Suguihara C, Hehre D, Huang J, Devia C, Bancalari E
University of Miami School of Medicine, Department of Pediatrics, FL 33101, USA.
J Pediatr. 1996 Mar;128(3):389-95. doi: 10.1016/s0022-3476(96)70290-1.
Infants exposed to cocaine in utero have been reported to have a higher incidence of apnea and altered ventilatory response to carbon dioxide and hypoxia. We investigated whether in utero cocaine exposure results in greater ventilatory depression during hypoxia in piglets.
Cocaine hydrochloride, 1.0 or 2.0 mg/kg given intramuscularly, or saline solution was administered daily to pair-fed pregnant sows during the last month of gestation. Thirteen cocaine-exposed piglets (mean +/- SD: age, 4.4 +/- 1.3 days; weight, 2.10 +/- 0.10 kg) and 15 saline solution-exposed piglets (age, 4.6 +/- 1.1 days; weight, 2.32 +/- 0.42 kg) were studied under chloral hydrate sedation. Minute ventilation (VE), arterial blood pressure (BP), heart rate (HR), oxygen consumption (VO2), and arterial blood gases were measured in room air. During hypoxia (fraction of inspired oxygen = 0.10), the values for VE, BP, and HR were obtained at 1, 5, and 10 minutes, VO2 was calculated during the last 5 minutes, and arterial blood gas samples taken after 10 minutes.
Basal VE did not differ between saline solution- and cocaine-exposed animals. The increase in VE at 1 minute of hypoxia was also similar. However, at 5 and 10 minutes of hypoxia, VE was significantly lower in the cocaine group than in the saline group (6% +/- 9% and 4% +/- 10% vs 15% +/- 13% and 21% +/- 14%; p < 0.02). Mean baseline BP and the initial increase in BP during hypoxia were not different between groups. However, BP remained increased throughout hypoxia only in the saline solution-exposed animals (p < 0.05). Changes in HR, VO2, arterial oxygen tension, and base excess during hypoxia were similar between groups.
These results show a decrease in the ventilatory response to hypoxia in newborn piglets prenatally exposed to cocaine. This change is most likely to be centrally mediated because the initial hypoxic hyperventilation was not modified by the intrauterine cocaine exposure. This decrease in ventilation cannot be explained by changes in metabolic rate or in cardiovascular or acid-base status.
据报道，子宫内暴露于可卡因的婴儿呼吸暂停的发生率较高，并且对二氧化碳和低氧的通气反应发生改变。我们研究了子宫内可卡因暴露是否会导致仔猪在低氧期间出现更大程度的通气抑制。
在妊娠最后一个月，对配对饲养的怀孕母猪每天肌肉注射1.0或2.0mg/kg盐酸可卡因或生理盐水。在水合氯醛镇静下，对13只暴露于可卡因的仔猪（平均±标准差：年龄，4.4±1.3天；体重，2.10±0.10kg）和15只暴露于生理盐水的仔猪（年龄，4.6±1.1天；体重，2.32±0.42kg）进行研究。在室内空气中测量分钟通气量（VE）、动脉血压（BP）、心率（HR）、氧耗量（VO2）和动脉血气。在低氧期间（吸入氧分数=0.10），在1、5和10分钟时获取VE、BP和HR的值，在最后5分钟计算VO2，并在10分钟后采集动脉血气样本。
暴露于生理盐水和可卡因的动物之间基础VE无差异。低氧1分钟时VE的增加也相似。然而，在低氧5分钟和10分钟时，可卡因组的VE显著低于生理盐水组（分别为6%±9%和4%±10% vs 15%±13%和21%±14%；p<0.02）。两组之间的平均基线BP和低氧期间BP的初始升高无差异。然而，仅在暴露于生理盐水的动物中，BP在整个低氧期间持续升高（p<0.05）。两组之间低氧期间HR、VO2、动脉血氧张力和碱剩余的变化相似。
这些结果表明，产前暴露于可卡因的新生仔猪对低氧的通气反应降低。这种变化很可能是由中枢介导的，因为最初的低氧性通气过度并未因子宫内可卡因暴露而改变。通气的这种降低不能用代谢率、心血管或酸碱状态的变化来解释。
