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Biomedical subjects

M A Matlib

Publications and source records attributed to M A Matlib.

At least 55 records · Page 3Linked to original sources
PubMed1983

Mitochondrial function in canine experimental cardiac hypertrophy.

Concentric left ventricular hypertrophy was produced in puppies by coarctation banding of the aorta at age 7 weeks. Hemodynamic, morphologic and biochemical studies were carried out 18 months after the operation. Systolic blood pressure proximal to the aortic constriction was 216 +/- 16 mmHg in experimental dogs compared with 115 +/- 5 mmHg in littermate control dogs. Ejection fraction of control and experimental dogs were 59 +/- 4 and 64 +/- 7, respectively. The left ventricular end-diastolic pressure was 6.0 +/- 0.4 in control and 8.4 +/- 1.1 in experimental dogs. There was no sign of overt heart failure in the experimental dogs. Anatomical analysis of different regions of the heart indicated that LV mass in the experimental dogs was increased by about 60%. Ultrastructure of mitochondria in situ, as observed under electron microscope, was normal both in control and hypertrophic hearts. Mitochondria isolated from epicardial and endocardial regions of the stable hypertrophic hearts showed normal rates of respiration, phosphorylation, citrate synthase, and cytochrome c oxidase activities compared to those isolated from hearts of littermate control dogs. It was, therefore, concluded that mitochondrial function is adequately preserved to meet the increased demand for energy in this model of stable cardiac hypertrophy of long duration.

Animals↗
PubMed1982

Selective inhibition of Na+-induced Ca2+ release from heart mitochondria by diltiazem and certain other Ca2+ antagonist drugs.

The effect of Ca2+ antagonist drugs on Ca2+ uptake and Na+-induced Ca2+ release by isolated rabbit heart mitochondria has been studied using arsenazo III and dansylaziridine-labeled troponin C as Ca2+ indicators. Mitochondria accumulated 20 nmol of Ca2+/mg of protein by a respiration-dependent process. A23187, carbonyl cyanide p-trifluoromethoxyphenylhydrazone, or Na+ induced a release of Ca2+ from Ca2+-loaded and ruthenium red (RR)-treated mitochondria. Ca2+ antagonist drugs had no effect on the Ca2+ uptake process or on Ca2+ release induced either by A23187 or by carbonyl cyanide p-trifluoromethoxyphenylhydrazone but they were effective in inhibiting the Na+-induced Ca2+ release process. The drug concentrations that resulted in 50% inhibition of Na+-induced Ca2+ release were 7, 12, 13, 66, and 150 microM for diltiazem, prenylamine, fendiline, nifedipine, and verapamil, respectively. In the absence of RR, the net amount of Ca2+ released by Na+ was less than that which occurred in the presence of RR due to the simultaneous operation of both the Ca2+ uptake and the Ca2+ release processes. Under these conditions, the inhibition of Ca2+ uptake by RR brought about a complete release of Ca2+ from the mitochondria, and the inhibition of the Na+-induced Ca2+ release by diltiazem resulted in an apparent uptake of Ca2+ by the mitochondria. These results indicate that diltiazem and certain other Ca2+ antagonist drugs may be selective inhibitors of the Na+/Ca2+ antiporter in heart mitochondria much like ruthenium red is a selective inhibitor of the Ca2+ uniporter.

Animals↗
PubMed1980

Effects of RMI 12330A, a new inhibitor of adenylate cyclase on myocardial function and subcellular activity.

1 RMI 12330A, a lactam-imine, at concentrations of 10(-4) M and higher, inhibited basal as well as isoprenaline and NaF-stimulated adenylate cyclase activity of guinea-pig heart homogenates. However, RMI 12330A was a more potent inhibitor of histamine-stimulated adenylate cyclase (IC50 of 1.5 X 10(-5) M). 2 In the isolated work-performing heart of the guinea-pig, RMI 12330A (IC50 of 1.1 X 10(-6) M) depressed all cardiac functions: pressures developed, dP/dt, contractile force, dF/dt, work performance and stroke work. Left atrial pressure rose and the positive inotropic response to increasing heart rate (staircase) became negative. Histamine, isoprenaline and ouabain no longer caused positive inotropic effects. 3 Increasing the perfusate calcium concentration from 2.5 mM to 4.5 and 6.5 mM completely restored cardiac function after its depression by RMI 12330A. 4 RMI 12330A uncoupled mitochondrial oxidative phosphorylation; the classical uncoupler, dinitrophenol, had the same effects on cardiac dynamics as RMI 12330A. 5 RMI in high doses inhibited hydrolytic activity of Na+, K+-ATPase of crude and purified heart preparations (IC50 of 1.7 X 10(-4) M) and inhibited ouabain binding to the same enzymes (IC50 of 1.5 X 10(-4) M). 6 A lactam-imine analogue of RMI 12330A that had no effect on adenylate cyclase, was also without effect on any of the systems examined.

Adenylyl Cyclase Inhibitors↗
PubMed1978

Localization of the oxytocin receptor in the plasma membrane of rat myometrium.

The distribution of [3H]oxytocin binding sites among various subcellular fractions of rat myometrium paralleled the distribution of 5'-nucleotidase, a plasma membrane marker enzyme, but not of NADPH-cytochrome c reductase or succinate-cytochrome c reductase, which are endoplasmic reticulum and mitochondrial marker enzymes respectively. [3H]Oxytocin binding to the most enriched plasma membrane fraction showed the degree of selectivity with respect to hormone analogues that is expected for the oxytocin receptor. The binding of oxytocin to this fraction showed an apparent Kd of 1.98 X 10(-9) M and a capacity of 1.28 pmol mg-1. It is concluded that the oxytocin receptor is located on the plasma membrane of the smooth muscle cells of the rat uterus.

Animals↗