Perbeck L, Hedqvist P
Acta Chir Scand. 1982;148(1):3-8.
Blood pressure responses to noradrenaline were studied in anesthetised rats subjected to hypovolemia by a constant pressure--open reservoir technique. Hypovolemia resulted in a decrease of the noradrenaline response, which correlated well to the length of the hypovolemic period and to the arterial perfusion pressure when lower than 60 mmHg. Early after retransfusion of the shed blood the pressure response to noradrenaline continued to decrease and began to recover only after additional 30-60 min. The decline in blood pressure response to noradrenaline during hemorrhagic shock was not significantly altered by adrenalectomy, infusion of various metabolic substrates, such as fat emulsion, Na-pyruvate or ATP-MgCl2, or by protection against respiratory and metabolic acidosis. The results imply that high levels of circulating catecholamines, substrate exhaustion and acidosis may be regarded as secondary factors rather than primary causes of decreased blood pressure response and development of irreversible hemorrhagic shock, and they stress the importance of adequate tissue perfusion in the protection against these disorders.
采用恒压-开放贮液器技术，对麻醉状态下造成低血容量的大鼠的去甲肾上腺素血压反应进行了研究。低血容量导致去甲肾上腺素反应降低，这与低血容量期的时长以及低于60 mmHg时的动脉灌注压密切相关。回输失血后早期，对去甲肾上腺素的血压反应持续降低，仅在额外30 - 60分钟后才开始恢复。出血性休克期间对去甲肾上腺素的血压反应下降，并未因肾上腺切除术、输注各种代谢底物（如脂肪乳剂、丙酮酸钠或ATP - MgCl₂）或预防呼吸性和代谢性酸中毒而发生显著改变。结果表明，循环儿茶酚胺水平升高、底物耗竭和酸中毒可能被视为次要因素，而非血压反应降低和不可逆性出血性休克发生的主要原因，并且这些结果强调了充足的组织灌注在预防这些病症中的重要性。
