Salak N, Pajk W, Knotzer H, Hofstötter H, Schwarz B, Mayr A, Labeck B, Kafka R, Ulmer H, Mutz N, Hasibeder W
Division of General and Surgical Intensive Care Medicine, Department of Anesthesia and Critical Care Medicine, The Leopold Franzens University of Innsbruck, Innsbruck, Austria.
Crit Care Med. 2001 Feb;29(2):367-73. doi: 10.1097/00003246-200102000-00027.
To study the effects of increasing dosages of epinephrine given intravenously on intestinal oxygen supply and, in particular, mucosal tissue oxygen tension in an autoperfused, innervated jejunal segment.
Prospective, randomized experimental study.
Animal research laboratory.
Domestic pigs.
Sixteen pigs were anesthetized, paralyzed, and normoventilated. A small segment of the jejunal mucosa was exposed by midline laparotomy and antimesenteric incision. Mucosal oxygen tension was measured by using Clark-type surface oxygen electrodes. Microvascular hemoglobin oxygen saturation and microvascular blood flow (perfusion units) were determined by tissue reflectance spectrophotometry and laser-Doppler velocimetry. Systemic hemodynamics, mesenteric-venous acid-base and blood gas variables, and systemic acid-base and blood gas variables were recorded. Measurements were performed after a resting period and at 20-min intervals during infusion of increasing dosages of epinephrine (n = 8; 0.01, 0.05, 0.1, 0.5, 1, and 2 microg x kg(-1) x min(-1)) or without treatment (n = 8). In addition, arterial and mesenteric-venous lactate concentrations were measured at baseline and at 60 and 120 mins.
Epinephrine infusion led to significant tachycardia; an increase in cardiac output, systemic oxygen delivery, and oxygen consumption; and development of lactic acidosis. Epinephrine significantly increased jejunal microvascular blood flow (baseline, 267 +/- 39 perfusion units; maximum value, 443 +/- 35 perfusion units) and mucosal oxygen tension (baseline, 36 +/- 2.0 torr [4.79 +/- 0.27 kPa]; maximum value, 48 +/- 2.8 torr [6.39 +/- 0.37 kPa]) and increased hemoglobin oxygen saturation above baseline. Epinephrine increased mesenteric venous lactate concentration (baseline, 2.9 +/- 0.6 mmol x L(-1); maximum value, 5.5 +/- 0.2 mmol x L(-1)) without development of an arterial-mesenteric venous lactate concentration gradient.
Epinephrine increased jejunal microvascular blood flow and mucosal tissue oxygen supply at moderate to high dosages. Lactic acidosis that develops during infusion of increasing dosages of epinephrine is not related to development of gastrointestinal hypoxia.
研究静脉注射递增剂量肾上腺素对肠道氧供的影响,特别是对自身灌注、有神经支配的空肠段黏膜组织氧分压的影响。
前瞻性、随机实验研究。
动物研究实验室。
家猪。
16头猪麻醉、麻痹并进行正常通气。通过中线剖腹术和系膜对侧切口暴露一小段空肠黏膜。使用Clark型表面氧电极测量黏膜氧分压。通过组织反射分光光度法和激光多普勒测速法测定微血管血红蛋白氧饱和度和微血管血流量(灌注单位)。记录全身血流动力学、肠系膜静脉酸碱和血气变量以及全身酸碱和血气变量。在休息期后以及在输注递增剂量肾上腺素(n = 8;0.01、0.05、0.1、0.5、1和2微克×千克⁻¹×分钟⁻¹)期间每隔20分钟进行测量,或不进行治疗(n = 8)。此外,在基线以及60和120分钟时测量动脉和肠系膜静脉乳酸浓度。
输注肾上腺素导致显著心动过速;心输出量、全身氧输送和氧消耗增加;并出现乳酸酸中毒。肾上腺素显著增加空肠微血管血流量(基线,267±39灌注单位;最大值,443±35灌注单位)和黏膜氧分压(基线,36±2.0托[4.79±0.27千帕];最大值,48±2.8托[6.39±0.37千帕]),并使血红蛋白氧饱和度高于基线水平。肾上腺素增加肠系膜静脉乳酸浓度(基线,2.9±0.6毫摩尔×升⁻¹;最大值,5.5±0.2毫摩尔×升⁻¹),但未形成动脉 - 肠系膜静脉乳酸浓度梯度。
肾上腺素在中高剂量时增加空肠微血管血流量和黏膜组织氧供。在输注递增剂量肾上腺素期间出现的乳酸酸中毒与胃肠道缺氧的发生无关。