Torbati D, Mangino M J, Garcia E, Estrada M, Totapally B R, Wolfsdorf J
Division of Critical Care Medicine, Miami Children's Hospital, FL 33155-3009, USA.
Crit Care Med. 1998 Nov;26(11):1863-7. doi: 10.1097/00003246-199811000-00030.
To test the hypothesis that PaCO2 levels generated during permissive hypercapnia may enhance arterial oxygenation, when ventilation is maintained.
Prospective study.
Research laboratory in a hospital.
One group of eight mongrel dogs (four male; four female).
The dogs were anesthetized (30 mg/kg iv pentobarbital), intubated, and cannulated in one femoral artery and vein. While paralyzed with 0.1 mg/kg/hr iv vecouronium bromide, all subjects were ventilated with room air. Anesthesia was maintained, using 2 to 3 mg/kg/hr iv pentobarbital. Arterial hypercapnia at the levels generated during permissive hypercapnia was produced by stepwise increases in the dry, inspired Pco2 (PiCO2) (0, 30, 45, 60 and 75 torr [0, 4, 6, 8, and 10 kPa]; 15 mins each).
Blood gas profiles were determined at each level of hypercapnia. The minute volume was maintained at the baseline level during all exposures. Arterial hypercapnia produced gradual and significant increases in the hemoglobin concentration. These increases were approximately 6%, 7%, 11%, and 14% at PiCO2 of 30, 45, 60, and 75 torr (4, 6, 8, and 10 kPa), respectively (p < .05; repeated analysis of variance followed by Dunnett multiple comparisons test). In parallel, the oxygen content increased by approximately 6%, 7%, 11%, and 13%, respectively. During hypercapnic trials, the PaO2 remained at the normal range, whereas the dry, inspired PO2 (PiO2) was reduced from 150 to 138 torr (20 to 18.4 kPa). The average PaO2 at the highest investigated level of arterial hypercapnia was at a normal range. The hemoglobin concentration and oxygen content returned to baseline values 30 mins after hypercapnic trials. The PaCO2 and pH became normalized 15 mins after hypercapnic trials. Indirect evidence for a similar response to hypercapnia in humans is presented.
Permissive hypercapnia due to inhaled CO2 increases oxygen-carrying capacity in dogs. The PaO2 remains at normal range even at a PiCO2 of 75 torr (10 kPa). The benefits of these effects during permissive hypercapnia, due to controlled hypoventilation, warrants investigation.
检验如下假设,即在维持通气时,允许性高碳酸血症期间产生的动脉血二氧化碳分压(PaCO₂)水平可能会增强动脉氧合作用。
前瞻性研究。
一家医院的研究实验室。
一组八只杂种犬(四只雄性;四只雌性)。
给犬只静脉注射戊巴比妥(30mg/kg)进行麻醉,插管,并在一条股动脉和静脉中插入导管。在静脉注射维库溴铵(0.1mg/kg/hr)使其麻痹的同时,所有研究对象均使用室内空气进行通气。使用静脉注射戊巴比妥(2至3mg/kg/hr)维持麻醉。通过逐步增加干燥吸入二氧化碳分压(PiCO₂)(0、30、45、60和75托[0、4、6、8和10kPa];每次15分钟),产生允许性高碳酸血症期间出现的动脉血二氧化碳水平升高。
在每个高碳酸血症水平测定血气指标。在所有暴露期间,每分通气量维持在基线水平。动脉血二氧化碳水平升高使血红蛋白浓度逐渐且显著增加。在PiCO₂为30、45、60和75托(4、6、8和10kPa)时,这些增加分别约为6%、7%、11%和14%(p<0.05;重复方差分析后进行Dunnett多重比较检验)。与此同时,氧含量分别增加了约6%、7%、11%和13%。在高碳酸血症试验期间,动脉血氧分压(PaO₂)保持在正常范围内,而干燥吸入氧分压(PiO₂)从150托降至138托(20至18.4kPa)。在研究的最高动脉血二氧化碳水平时,平均PaO₂处于正常范围。高碳酸血症试验30分钟后,血红蛋白浓度和氧含量恢复至基线值。高碳酸血症试验15分钟后,PaCO₂和pH恢复正常。文中还提供了人类对高碳酸血症有类似反应的间接证据。
吸入二氧化碳导致的允许性高碳酸血症可增加犬类的携氧能力。即使在PiCO₂为75托(10kPa)时,PaO₂仍保持在正常范围内。由于控制性低通气导致的允许性高碳酸血症期间这些效应的益处值得研究。