Curtis M T, Lefer A M
Am J Physiol. 1980 Sep;239(3):H416-21. doi: 10.1152/ajpheart.1980.239.3.H416.
The opiate antagonist, naloxone, was infused at 8 mg x kg-1 x h-1 in cats to determine its effect in hemorrhagic shock. Hemorrhaged cats treated with naloxone maintained postreinfusion mean arterial blood pressure at a higher value compared to those receiving only the vehicle. Final pressures were 77 +/- 9 mmHg for cats receiving vehicle compared to 120 +/- 6 mmHg for cats receiving naloxone. These values represent 58 +/-7 and 98 +/- 6% of initial pressures for vehicle- and naloxone-treated cats, respectively (P < 0.001). Naloxone also moderated increases in circulating lysosomal hydrolase activity (4- vs. 23-fold increase) and total plasma proteolysis (33 vs. 100% increase). Plasma myocardial depressant factor activity was also significantly reduced in naloxone-treated hemorrhaged cats compared to shock cats given 0.9% NaCl (16 +/- 3 vs. 58 +/- 4 U, respectively; P < 0.001). Studies on cat papillary muscles demonstrated that naloxone at concentrations slightly higher than estimated plasma values during shock exerted a moderate positive inotropic effect. Our results show that naloxone improved the hemodynamic and biochemical state of cats in hemorrhagic shock. Inhibition of proteolysis and stabilization of lysosomal membranes appear to be ivolved in the protective action of naloxone, along with the well-known opiate-antagonistic action of this agent.
给猫以8毫克×千克-1×小时-1的剂量输注阿片拮抗剂纳洛酮,以确定其在失血性休克中的作用。与仅接受赋形剂的猫相比,用纳洛酮治疗的出血猫在再输注后平均动脉血压维持在更高水平。接受赋形剂的猫的最终血压为77±9毫米汞柱,而接受纳洛酮的猫为120±6毫米汞柱。这些值分别代表接受赋形剂和纳洛酮治疗的猫初始血压的58±7%和98±6%(P<0.001)。纳洛酮还减轻了循环中溶酶体水解酶活性的增加(4倍与23倍增加)和血浆总蛋白水解(33%与100%增加)。与给予0.9%氯化钠的休克猫相比,纳洛酮治疗的出血猫血浆心肌抑制因子活性也显著降低(分别为16±3与58±4单位;P<0.001)。对猫乳头肌的研究表明,在休克期间浓度略高于估计血浆值的纳洛酮发挥了适度的正性肌力作用。我们的结果表明,纳洛酮改善了失血性休克猫的血流动力学和生化状态。抑制蛋白水解和稳定溶酶体膜似乎参与了纳洛酮的保护作用,以及该药物众所周知的阿片拮抗作用。