Cardiopulmonary effects of dexmedetomidine in sevoflurane-anesthetized sheep with and without nitric oxide inhalation
Cardiopulmonary effects of dexmedetomidine in sevoflurane-anesthetized sheep with and without nitric oxide inhalation
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DOI：
10.2460/ajvr.2005.66.1496
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发表时间：
2005-09-01
影响因子：
1
通讯作者：
Huhtinen, MK
中科院分区：
文献类型：
--
作者：
K채stner, SBR;Kull, S;Huhtinen, MK
目的-确定在麻醉绵羊中静脉推注右美托咪定后，吸入一氧化氮（NO）是否可预防肺动脉高压并改善氧合。动物-6只健康成年绵羊。程序-在一项交叉研究中，七氟烷麻醉的绵羊接受右美托咪定（2 μ g/kg，IV），无NO（DEX治疗）或吸入NO（DEX-NO治疗）。在右美托咪定推注前和推注后120分钟测量心脏变量，包括呼吸力学。结果：右美托咪定引起心率和心输出量一过性降低。平均动脉压（MAP）和全身血管阻力（SVR）短暂升高，随后MAP和SVR显著降低，持续90分钟。右美托咪定注射后，平均肺动脉压（MPAP）和肺血管阻力一过性升高。注射后3分钟PaO 2显著降低，注射后10分钟达到最低值（平均SEM）13.3 - 78 kPa。PaO 2的降低伴随着动态顺应性的突然和长期降低以及气道阻力、分流分数和肺泡死腔的显著增加。MPAP的峰值变化在两种治疗之间没有差异。对于DEX-NO治疗，PaO 2显著低于DEX治疗，分流分数显著高于DEX治疗。结论和临床相关性-吸入NO不能预防右美托咪定IV给药引起的肺动脉压升高。预先吸入NO可能通过增加肺内分流而加重氧合损伤。
Objective-To determine whether inhaled nitric oxide (NO) prevents pulmonary hypertension and improves oxygenation after IV administration of a bolus of dexmedetomidine in anesthetized sheep. Animals-6 healthy adult sheep. Procedure-In a crossover study, sevoflurane-anesthetized sheep received dexmedetomidine (2 mu g/kg, IV) without NO (DEX treatment) or with inhaled NO (DEX-NO treatment). Cardiopulmonary variables, including respiratory mechanics, were measured before and for 120 minutes after bolus injection of dexmedetomidine. Results-Dexmedetomidine induced a transient decrease in heart rate and cardiac output. A short-lived increase in mean arterial pressure (MAP) and systemic vascular resistance (SVR) was followed by a significant decrease in MAP and SVR for 90 minutes. Mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance increased transiently after dexmedetomidine injection. The PaO2 was significantly decreased 3 minutes after injection and reached a minimum of (mean SEM) 13.3 78 kPa 10 minutes after injection. The decrease in PaO2 was accompanied by a sudden and prolonged decrease in dynamic compliance and a significant increase in airway resistance, shunt fraction, and alveolar dead space. Peak changes in MPAP did not differ between the 2 treatments. For the DEX-NO treatment, PaO2 was significantly lower and the shunt fraction significantly higher than for the DEX treatment. Conclusions and Clinical Relevance-Inhalation of NO did not prevent increases in pulmonary arterial pressures induced by IV administration of dexmedetomidine. Preemptive inhalation of NO intensified oxygenation impairment, probably through increases in intrapulmonary shunting.