process suggest the leading role of a toxic and infectious agent in myocardial damage.

Cardiac Output↗
PubMed1993

The role of endocardial endothelium in the modulation of myocardial contraction in the isolated whole heart.

Selective damage to the endocardial endothelium in isolated papillary muscle preparations has been shown to produce an abbreviation of contraction, changes which were also observed following an increase in myocardial cyclic GMP in those preparations. In the present study we have investigated the effects of removing the endocardium and increasing myocardial cyclic GMP on contractile parameters in isolated Langendorff perfused ferret hearts, where the myocardial mass underlying the endocardium is much greater. Selective damage to left ventricular endocardial endothelium without damaging the underlying myocardium was achieved by brief exposure to a weak detergent solution (Triton X-100 0.005% v/v). This resulted in a significant abbreviation of the left ventricular pressure-time curve due to the earlier onset of relaxation, but there was little effect on early systole. The direct intraventricular infusion for 15 minutes of 10 microM sodium nitroprusside, a donor of nitric oxide, or of 1 microM substance P, to stimulate release of endothelium-derived relaxing factor, did not increase myocardial cyclic GMP levels or alter left ventricular contractile performance. Myocardial cyclic GMP levels were significantly increased by 15 minute intracoronary infusions of 10 microM nitroprusside and 1 microM substance P, approximately ten-fold and two-fold respectively. Intracoronary nitroprusside induced an abbreviation of the left ventricular pressure-time curve with an earlier onset of relaxation, but contraction was unaltered by intracoronary substance P. These results show that, in the isolated Langendorff perfused ferret heart, both selective removal of endocardial endothelium and an increase in myocardial cyclic GMP cause an abbreviation of left ventricular pressure and an earlier onset of relaxation with little change in early systole.

Animals↗