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钙离子进入肌丝的速率及数量的变化,控制心肌张力的增长及其速率;心肌舒张时,从收缩机制中钙离子析出的速率,控制张力的减弱,因此心室压力增加的速率以及射血速度,以及压力减弱及心室充盈度,这二者均依赖于细胞内Ca~(++)的动力学。Ca~(++)能增强正性收缩能药物的作用。酸中毒时从肌浆网(SR)释出的Ca~(++)减少,这是局部缺血致负性收缩能效应的部分原因。舒张时,心肌胞浆中Ca~(++)浓度低于10~(-7)M,此时SR主动地摄入Ca~(++)。当Ca~(++)再被释入到胞浆中,其浓度可增至100倍,便激活收缩因素产生收
Changes in the rate and amount of calcium ions entering the myofilament control the growth and rate of myocardial tension; the rate of calcium ion withdrawal from the contractile mechanism during myocardial relaxation reduces the control of the tension, thus the rate of ventricular pressure increase and the rate of ejection , As well as decreased stress and ventricular filling, both of which depend on intracellular Ca ~ (++) kinetics. Ca ~ (++) can enhance the role of positive systolic drug. Ca (++) released from sarcoplasmic reticulum (SR) during acidosis is reduced, which is partly responsible for the negative contractile energy effects of ischemia. When diastolic, the concentration of Ca ~ (++) in the cytoplasm of myocardium was lower than 10 ~ (-7) M, at this time, SR actively ingested Ca ~ (++). When Ca ~ (++) is released into the cytoplasm again, its concentration can be increased to 100 times to activate the contraction factor