Filuk R B, Berezanski D J, Anthonisen N R
Respiratory Investigation Unit, University of Manitoba, Winnipeg, Canada.
J Appl Physiol (1985). 1988 Sep;65(3):1050-4. doi: 10.1152/jappl.1988.65.3.1050.
In nine normal subjects we measured the ventilatory response to isocapnic hypoxia with and without an intravenous infusion of 1 mg of somatostatin. Arterial O2 saturation was rapidly lowered to 80 +/- 2% in 2 min and maintained for 30 min. During control experiments, ventilation increased immediately (3-5 min) and then declined so that at 25 min of hypoxia ventilation was little above that in room air. Somatostatin was associated with a small decrease in ventilation while the subjects breathed room air. With hypoxia there was no immediate increase in ventilation for the group as a whole, although an increase was observed in one subject. With somatostatin, after 25 min of hypoxia, mean ventilation was lower than at any other time in the study; as hypoxia was discontinued ventilation increased slightly. Somatostatin causes profound depression of the ventilatory response to hypoxia by a mechanism that is not known but may be central. With somatostatin hypoxia of 25-min duration tends to depress ventilation.
在9名正常受试者中，我们测量了在静脉输注1毫克生长抑素和未输注生长抑素的情况下，对等碳酸血症性低氧的通气反应。动脉血氧饱和度在2分钟内迅速降至80±2%，并维持30分钟。在对照实验中，通气立即增加（3 - 5分钟），然后下降，因此在低氧25分钟时，通气仅略高于室内空气中的通气水平。当受试者呼吸室内空气时，生长抑素使通气量略有下降。在低氧状态下，尽管在一名受试者中观察到通气增加，但就整个组而言，通气并没有立即增加。使用生长抑素时，在低氧25分钟后，平均通气量低于研究中的任何其他时间；随着低氧状态的解除，通气量略有增加。生长抑素通过一种未知的机制导致对低氧的通气反应严重抑制，这种机制可能是中枢性的。使用生长抑素时，持续25分钟的低氧倾向于抑制通气。
