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Summary
Gasser R et al.  
Some observations on Ca-overload in rat ventricular tissue

Journal of Clinical and Basic Cardiology 1999; 2 (2): 255-258

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Fig. 1: Myokard - Kalzium Fig. 2: Mykard - Kalzium Fig. 3: Myokard - Kalzium Fig. 4: Myokard - Kalzium



Keywords: Kalzium-OverloadKalziumantagonistMikroelektrodeMyokardRatteCa antagonistCa-overloadmicroelectrodemyocardiumrat

It is well known that Ca-antagonists are able to protect myocardium, arterial wall and other tissue from deleterious Ca uptake. This has been shown using atomic absorption spectroscopy as far as the total Ca-content of the tissue is concerned. The behaviour of free intracellular Ca in this context has, however, remained unknown so far. In our experiments myocardial Ca-overload has been induced by a single high dose of vit. D3. Here we show that vitamin D3-induced myocardial Ca-overload can be prevented by diltiazem. Using Ca++-selective microelectrodes in Sprague-Dawley rats we demonstrate that a single high dose of vit. D3 led to an excessive rise in intracellular free resting calcium ((Ca++)i). This myocardial (Ca++)i-overload has been effectively prevented by s.c. diltiazem (300 mg/kg/d) and verapamil (60 mg/kg/d). Thus, we found resting values of myocardial (Ca++)i of 2.0 0.2 x 10-7 mol/l (n = 7). In vit. D3 treated rats (Ca++)i amounted to 3.2 1.0 x 10-5 mol/l (n = 7). Conversely, in the vit. D3 + diltiazem and vit. D3 + verapamil groups (Ca++)i was 1.6 0.8 x 10-6 mol/l and 2.1 0.7 x 10-6 mol/l, respectively. We conclude that Ca++-antagonists can prevent the vit. D3-induced excessive rise in myocardial free intracellular Ca++-concentrations. In addition, we show that Ca++-selective microelectrodes constitute a suitable means for studying the effect of pharmacological agents on (Ca++)i. J Clin Basic Cardiol 1999; 2: 255-8.
 
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