Thoracic peridural block in experimental endotoxin shock.
The influence of thoracic peridural block (PDB) on the metabolic and hemodynamic changes in endotoxin shock were investigated in rabbits. During the first 6 h of endotoxin shock, sensomotoric and sympathetic blockade distal to spinal segment T4 was achieved by intermittent administration of bupivacaine into a thoracic peridural catheter. The increase of plasma glucose, lactate, and free glycerol 2 h after endotoxin (50 micrograms/kg) administration was prevented by PDB. Animals with PDB had an accelerated clearance of glucose as indicated by a shorter plasma half-life of intravenously injected glucose (0.33 g/kg) 1 h after endotoxin administration. Hemodynamic parameters were measured during the first 210 min after endotoxin application. Compared with controls, PDB reduced mean arterial pressure and total peripheral resistance. PDB did not affect the initial increase of right ventricular pressure or the progressive decrease in O2 consumption and cardiac output after the endotoxin injection. The mortality at 24 h was not significantly reduced by the PDB (controls, n = 22: 68%; PDB, n = 21: 57%). The results demonstrate that thoracic PDB effectively blocks the sympathetic response in endotoxin shock. Hence, PDB causes peripheral vasodilatation, and, moreover, the metabolic data are consistent with an inhibition of the reactive glycogenolytic and lipolytic responses in shock. Although PDB altered the metabolic disturbances caused by endotoxin shock, mortality was not significantly affected.
D000818:Animals; D001340:Autonomic Nerve Block; D001786:Blood Glucose / Q000378:metabolism; D002045:Bupivacaine; D005260:Female; D005990:Glycerol / Q000378:metabolism; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000378:metabolism; D008297:Male; D011817:Rabbits; D012772:Shock, Septic / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*
D001786:Blood Glucose; D007773:Lactates; D005990:Glycerol; D002045:Bupivacaine