Gelpi R J, Mosca S M, Cingolani H E
Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, La Plata, Argentina.
J Mol Cell Cardiol. 1990 Nov;22(11):1285-96. doi: 10.1016/0022-2828(90)90064-9.
The effects of increased cytosolic calcium on cardiac mechanics were studied in open chest dogs instrumented with ultrasonic crystals and a miniature pressure transducer. Calcium was increased either by promoting calcium influx with Bay K 8644 (Bay K) or by increasing extracellular calcium concentration. A single dose of Bay K (10 micrograms/kg/min) was administered to each dog. Bay K increased LV systolic pressure, maximal rate of rise of LV pressure (LV + dP/dt), mean velocity of circumferential fiber shortening (Vcf), and calculated LV end-systolic wall stress. The time constant of isovolumic pressure decay (T) was calculated following two different methods: (a) a semilogarithmic method (Tz), and (b) using the linear relation between LV - dP/dt vs LV pressure (T1). Whereas Tz decreased from 31.7 +/- 2.6 to 26.7 +/- 1.7 ms (P less than 0.05), no changes were detected in T1 (46.3 +/- 4.4 vs 50.9 +/- 4.0 ms N.S.) The asymptote value (PB) decreased after Bay K from -9 +/- 2.8 to -22.5 +/- 4.2 mmHg (P less than 0.05). The same results were obtained when the changes in the loading conditions of the heart produced by Bay K were controlled by mechanical manoeuvers or after beta-blockade with propranolol. When calcium chloride was administered in amounts that will produce equal contractile changes as Bay K, a decrease in PB was also observed (from -14.7 +/- 1.6 to -27.7 +/- 6.1 mmHg (P less than 0.05]. Tz decreased from 29.6 +/- 3.6 to 22.5 +/- 2.9 ms (P less than 0.05) and no changes in T1 (52.5 +/- 5 vs 52.4 +/- 7.3 ms, N.S.) were detected. The decrease in the asymptote reported herein could induce a false decrease in the time constant if the altered values of PB are not considered, or another method of calculation of the time constant is used. Neither Bay K nor elevated extracellular calcium concentration modified the diastolic compliance. Changes in loading conditions or a cAMP pathway can be ruled out as a cause of the decrease in PB, since the results were reproduced under controlled loading conditions and beta blockade. These data suggest that increasing cytosolic calcium does not alter either the relaxation rate or the diastolic compliance but does decrease the value toward left ventricular pressure decays.
在开胸犬身上，通过植入超声晶体和微型压力传感器来研究细胞溶质钙增加对心脏力学的影响。钙的增加可通过用Bay K 8644（Bay K）促进钙内流或增加细胞外钙浓度来实现。给每只犬单次注射Bay K（10微克/千克/分钟）。Bay K可增加左心室收缩压、左心室压力最大上升速率（左心室 + dP/dt）、圆周纤维缩短平均速度（Vcf）以及计算得出的左心室收缩末期壁应力。等容压力衰减时间常数（T）通过两种不同方法计算：（a）半对数法（Tz），以及（b）利用左心室 - dP/dt与左心室压力之间的线性关系（T1）。Tz从31.7 ± 2.6毫秒降至26.7 ± 1.7毫秒（P < 0.05），而T1未检测到变化（46.3 ± 4.4对50.9 ± 4.0毫秒，无显著差异）。Bay K注射后渐近线值（PB）从 -9 ± 2.8毫米汞柱降至 -22.5 ± 4.2毫米汞柱（P < 0.05）。当通过机械操作或用普萘洛尔进行β受体阻断来控制Bay K引起的心脏负荷条件变化时，得到了相同的结果。当给予氯化钙，使其产生与Bay K相等的收缩变化量时，也观察到PB降低（从 -14.7 ± 1.6降至 -27.7 ± 6.1毫米汞柱（P < 0.05））。Tz从29.6 ± 3.6毫秒降至22.5 ± 2.9毫秒（P < 0.05），未检测到T1有变化（52.5 ± 5对52.4 ± 7.3毫秒，无显著差异）。如果不考虑PB的改变值或使用另一种时间常数计算方法，本文报道的渐近线降低可能会导致时间常数出现假性降低。Bay K和升高的细胞外钙浓度均未改变舒张期顺应性。由于在控制负荷条件和β受体阻断下重复得到了结果，因此可以排除负荷条件变化或cAMP途径是PB降低的原因。这些数据表明，增加细胞溶质钙既不改变舒张速率也不改变舒张期顺应性，但确实会降低左心室压力衰减值。
