We investigated the contribution of maximal Ca(2+)-activated force to the positive inotropism induced by mild hypothermia. Phosphorus-31 nuclear magnetic resonance spectroscopy revealed that neither energy-related phosphorus compounds in myocardium nor intracellular pH was responsible for the change in contractility. Maximal Ca(2+)-activated pressure (MCAP), the intact-heart correlate of maximal Ca(2+)-activated force, was determined in isolated perfused rabbit hearts by measuring isovolumic left ventricular pressure during tetani at extracellular Ca2+ concentrations greater than or equal to 10 mM. Tetani were elicited by rapid pacing after exposure to ryanodine. MCAP increased by 2.17 +/- 0.28% (mean +/- SE, P less than 0.001, n = 19) for each degree of myocardial cooling between 30 and 38 degrees C. Our results indicate that a primary change in myofilament Ca2+ responsiveness underlies the positive inotropism in hypothermia. The increase in maximal Ca(2+)-activated force may explain the observation of positive inotropism without an upward shift in the relation between oxygen consumption and pressure-volume area, as previously reported for cooled whole hearts.

Abstract. The previous Northern blot analysis and in situ hybridization studies showed that histamine H 1 -receptor (H 1 R) mRNA is expressed in human placenta and suggested that H 1 R plays some roles in the function of placenta in pregnancy. To investigate further, it is essential to show the precise location of H 1 R in the placenta. In the present study, we investigated H 1 R expression in human placenta by radioligand binding assay and immunohistochemical study using an antibody against human H 1 R. Placentas were obtained from normal uncomplicated deliveries. Membranes prepared from the tissue exhibited saturable [

We report a familial case of macrothrombocytopenia without inclusion bodies in polymorphonuclear cells or any congenital abnormalities.The results of the hemostatic and platelet function tests were all normal except for the platelet retention rate. The number ofmegakaryocytes increased slightly and some were relatively small. Electron microscopic studies revealed a unique morphological abnormality of the platelets' mitochondria.