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利多卡因和乙醇对大鼠心脏乳头肌的温度依赖性变力作用。

Temperature-dependent inotropic effects of lignocaine and ethanol on rat heart papillary muscles.

作者信息

Schulz C S, Salvatici R P, Standen D J, Cabezas M E, Carpentier R G

机构信息

Department of Preclinical Sciences, Faculty of Medicine, Universidad de La Frontera, Temuco, Chile.

出版信息

Clin Exp Pharmacol Physiol. 1998 Nov;25(11):913-8. doi: 10.1111/j.1440-1681.1998.tb02343.x.

Abstract
  1. The main objective of the present study was to investigate the temperature dependence of the cardiac inotropic effects of lignocaine and ethanol (EtOH). 2. We studied the in vitro inotropic actions and interactions of EtOH (2.4 g/L) and lignocaine (25 mg/L) on rat papillary muscles superfused with Tyrode's solution and stimulated at 1 Hz at either 37 or 30 degrees C. Peak tension developed (PTD), maximum velocity of development of tension (VmaxT) and time to peak tension (TPT) were measured. 3. At 37 degrees C, EtOH depressed PTD, while VmaxT and TPT remained unchanged. At 37 degrees C, lignocaine alone or in combination with EtOH depressed all three parameters. 4. At 30 degrees C, EtOH did not modify PTD or VmaxT, whereas TPT decreased. At 30 degrees C, lignocaine decreased TPT, but VmaxT did not change and the effect of lignocaine on PTD was smaller at 30 degrees C than at 37 degrees C. Ethanol and lignocaine in combination decreased all three parameters at 30 degrees C. However, the depression of VmaxT by the combination of lignocaine and EtOH was less at 30 degrees C than at 37 degrees C. 5. Hypothermia (30 degrees C) protected the myocardium against the depressant actions of EtOH and lignocaine, alone or in combination. With EtOH alone, the protection resulted in no change in PTD. When lignocaine was involved, the protection resulted in a weaker action on PTD and VmaxT. The temperature dependence of the action of lignocaine may explain, at least in part, the development of ventricular failure in cardiac surgical patients exposed to lignocaine during hypothermia and rewarming.
摘要
  1. 本研究的主要目的是探究利多卡因和乙醇(EtOH)对心脏变力作用的温度依赖性。2. 我们研究了EtOH(2.4 g/L)和利多卡因(25 mg/L)在37或30摄氏度下对用台氏液灌注并以1 Hz频率刺激的大鼠乳头肌的体外变力作用及相互作用。测量了产生的峰值张力(PTD)、张力发展的最大速度(VmaxT)和达到峰值张力的时间(TPT)。3. 在37摄氏度时,EtOH降低了PTD,而VmaxT和TPT保持不变。在37摄氏度时,单独使用利多卡因或与EtOH联合使用均降低了所有这三个参数。4. 在30摄氏度时,EtOH未改变PTD或VmaxT,而TPT降低。在30摄氏度时,利多卡因降低了TPT,但VmaxT未改变,且利多卡因对PTD的作用在30摄氏度时比在37摄氏度时小。在30摄氏度时,乙醇和利多卡因联合使用降低了所有这三个参数。然而,利多卡因和EtOH联合使用对VmaxT的抑制在30摄氏度时比在37摄氏度时小。5. 低温(30摄氏度)可保护心肌免受单独或联合使用的EtOH和利多卡因的抑制作用。单独使用EtOH时,这种保护作用导致PTD无变化。当涉及利多卡因时,这种保护作用导致对PTD和VmaxT的作用较弱。利多卡因作用的温度依赖性可能至少部分解释了在低温和复温过程中接受利多卡因治疗的心脏手术患者发生心力衰竭的原因。

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