Tveita T, Ytrehus K, Myhre E S, Hevrøy O
Department of Medical Physiology, University of Tromso, N-9037 Tromso, Norway.
J Appl Physiol (1985). 1998 Dec;85(6):2135-9. doi: 10.1152/jappl.1998.85.6.2135.
This study was aimed at elucidating whether ventricular hypothermia-induced dysfunction persisting after rewarming the unsupported in situ dog heart could be characterized as a systolic, diastolic, or combined disturbance. Core temperature of 8 mongrel dogs was gradually lowered to 25 degreesC and returned to 37 degreesC over a period of 328 min. Systolic function was described by maximum rate of increase in left ventricular (LV) pressure (dP/dtmax), relative segment shortening (SS%), stroke volume (SV), and the load-independent contractility index, preload recruitable stroke work (PRSW). Diastolic function was described by the isovolumic relaxation constant (tau) and the LV wall stiffness constant (Kp). Compared with prehypothermic control, a significant decrease in LV functional variables was measured at 25 degreesC: dP/dtmax 2,180 +/- 158 vs. 760 +/- 78 mmHg/s, SS% 20.1 +/- 1.2 vs. 13.3 +/- 1.0%, SV 11.7 +/- 0.7 vs. 8.5 +/- 0.7 ml, PRSW 90.5 +/- 7.7 vs. 29.1 +/- 5.9 J/m. 10(-2), Kp 0.78 +/- 0.10 vs. 0.28 +/- 0.03 mm-1, and tau 78.5 +/- 3.7 vs. 25.8 +/- 1.6 ms. After rewarming, the significant depression of LV systolic variables observed at 25 degreesC persisted: dP/dtmax 1,241 +/- 108 mmHg/s, SS% 10.2 +/- 0.8 J, SV 7.3 +/- 0.4 ml, and PRSW 52.1 +/- 3.6 m. 10(-2), whereas the diastolic values of Kp and tau returned to control. Thus hypothermia induced a significant depression of both systolic and diastolic LV variables. After rewarming, diastolic LV function was restored, in contrast to the persistently depressed LV systolic function. These observations indicate that cooling induces more long-lasting effects on the excitation-contraction coupling and the actin-myosin interaction than on sarcoplasmic reticulum Ca2+ trapping dysfunction or interstitial fluid content, making posthypothermic LV dysfunction a systolic perturbation.
本研究旨在阐明在无辅助原位犬心脏复温后持续存在的心室低温诱导功能障碍是否可被描述为收缩期、舒张期或联合性紊乱。8只杂种犬的核心体温逐渐降至25℃，并在328分钟内恢复至37℃。收缩功能通过左心室（LV）压力最大上升速率（dP/dtmax）、相对节段缩短率（SS%）、每搏输出量（SV）以及负荷独立收缩性指数、前负荷可募集每搏功（PRSW）来描述。舒张功能通过等容舒张常数（tau）和LV壁僵硬度常数（Kp）来描述。与低温前对照相比，在25℃时LV功能变量显著降低：dP/dtmax为2180±158 vs. 760±78 mmHg/s，SS%为20.1±1.2 vs. 13.3±1.0%，SV为11.7±0.7 vs. 8.5±0.7 ml，PRSW为90.5±7.7 vs. 29.1±5.9 J/m·10⁻²，Kp为0.78±0.10 vs. 0.28±0.03 mm⁻¹，tau为78.5±3.7 vs. 25.8±1.6 ms。复温后，在25℃时观察到的LV收缩期变量显著降低持续存在：dP/dtmax为1241±108 mmHg/s，SS%为10.2±0.8 J，SV为7.3±0.4 ml，PRSW为52.1±3.6 m·10⁻²，而Kp和tau的舒张期值恢复至对照水平。因此，低温诱导LV收缩期和舒张期变量均显著降低。复温后，LV舒张功能恢复，与持续降低的LV收缩功能形成对比。这些观察结果表明，降温对兴奋-收缩偶联和肌动蛋白-肌球蛋白相互作用的影响比对肌浆网Ca²⁺捕获功能障碍或细胞间液含量的影响更持久，使得低温后LV功能障碍成为一种收缩期扰动。
