[Rib fracture following radiotherapy after radical mastectomy].
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Biomedical subjects
Publications and source records attributed to S Imai.
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1. Using a calcium buffer system, the effect of severe calcium lack on the shape of K-contracture of the guinea-pig's taenia coli was studied. Under conditions of calcium lack, the initial phasic response was preferentially affected and it disappeared completely at concentrations below 10(-7)M, while the ensuing tonic response persisted, though considerably diminished in size, even at the concentration of 10(-8)M.2. In calcium-free media, various multivalent cations, which according to Frank (1962) can support the K-contracture of a skeletal twitch muscle fibre in calcium-free solution, augmented the remaining tonic response, but did not restore the phasic response, when it was eliminated in calcium free environment.3. When K-contractures were induced in normal calcium media, these cations produced, in contrast, an abolition of the phasic response together with a partial depression of the tonic phase. They also inhibited a part of the fully developed contracture. The last effect was no longer obtainable in calcium-free media.4. It is concluded that the phasic response and a part of the tonic response of taenia coli depend upon the extracellular calcium for their initiation (and also for maintenance of tension in the case of the latter) and that the rest of the tonic response draws on a store of ;bound' calcium for its evolution.
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In an attempt to clarify the mechanism of sarcoplasmic reticulum (SR) dysfunction during the genesis of irreversible damage in the ischemic-reperfused myocardium, the changes in SR Ca2(+)-pumping ATPase (Ca2(+)-activated, Mg2(+)-dependent ATPase; Ca2(+)-ATPase) activity were studied during ischemia and subsequent reperfusion in the isolated perfused guinea pig heart preparation and correlated with the accumulation of calcium in the myocardium. Although the SR Ca2(+)-ATPase activity was not affected by ischemia of 40 min, reperfusion of the ischemic myocardium resulted in a definite time-dependent decrease in the enzyme activity. The reduction of SR Ca2(+)-ATPase activity was associated with a concomitant decrease in the enzyme concentration in the isolated SR and was in a good correlation with a substantial accumulation within the myocardium. As the results indicated the possibility that proteolytic degradation by a calcium-activated protease(s) was responsible for the reduction of enzyme activity, we examined for the possible involvement of calcium-activated neutral protease (CANP). However, SR Ca2(+)-ATPase obtained either from the normal hearts or from the hearts after 40-min ischemia was found to be quite resistant to proteolytic actions of the two forms of CANP, i.e., microCANP and mCANP partially purified from the guinea pig heart. These results suggest that a destructive process leading to the degradation of SR Ca2(+)-ATPase is activated by reperfusion, but not by ischemia per se, and that CANP is not implicated in the degradation of SR Ca2(+)-ATPase.