Tarasiuk A, Janco J, Sofer S
Pediatric Intensive Care Unit, Soroka Medical Center, Israel.
Acta Physiol Scand. 1997 Oct;161(2):141-9. doi: 10.1046/j.1365-201X.1997.00202.x.
Scorpion venom can induce in dogs severe haemodynamic changes leading to rapid rise in systemic blood pressure and cardiac output, followed by reduction of cardiac output and blood pressure within 1 h. The decrease in cardiac output is not related to myocardial dysfunction (Tarasiuk et al. 1994). We hypothesized that scorpion venom affects cardiac output by reducing venous return to the heart. Venous return was studied by steady-state measurements of cardiac output, the pressure gradient and resistance to venous return, in 16 dogs following injection of 0.05 mg kg-1 venom obtained from the scorpion species Leiurus quinquestriatus. In eight of the 16 dogs, atropine (0.1 mg kg-1) was given 15 min prior to venom injection (n = 4) or 85 min (n = 4) after venom administration. In five additional dogs, the stability of the preparation over time was evaluated following the same protocol without the injection of the venom. At 15 min, the venom induced an increase in blood pressure (80%) and cardiac output (250%) (P < 0.001) with little effect on heart rate. At 90 min, cardiac output and heart rate declined considerably below baseline (P < 0.001). Atropine prevented the decrease in heart rate, but did not affect the reduction of cardiac output. Five minutes after venom injection, mean circulatory pressure increased by 300% (P < 0.001), which was accompanied by a rightward shift of the venous return curve with no effect on resistance to venous return. At 120 min, mean circulatory pressure recovered and resistance to venous return remained at 40% (P < 0.01) above baseline. This study indicates that, in dogs, scorpion venom affects cardiac output by modifying the determinants of venous return. The initial increase in cardiac output is related to increased mean circulatory pressure since resistance to venous return did not change. The later fall in cardiac output is related to the reduction of mean circulatory pressure and increased resistance to venous return.
蝎毒可在犬类中诱发严重的血流动力学变化，导致全身血压和心输出量迅速升高，随后在1小时内心输出量和血压降低。心输出量的降低与心肌功能障碍无关（塔拉修克等人，1994年）。我们推测蝎毒通过减少静脉回心血量来影响心输出量。通过对16只犬注射从以色列金蝎获取的0.05毫克/千克毒液后，对心输出量、压力梯度和静脉回心血量阻力进行稳态测量，研究静脉回心血量。在16只犬中的8只，在注射毒液前15分钟（n = 4）或注射毒液后85分钟（n = 4）给予阿托品（0.1毫克/千克）。另外5只犬按照相同方案但不注射毒液来评估制剂随时间的稳定性。在15分钟时，毒液使血压升高（80%）和心输出量增加（250%）（P < 0.001），对心率影响很小。在90分钟时，心输出量和心率大幅降至基线以下（P < 0.001）。阿托品可防止心率下降，但不影响心输出量的降低。注射毒液5分钟后，平均循环压力增加300%（P < 0.001），同时静脉回心血量曲线右移，对静脉回心血量阻力无影响。在120分钟时，平均循环压力恢复，静脉回心血量阻力仍比基线高40%（P < 0.01）。这项研究表明，在犬类中，蝎毒通过改变静脉回心血量的决定因素来影响心输出量。心输出量最初的增加与平均循环压力升高有关，因为静脉回心血量阻力没有变化。随后心输出量的下降与平均循环压力降低和静脉回心血量阻力增加有关。
