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The effect of halothane on Ca2+ uptake or release by the sarcoplasmic reticulum (SR) was compared in the newborn and adult rabbit myocardium. The sarcolemma of right ventricular myocardium was disrupted (skinned) by homogenization. Fiber bundles were dissected from the homogenate, mounted on tension transducers, and immersed sequentially in five solutions that loaded Ca2+ into the SR, then in solutions containing either 2 or 25 mM caffeine to release SR-stored Ca2+, resulting in transient tension development. Experimental solutions were saturated with halothane in N2 gas during Ca2+ uptake by SR, Ca2+ release by SR, or during both SR Ca2+ uptake and release. Halothane (0.5-1.7%) resulted in dose-dependent depression of SR Ca2+ uptake in both newborn and adult skinned fibers. Less tension transient depression resulted in newborn (35%) than adult skinned fibers (49.5%, P less than 0.05) with 0.5% halothane exposure during SR Ca2+ uptake. Similar depression resulted in newborn (53.7% and 73.4%) and adult fibers (65.2% and 77.9%) with 1.0% and 1.7% halothane. Halothane had little effect on SR Ca2+ release by 25 mM caffeine but enhanced submaximal SR Ca2+ release by 2 mM caffeine more in newborn than adult myocardium. Increased Ca2+ efflux from newborn SR may contribute to the greater sensitivity of intact newborn cardiac muscle to exposure to halothane.

The mechanism of quinidine action on rabbit cardiac and skeletal muscle was examined with "functionally skinned" muscle-fiber preparations. By using these preparations we could correlate measurements of muscle tension with the effect of quinidine on the Ca2+ activation of the contractile proteins and on the Ca2+ uptake and release from the sarcoplasmic reticulum (SR).

The antishock effect of anisodamine (654-2) was observed in different kinds of experimental shock in groups of rabbits--due to late hemorrhage, superior mesenteric artery occlusion, and septic shock from peritonitis. The drug 654-2 significantly alleviated the progress of shock and increased the survival rate of the animals. The therapeutic effect of 654-2 was much better than that of other vasoactive drugs commonly used, such as norepinephrine, phenoxybenzamine, dopamine, and aramine. The antishock mechanism of 654-2 is probably partly due to its protective action on intestinal shock in preventing its effects becoming irreversible. The antishock action of 654-2 both by basic research workers and clinicians merits further study.

Rat's Ca-resistant ventricular myocytes and reconstituted liposomes of canine cardiac sarcolemma were used in analysing factors affecting Na(+)-Ca2+ exchange system. Decrease in extracellular (extravesicular) Na+ or increase in intracellular Na+ by inhibition of the Za(+)-K(+)-ATPase with ouabain stimulated the Na(+)-Ca2+ exchange. Mn2+, an antagonist of Na(+)-Ca2+ exchange, dose-dependently inhibited the Na(+)-dependent Ca2+ uptake. However, verapamil had no effect on it. Arachidonic acid and lipid peroxides caused by incubation with-H2O2 significantly stimulated Na(+)-Ca2+ exchange in a dose-dependent fashion.

The effect of methylmercury hydroxide (MMH) on the frequency of spontaneously beating atrial-SA node and on the isometric tension of electrically stimulated left atrial (1 Hz) preparation isolated from rats were investigated. The tissues were also fixed for ultrastructural study at the end of the experiments. We found that MMH, at low doses (0.5 and 2ppm), increased the frequency of contractions and the isometric tension of isolated atria and decreased the isometric tension of isolated papillar muscles, and at higher doses (greater than 2ppm), decreased all the above parameter. Morphologically, there were dilation and swelling of mitochondrial and sarcoplasmic reticulum. Occasionally, deposits of amorphous material in the mitochondria and myofibrillary degeneration of myocardial fibers were noted. It is concluded the MMH has direct effect on intracellular organelles (mitochondria, sarcoplasmic reticulum, and myofibril) of myocardial tissue and induces functional changes of atria and papillary muscles

Endothelin is a recently discovered bioactive peptide produced by vascular endothelial cells. By means of specific radioimmunoassay we found that plasma endothelin level in patients with late septic shock was significantly increased. And a typical shock model in healthy rats was reproduced by continuous infusion of endothelin (endothelin shock). Infusion of endothelin at a small dose to hemorrhagic shocked rats deteriorated the shock process and resulted in an irreversible development. From these results it is suggested that endothelin may be an endogenous injury-inducing factor, acting as one of the important humoral factors involved in shock pathogenesis.