Pfenninger E, Bowdler I, Novak R, Grünert A, Kilian J
Resuscitation. 1987 Jun;15(2):125-33. doi: 10.1016/0300-9572(87)90023-2.
The effects of spontaneous respiration and mechanical ventilation were examined by investigating the interaction between elevated intracranial pressure and alcohol intoxication. Ethanol (200 ml 48%) was infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (group 1), 7 young pigs with elevated cerebral pressure during spontaneous respiration (group 2), and 4 young pigs without elevated cerebral pressure during spontaneous respiration (group 3). While the behavior of intracranial pressure during mechanical ventilation in the animals from group 1 was inhomogeneous with a tendency to rise (29-34 mmHg), cerebral pressure (28-55 mmHg) increased drastically in the animals from group 2. This increase was associated with a sharp rise of Pa,CO2 (37.6-73.3 mmHg) and a decrease of Pa,O2 (74 mmHg to 13 mmHg). None of the animals in group 2 survived. Pa,CO2 also rose in alcoholized animals without elevated cerebral pressure (group 3) (41.9-63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory center. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure generally avoided.
通过研究颅内压升高与酒精中毒之间的相互作用，来考察自主呼吸和机械通气的影响。在机械通气期间，给11头颅内压升高的幼猪输注乙醇（200毫升48%）（第1组）；在自主呼吸期间，给7头颅内压升高的幼猪输注乙醇（第2组）；在自主呼吸期间，给4头颅内压未升高的幼猪输注乙醇（第3组）。第1组动物在机械通气期间颅内压的变化不均匀，有升高趋势（29 - 34 mmHg），而第2组动物的脑压（28 - 55 mmHg）急剧升高。这种升高与动脉血二氧化碳分压（Pa,CO2）的急剧上升（37.6 - 73.3 mmHg）和动脉血氧分压（Pa,O2）的下降（从74 mmHg降至13 mmHg）相关。第2组动物无一存活。在颅内压未升高的酒精化动物（第3组）中，Pa,CO2也升高了（41.9 - 63.9 mmHg）；然而，颅内压仍在正常范围内。第3组所有动物均存活。我们的研究结果表明，颅内压升高和酒精中毒对呼吸中枢的抑制有累积或增强作用。机械通气可预防呼吸抑制，因此通常可避免颅内压进一步升高。
