Biomedical subjects

R J Barsotti

Publications and source records attributed to R J Barsotti.

21 records · Page 2Linked to original sources

PubMed1983

Myosin light chain phosphorylation does not modulate cross-bridge cycling rate in mouse skeletal muscle.

An attempt was made to determine whether phosphorylation of the myosin light chain represents a thick filament-associated mechanism for modulating the rate of cross-bridge cycling in mouse skeletal muscle. When the degree of light chain phosphorylation was varied independently of tetanus duration, there was no correlation of phosphorylation with cross-bridge turnover rate, as measured by the shortening velocity of the muscle. It is concluded that in intact skeletal muscle phosphorylation of the myosin light chain does not in itself modulate cross-bridge cycling rate and that previously reported changes in cycling rate were due to other factors that may vary with tetanus duration.

Animals↗

PubMed1982

Blood flow and ultrastructure in ischemic myocardium of cats given dexamethasone.

Regional myocardial blood flow or myocardial creatine kinase activity and ultrastructure was studied in anesthetized cats subjected to sham operation, 5 h of circumflex-artery ligation, or 2 h of coronary-artery ligation with 3 h of reperfusion. Sham-operated cats were given dexamethasone sodium phosphate (8 mg/kg iv) at the beginning of the experiment. Cats subjected to coronary-artery ligation were given steroid or vehicle before ligation. In sham-operated cats the average blood flow in tissue of the anterior wall was 2.11 +/- 0.37 (SER) ml.g-1.min-1. The corresponding flow for tissue of the posterior wall was 2.22 +/- 0.42 ml.g-1.min-1. Ligation of the circumflex artery produced a range of average blood flow in the posterior basal myocardium that was 52-92% less than that of sham-operated cats. Within the tissue of the posterior left ventricular wall, steroid pretreatment did not prevent loss of creatine kinase activity after coronary-artery ligation. Moreover, steroid pretreatment was ineffective in maintaining myocardial structure in reperfused myocardial tissue. These results indicate that 1) dexamethasone does not effectively increase blood flow within ischemic or reperfused myocardial tissue, and 2) dexamethasone may stabilize ischemic myocardial tissue. However, upon reperfusion, dexamethasone is unable to maintain myocardial ultrastructure in moderately to severely ischemic tissue.

Animals↗

PubMed1975

The reversibility of skeletal muscle pyruvate kinase and an assessment of its capacity to support glyconeogenesis.

The kinetics of pyruvate phosphorylation by rabbit skeletal muscle pyruvate kinase (EC 2.7.1.40) has been studied with a coupled assay using P-enolpyruvate carboxylase (EC 4.1.1.31) and malate dehydrogenase (EC 1.1.1.37). The reaction sequence is (See journal for formula). Although the equilibrium of the pyruvate kinase reaction by itself strongly favors pyruvate production, the over-all equilibrium of this coupled system favors the depletion of pyruvate, thus greatly reducing the problem of back reaction during the assay. In addition, the oxidation of NADH by malate dehydrogenase makes it possible to monitor the system with a spectrophotometer. The Michaelis constant of pyruvate kinase was found to be 0.9 mM for ATP and 7 mM for pyruvate, values that agree reasonably well with earlier studies using direct assays. However, the maximum velocity is about 6 mumol of pyruvate phosphorylated/min/mg of enzyme, which is very much faster than that indicated by earlier studies. These results suggest that the metabolic significance of the reverse reaction of muscle pyruvate kinase may have been underestimated. In particular, the data given here suggest that its rate in vivo is probably comparable to the observed rate of glycogen synthesis from lactate, making possible glyconeogenesis in muscle by pyruvate kinase reversal without the need for an enzymatic bypass of the kind employed by liver and kidney.

Adenosine Triphosphate↗