NEUROHORMONAL REGULATION OF SYSTEMATIC HEMOSTATIC FUNCTION

不明原因的酸中毒发生在多达15%的心脏手术后的患者中，由于这种疾病自发消退，并且有和没有乳酸酸中毒的患者的心输出量相似，因此这可能代表2型乳酸酸中毒。 目前对这种明显的2型乳酸酸中毒的机制知之甚少。 这项研究源于先前对全身止血功能的神经激素调节的研究，旨在评价应激激素对酸碱平衡和乳酸浓度的影响。在止血功能的原始研究中，志愿者在随机接受含有肾上腺素、皮质醇、胰高血糖素、血管紧张素II和加压素的应激激素输注时发生了明显的2型乳酸酸中毒。 随后，我们研究了接受所有f激素、四种激素（不含血管紧张素II）、三种激素（不含血管紧张素或加压素）的应激激素输注的健康志愿者，在所有这些输注期间，志愿者都出现了明显的2型乳酸酸中毒。目前，我们正在研究单独接受肾上腺素的健康志愿者。最初的志愿者也发生了2型乳酸酸中毒，考虑到常规评估术后乳酸酸中毒的成本，我们渴望评估后续志愿者。

Unexplained acidosis occurs in up to 15% of patients following cardiac surgery, Since this disorder resolves spontaneously and cardiac output is similar in patients with and without lactic acidosis, it is likely this represents a type 2 lactic acidosis. Little is presently known regarding the mechanism responsible for this apparent Type 2 lactic acidosis. This study, which stems from a previous investigation on the neurohormonal regulation of systemic hemostatic function, is designed to evaluate the impact of stress hormones on acid-base balance and lactate concentrations. Volunteers in the original study on hemostatic function were noted to develop an apparent Type 2 lactic acidosis when randomized to the stress hormone infusion that contained epinephrine, cortisol, glucagon, angiotensin Ii, and vasopressin. Subsequently we have studied healthy volunteers receiving stress hormone infusion of all f hormones, four hormones (without angiotensin II), three hormones (without angiotensin or vasopressin) and during all of these infusions the volunteers have developed an apparent Type 2 lactic acidosis of the same magnitude. Presently we are studying healthy volunteers receiving epinephrine alone. The initial volunteer also has developed a type 2 lactic acidosis and given the cost of routinely evaluating postoperative lactic acidosis we are eager to evaluate subsequent volunteers.