Mitsuhata H, Takeuchi H, Saitoh J, Hasome N, Horiguchi Y, Shimizu R
Department of Anesthesiology, Jichi Medical School, Tochigi, Japan.
Shock. 1995 Jun;3(6):447-53; discussion 454.
We investigated whether a nitric oxide synthase (NOS) inhibitor improves cardiovascular depression associated with anaphylaxis. After induction of anaphylactic circulatory depression, one group received an NOS inhibitor (Group I, n = 6) and the other received saline solution (Group II, n = 5). Mean arterial pressure and right atrial pressure were significantly higher in Group I than in Group II. Hematocrit was significantly lower in Group I than in Group II. Cardiac output, stroke volume, mean pulmonary arterial pressure, the maximum rate of increase in left ventricular pressure, and the time constant of the fall in isovolumic left ventricular pressure did not differ between the groups. In conclusion, L-NAME attenuates hypotension, but does not improve cardiac depression in anaphylaxis in dogs. Our finding that NOS inhibitor did not improve cardiac function implies that the production of NO in anaphylaxis may have a protective effect with regard to cardiac performance.
我们研究了一氧化氮合酶（NOS）抑制剂是否能改善与过敏反应相关的心血管抑制。在诱导过敏反应性循环抑制后，一组接受NOS抑制剂（I组，n = 6），另一组接受盐溶液（II组，n = 5）。I组的平均动脉压和右心房压显著高于II组。I组的血细胞比容显著低于II组。两组之间的心输出量、每搏量、平均肺动脉压、左心室压力最大上升速率以及等容性左心室压力下降的时间常数没有差异。总之，L - 精氨酸甲酯（L - NAME）可减轻低血压，但不能改善犬类过敏反应中的心脏抑制。我们发现NOS抑制剂不能改善心脏功能，这意味着过敏反应中一氧化氮的产生可能对心脏功能有保护作用。
