Rocchini A P, Gallagher K P, Botham M J, Lemmer J H, Szpunar C A, Behrendt D
Am J Physiol. 1985 Sep;249(3 Pt 2):H577-84. doi: 10.1152/ajpheart.1985.249.3.H577.
The ability of a chronic high-salt diet to prevent fatal hemorrhagic shock was examined in 36 mongrel dogs. Twenty-one dogs received a dietary supplement of 9 g sodium chloride/day for 6 wk, and 15 dogs received the same basic diet for 6 wk but without the sodium chloride supplement. Hemorrhagic shock was induced in all dogs by bleeding into an overhanging sealed reservoir. After 3 h of shock, salt-pretreated dogs had a lower systemic vascular resistance of 0.70 +/- 0.02 versus 1.44 +/- 0.04 mmHg X ml-1 X min X kg (P less than 0.01) and a higher cardiac output of 53 +/- 3 versus 26 +/- 3 ml X min-1 X kg-1 (P less than 0.01) than was observed in controls. At 2.5 h of shock, the salt-pretreated dogs also experienced an increase in gastrointestinal (P less than 0.01), hepatic arterial, (P less than 0.05), kidney (P less than 0.05), brain (P less than 0.01), and heart blood flows (P less than 0.001) compared with 0.5 h of shock, whereas the control dogs experienced no increased flow during this same period. We also observed that after 3 h of hypotension there was a significantly smaller increase in plasma renin activity in the salt-pretreated dogs. Administration of 0.1 U X kg-1 X min-1 of hog renin eliminated the differences in systemic vascular resistance, cardiac output, and survival in five salt-pretreated dogs.
在36只杂种狗身上研究了慢性高盐饮食预防致命性失血性休克的能力。21只狗接受了每天9克氯化钠的饮食补充,持续6周;15只狗接受相同的基础饮食6周,但不补充氯化钠。所有狗均通过向悬垂的密封储液器内放血诱导失血性休克。休克3小时后,经盐预处理的狗的全身血管阻力较低,为0.70±0.02,而对照组为1.44±0.04 mmHg·ml⁻¹·min·kg(P<0.01);心输出量较高,为53±3,而对照组为26±3 ml·min⁻¹·kg⁻¹(P<0.01)。在休克2.5小时时,与休克0.5小时相比,经盐预处理的狗的胃肠道血流(P<0.01)、肝动脉血流(P<0.05)、肾血流(P<0.05)、脑血流(P<0.01)和心脏血流(P<0.001)也有所增加,而对照组在此期间血流没有增加。我们还观察到,低血压3小时后,经盐预处理的狗血浆肾素活性的增加明显较小。给5只经盐预处理的狗注射0.1 U·kg⁻¹·min⁻¹的猪肾素消除了全身血管阻力、心输出量和存活率方面的差异。