- 作者: Mario Vassalle; Cheng-I Lin
- 作者服務機構: Department of Physiology and Pharmacology, State University of New York, Downstate Medical Center, Brooklyn, N.Y., USA, and Department of Physiology and Biophysics, National Defense Medical Center, Taipei, Taiwan(ROC)
- 中文摘要: --
- 英文摘要: The changes in cardiac function caused by calcium over-load are reviewed.Intracellular Ca2+ may increase in dif-ferent structures【e.g.sarcoplasmic reticulum(SR),cyto-plasm and mitochondria] to an excessive level whichinduces electrical and mechanical abnormalities in car-diac tissues. The electrical manifestations of Ca2+ over-load include arrhythmias caused by oscillatory (Vos) andnon-oscillatory (Vex) potentials.The mechanical manifes-tations include a decrease in force of contraction,con-tracture and aftercontractions. The underlying mecha-nisms involve a role of Na+ in electrical abnormalities asa charge carrier in the Na+-Ca2+ exchange and a role ofCa2+ in mechanical toxicity. Ca2+ overload may be in-duced by an increase in【Na+]i through the inhibition ofthe Na+-K+ pump(e.g. toxic concentrations of digitalis)orby an increase in Ca2+ load(e.g.catecholamines).TheCa2+ overload is enhanced by fast rates. Purkinje fibersare more susceptible to Ca2+ overload than myocardialfibers, possibly because of their greater Na+ load.If theSR is predominantly Ca2+ overloaded,Vos and fast dis-charge are induced through an oscillatory release of Ca2+in diastole from the SR; if the cytoplasm is Ca2+ over-loaded,the non-oscillatory Vex tail is induced at negativepotentials. The decrease in contractile force by Cat+over-load appears to be associated with a decrease in highenergy phosphates, since it is enhanced by metabolicinhibitors and reduced by metabolic substrates.Theionic currents Ios and Iex underlie Vos and Vex, respective-1y, both being due to an electrogenic extrusion of Ca2+through the Na+-Ca2+ exchange.Ios is an oscillatory cur-rent due to an oscillatory release of Ca2+ in early diastolefrom the Ca2+-overloaded SR,and lex is a non-oscillatorycurrent due to the extrusion of Ca2+ from the Cat+-over-loaded cytoplasm.Ios and Iex can be present singly orsimultaneously. An increase in【Ca2+]i appears to beinvolved in the short- and long-term compensatorymechanisms that tend to maintain cardiac output inphysiological and pathological conditions. Eventually,【Ca2+]; may increase to overload levels and contribute tocardiac failure.Experimental evidence suggests that clin-ical concentrations of digitalis increase force in Ca2+-overloaded cardiac cells by decreasing the inhibition ofthe Na+-K+ pump by Ca2+, thereby leading to a reductionin Ca2+ overload and to an increase in force of contrac-tion.
- 中文關鍵字: --
- 英文關鍵字: --