Hershenson M B, Schena J A, Lozano P A, Jacobson M J, Crone R K
Department of Anaesthesia, Harvard Medical School, Children's Hospital, Boston, Massachusetts 02115.
J Appl Physiol (1985). 1989 Jan;66(1):96-101. doi: 10.1152/jappl.1989.66.1.96.
At least two investigators have demonstrated a reduction in O2 extraction during induced hypothermia (Cain and Bradley, J. Appl. Physiol. 55: 1713-1717, 1983; Schumacker et al., J. Appl. Physiol. 63: 1246-1252, 1987). We hypothesized that administration of pentoxiphylline (PTX), a theobromine that lowers blood viscosity and has vasodilator effects, would increase O2 extraction during hypothermia. To test this hypothesis, we studied O2 transport in anesthetized, paralyzed, mechanically ventilated beagles exposed to hypoxic hypoxia during either 1) normothermia (38 degrees C), 2) hypothermia (30 degrees C), or 3) hypothermia + PTX (30 degrees C and PTX, 20 mg.kg-1.h-1). Measurements included arterial and mixed venous PO2, hemoglobin concentration and saturation, cardiac output, systemic vascular resistance (SVR), blood viscosity, and O2 consumption (VO2). Critical levels of O2 delivery (DO2, the product of arterial O2 content and cardiac output) were determined by a system of linear regression. Hypothermia significantly decreased base line cardiac output (-35%), DO2 (-37%), and VO2 (-45%), while increasing SVR and blood viscosity. Addition of PTX increased cardiac output (35%) and VO2 (14%), and returned SVR and blood viscosity to normothermic levels. Hypothermia alone failed to significantly reduce the critical level of DO2, but addition of PTX did [normothermia, 11.4 +/- 4.2 (SD) ml.kg-1.min-1; hypothermia, 9.3 +/- 3.6; hypothermia + PTX, 6.6 +/- 1.3; P less than 0.05, analysis of variance]. The O2 extraction ratio (VO2/DO2) at the critical level of DO2 was decreased during hypothermia alone (normothermia, 0.60 +/- 0.13; hypothermia, 0.42 +/- 0.16; hypothermia + PTX, 0.62 +/- 0.19; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
至少有两位研究者已证明，在诱导性体温过低期间氧摄取减少（Cain和Bradley，《应用生理学杂志》55：1713 - 1717，1983；Schumacker等人，《应用生理学杂志》63：1246 - 1252，1987）。我们推测，给予己酮可可碱（PTX），一种可降低血液粘度并具有血管舒张作用的可可碱，会在体温过低期间增加氧摄取。为验证这一假设，我们研究了在1）正常体温（38摄氏度）、2）体温过低（30摄氏度）或3）体温过低 + PTX（30摄氏度且PTX，20毫克·千克⁻¹·小时⁻¹）期间，暴露于低氧性缺氧的麻醉、麻痹、机械通气的比格犬的氧转运情况。测量指标包括动脉和混合静脉血氧分压、血红蛋白浓度和饱和度、心输出量、全身血管阻力（SVR）、血液粘度和氧消耗（VO₂）。通过线性回归系统确定氧输送（DO₂，动脉血氧含量与心输出量的乘积）的临界水平。体温过低显著降低基线心输出量（-35%）、DO₂（-37%）和VO₂（-45%），同时增加SVR和血液粘度。添加PTX可增加心输出量（35%）和VO₂（14%），并使SVR和血液粘度恢复到正常体温水平。单独的体温过低未能显著降低DO₂的临界水平，但添加PTX则可降低[正常体温，11.4 ± 4.2（标准差）毫升·千克⁻¹·分钟⁻¹；体温过低，9.3 ± 3.6；体温过低 + PTX，6.6 ± 1.3；P < 0.05，方差分析]。在DO₂临界水平时，单独体温过低期间的氧摄取率（VO₂/DO₂）降低（正常体温，0.60 ± 0.13；体温过低，0.42 ± 0.16；体温过低 + PTX，0.62 ± 0.19；P < 0.05）。（摘要截短于250字）
