Y Mizukoshi1, K Shibata, M Yoshida. 1. Department of Anesthesiology and Intensive Care Medicine, Kanazawa University School of Medicine, Japan.
Abstract
PURPOSE: We have previously observed that sympathetic blockade by epidural anesthesia (EA) modifies the cardiovascular response to marked hypercapnic acidosis in dogs. Our objective was to determine whether the combination of marked hypercapnic acidosis and EA reduce left ventricular contractility. METHODS: We randomly assigned 22 Japanese white rabbits anesthetized with isoflurane (1.0%) to two groups according to the absence (control group, n= 11) or presence (EA group, n= 11) of thoracolumbar EA. After epidural injection (0.5 mL.kg(-1) of 0.9% saline in the control group or 1% mepivacaine in the EA group) and during subsequent hypercapnia (mean arterial CO2 tension 85 mmHg), we measured left ventricular pressure, left ventricular volume by using conductance catheter and plasma catecholamine concentrations. Left ventricular contractility was assessed by the slope of the linear approximation of the left ventricular end-systolic pressure-volume relationship, [i.e., end-systolic elastance (Ees)]. RESULTS: The combination of hypercapnic acidosis and thoracolumbar EA caused a 65% decrease in Ees (P <0.05). Hypercapnic acidosis alone caused a 16% decrease (P <0.05) and thoracolumbar EA alone caused a 49% decrease in Ees (P <0.05). In the EA group, epidural injection caused an 85% decrease in the epinephrine concentration (P <0.05) and a 39% decrease in the norepinephrine concentration (P <0.05), even during hypercapnic acidosis. However, in the control group, hypercapnic acidosis caused no change in the circulating epinephrine concentration but a 74% increase in the circulating norepinephrine concentration (P <0.05). CONCLUSION: Combined hypercapnic acidosis and EA markedly reduce left ventricular contractility in an additive fashion in rabbits receiving general anesthesia.
PURPOSE: We have previously observed that sympathetic blockade by epidural anesthesia (EA) modifies the cardiovascular response to marked hypercapnic acidosis in dogs. Our objective was to determine whether the combination of marked hypercapnic acidosis and EA reduce left ventricular contractility. METHODS: We randomly assigned 22 Japanese white rabbits anesthetized with isoflurane (1.0%) to two groups according to the absence (control group, n= 11) or presence (EA group, n= 11) of thoracolumbar EA. After epidural injection (0.5 mL.kg(-1) of 0.9% saline in the control group or 1% mepivacaine in the EA group) and during subsequent hypercapnia (mean arterial CO2 tension 85 mmHg), we measured left ventricular pressure, left ventricular volume by using conductance catheter and plasma catecholamine concentrations. Left ventricular contractility was assessed by the slope of the linear approximation of the left ventricular end-systolic pressure-volume relationship, [i.e., end-systolic elastance (Ees)]. RESULTS: The combination of hypercapnic acidosis and thoracolumbar EA caused a 65% decrease in Ees (P <0.05). Hypercapnic acidosis alone caused a 16% decrease (P <0.05) and thoracolumbar EA alone caused a 49% decrease in Ees (P <0.05). In the EA group, epidural injection caused an 85% decrease in the epinephrine concentration (P <0.05) and a 39% decrease in the norepinephrine concentration (P <0.05), even during hypercapnic acidosis. However, in the control group, hypercapnic acidosis caused no change in the circulating epinephrine concentration but a 74% increase in the circulating norepinephrine concentration (P <0.05). CONCLUSION: Combined hypercapnic acidosis and EA markedly reduce left ventricular contractility in an additive fashion in rabbits receiving general anesthesia.