Rundgren Mats, Frithiof Robert, Hjelmqvist Hans, Ullman Johan E, Eriksson Stefan
Karolinska Institutet, Department of Physiology and Pharmacology, S-171 77 Stockholm, Sweden.
Physiol Behav. 2007 Sep 10;92(1-2):272-7. doi: 10.1016/j.physbeh.2007.05.029. Epub 2007 May 21.
During progressive blood loss several mechanisms act in concert to compensate for the reduced intravascular volume with the overall aim to provide sufficient blood supply to vital organs. The hemodynamic responses in this situation follow a characteristic course of events in conscious individuals with an initial phase of largely maintained blood pressure and tachycardia followed by an abrupt fall in pressure, accompanied by bradycardia and widespread inhibition of sympathetic nervous activity when 20-30% of the blood volume is lost. Our research has focussed on Na+ and angiotensin II effects on the brain for the cardiovascular compensatory mechanisms in response to hypotensive hemorrhage in sheep. We have found that intracerebroventricular infusion of hypertonic NaCl solution improves the tolerance to blood loss, i.e., increases the amount of blood loss needed to induce hypotension. Inhalation anesthesia abolished this effect of the infusion. Similarly, corresponding infusions of angiotensin II also increased the resistance to blood loss in conscious animals only, although accompanied by different hemodynamic compensatory mechanisms. The effects of intracerebroventricular hypertonic NaCl infusion on cardiovascular compensation during hemorrhage are similar to those achieved with treatment of hemorrhagic shock with intravenous infusions of small volumes of hypertonic NaCl solutions. We therefore suggest that a substantial part of the beneficial effect of that treatment is mediated via direct effects of the hypernatremia on the brain. These observations also illustrate the need for further elucidation of more possible influences on autonomic functions by increased Na+ concentration which, together with hypovolemia, is a hallmark of dehydration.
在进行性失血过程中，多种机制协同作用，以补偿血管内容量的减少，总体目标是为重要器官提供充足的血液供应。在清醒个体中，这种情况下的血流动力学反应遵循一系列特征性事件，最初阶段血压基本维持，伴有心动过速，随后血压急剧下降，伴有心动过缓和交感神经活动广泛抑制，此时失血量达血容量的20 - 30%。我们的研究聚焦于钠和血管紧张素II对大脑的作用，以探讨绵羊低血压性出血时的心血管代偿机制。我们发现，脑室内注入高渗氯化钠溶液可提高对失血的耐受性，即增加诱发低血压所需的失血量。吸入麻醉消除了注入的这种作用。同样，相应注入血管紧张素II也仅在清醒动物中增加了对失血的抵抗力，尽管伴有不同的血流动力学代偿机制。脑室内注入高渗氯化钠对出血时心血管代偿的作用与静脉输注少量高渗氯化钠溶液治疗失血性休克的效果相似。因此，我们认为该治疗的大部分有益作用是通过高钠血症对大脑的直接作用介导的。这些观察结果还表明，需要进一步阐明钠浓度升高对自主神经功能更可能产生的影响，钠浓度升高与血容量减少一起，是脱水的一个标志。
