Tibbs P A, Young B, McAllister R G, Brooks W H, Tackett L
J Neurosurg. 1978 Oct;49(4):558-62. doi: 10.3171/jns.1978.49.4.0558.
Two distinct and sequential patterns of hemodynamic alteration were observed after acute cervical spinal cord transection in anesthetized dogs. Interruption of the cord initially caused a 45% increase in mean arterial pressure (p less than 0.01), a 34% increase in systemic vascular resistance (p less than 0.05), and a 92% increase in left ventricular dp/dt (p less than 0.01), reflecting a generalized sympathetic response to trauma. Concomitant bradycardia and escape arrhythmias suggested relative parasympathetic hyperactivity. Resolution of the brief pressor response was followed by a second, more prolonged, period characterized by a fall in arterial pressure to 71% of control levels (p less than 0.05), a 16% decrease in systemic vascular resistance, and a 58.5% decrease in left ventricular dp/dt (p less than 0.01). These latter hemodynamic changes are consistent with sympathetic denervation and failure of regulatory mechanisms mediated by both alpha- and beta-adrenergic peripheral vascular and myocardial receptors.
在麻醉犬急性颈髓横断后,观察到两种不同且相继出现的血流动力学改变模式。脊髓横断最初导致平均动脉压升高45%(p<0.01),全身血管阻力升高34%(p<0.05),左心室dp/dt升高92%(p<0.01),这反映了对创伤的全身性交感反应。同时出现的心动过缓和逸搏性心律失常提示相对的副交感神经活动亢进。短暂的升压反应消退后,紧接着进入第二个更长的阶段,其特征为动脉压降至对照水平的71%(p<0.05),全身血管阻力降低16%,左心室dp/dt降低58.5%(p<0.01)。这些后期的血流动力学变化与交感神经去神经支配以及由α和β肾上腺素能外周血管和心肌受体介导的调节机制失效相一致。