TY - JOUR
T1 - Effects of isoflurane, enflurane, and halothane on skeletal muscle microcirculation in the endotoxemic rat
AU - Schumacher, Jan
AU - Pörksen, Matthies
AU - Klotz, Karl F.
N1 - Funding Information:
From the Department of Anesthesiology, Medical University of Luebeck, Luebeck, Germany. Supported by the Medical University of Luebeck, Luebeck, Germany. Received August 28, 2000. Accepted November 1, 2000. Address reprint requests to Jan Sehumacher, MD, Department of Anesthesiology, Medical University of Luebeck, Ratzebarger Allee 160, D-23538 Luebeck, Germany. Copyright 9 2001 by W.B. Saunders Company 0883-9441/01/1601-0001 $35.00/0 doi: lO.1053/jcrc.2001.21790
Funding Information:
The authors gratefully acknowledge the support of the Institute of Pathology, Medical University of Luebeck, Germany for the histopathological investigations and the technical support of Dunja Leffler from the Department of Anesthesiology, Medical University of Luebeck.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2001
Y1 - 2001
N2 - Purpose: The cardiovascular effects of volatile anesthetics during sepsis sets patients at high risk for hemodynamic deterioration. We compared the microcirculatory alterations in skeletal muscle under anesthesia with isoflurane, enflurane, and halothane in an endotoxemic rat preparation. Materials and Methods: Twenty-one Sprague-Dawley rats under continuous hemodynamic monitoring and intravital microscopy of the spinotrapezius muscle were studied during two level lipopolysaccharide (0.2 mg/kg and 2 mg/kg) induced sepsis. The effects of equianesthetic concentrations (1.5 minimum alveolar concentration [MAC]) of either isoflurane [n:7], enflurane [n:7], or halothane [n:7] on microcirculatory vasoregulation were measured and histopathologic changes were evaluated. Results: During low-dose endotoxemia, arteriolar vasodilation under isoflurane was nearly abolished (P < .05). At high-dose endotoxemia, this lack of vasodilatory effect was similar (P < .05). Animals receiving 1.5 MAC of enflurane during lowdose endotoxin presented a significant decrease in arteriolar diameter by -11.3 (±2.9%), this response was less during high-dose endotoxemia (-7.0, ±2.9%). Halothane caused pronounced vasoconstriction by -20 (±3.7%) during low-dose endotoxemia and moderate but significant constriction during high-dose endotoxemia (-7.9, ±2.6%). Conclusions: Isoflurane, enflurane, and halothane exert significantly different effects on vasoregulation of skeletal muscle arterioles in the endotoxemic rat.
AB - Purpose: The cardiovascular effects of volatile anesthetics during sepsis sets patients at high risk for hemodynamic deterioration. We compared the microcirculatory alterations in skeletal muscle under anesthesia with isoflurane, enflurane, and halothane in an endotoxemic rat preparation. Materials and Methods: Twenty-one Sprague-Dawley rats under continuous hemodynamic monitoring and intravital microscopy of the spinotrapezius muscle were studied during two level lipopolysaccharide (0.2 mg/kg and 2 mg/kg) induced sepsis. The effects of equianesthetic concentrations (1.5 minimum alveolar concentration [MAC]) of either isoflurane [n:7], enflurane [n:7], or halothane [n:7] on microcirculatory vasoregulation were measured and histopathologic changes were evaluated. Results: During low-dose endotoxemia, arteriolar vasodilation under isoflurane was nearly abolished (P < .05). At high-dose endotoxemia, this lack of vasodilatory effect was similar (P < .05). Animals receiving 1.5 MAC of enflurane during lowdose endotoxin presented a significant decrease in arteriolar diameter by -11.3 (±2.9%), this response was less during high-dose endotoxemia (-7.0, ±2.9%). Halothane caused pronounced vasoconstriction by -20 (±3.7%) during low-dose endotoxemia and moderate but significant constriction during high-dose endotoxemia (-7.9, ±2.6%). Conclusions: Isoflurane, enflurane, and halothane exert significantly different effects on vasoregulation of skeletal muscle arterioles in the endotoxemic rat.
UR - http://www.scopus.com/inward/record.url?scp=0035092023&partnerID=8YFLogxK
U2 - 10.1053/jcrc.2001.21790
DO - 10.1053/jcrc.2001.21790
M3 - Journal articles
C2 - 11230718
AN - SCOPUS:0035092023
SN - 0883-9441
VL - 16
SP - 1
EP - 7
JO - Journal of Critical Care
JF - Journal of Critical Care
IS - 1
ER -
