Experiments on smooth muscles of rat stomach showed that lysophosphatidylcholine in concentrations of 10(-8) and 10(-7) g/ml does not modulate the tonotropic effect of acetylcholine (10(-6) g/ml), in a concentration of 10(-6) g/ml potentiated this effect (similarly to phosphatidylcholine, 10(-6) g/ml), and reduced it in concentrations of 10(-5)-10(-4) g/ml (similarly to hen egg yolk in dilutions of 1:500, 1:100, and 1:500). These data indicate that lysophosphatidylcholine modifies signal transduction from the receptor to G protein.
It is known that women and rats have increased minute volume of blood flow (MV) during pregnancy. It is believed that this is due to an increase in heart rate. This remains unclear — whether pregnancy increases myocardial contractility (and consequently increases the stroke volume). There are no data on changes of myocardium electroexcitability during pregnancy. To clarify these issues, experiments were conducted on strips of right ventricular of 94 nonpregnant and 45 pregnant rats. The strips were perfused with Krebs solution at 37 °C, which is preenriched by pure oxygen, and after 30 minutes of adaptation evaluated force of contractions. They are caused by electrostimulation (5 ms, 1 Hz, 20 V) applied transmural. Then determined the excitation threshold, i.e, minimum voltage (V), wherein a single stimul (5 ms) induced contraction. It was found that the force of contraction (mN, mN/mg wet weight or mN/mg dry weight of strips ) and the excitation threshold do not depend on the phase of the estrous cycle, pregnancy, and the availability of its terms. This means that during pregnancy contractility of right ventricle of rats myocardial does not change, and even tends to decrease. Therefore, increasing of MV during pregnancy, most likely due to an increase in heart rate. It was also established that at the end of pregnancy water content increases (on 12 %) in the myocardium (perhaps by increasing the expression of aquaporins in cardiomyocytes) which is regarded as a reflection of adaptation. Refs 41. Figs 4.
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