Thoracic epidural anesthesia improves functional recovery from myocardial stunning in conscious dogs.
The effects of thoracic epidural anesthesia (TEA) on the contractile performance of ischemic and postischemic myocardium have not been well investigated. The purpose of this investigation was to examine the effects of TEA on severity and duration of myocardial stunning in an experimental model for sublethal acute myocardial ischemia. Seven dogs were chronically instrumented for measurement of heart rate (HR), left atrial (LAP), aortic and left ventricular pressure (LVP), LV dP/dtmax' and myocardial wall-thickening fraction (WTF). An occluder around the left anterior descending artery (LAD) allowed induction of reversible LAD ischemia. TEA was performed with lidocaine 4 mg/kg through a chronically implanted epidural catheter at the second thoracic level. Regional myocardial blood flow was determined with colored microspheres. Two experiments were performed in a cross-over design on separate days: Experiment 1, induction of 10 min of LAD ischemia without TEA; and Experiment 2, induction of 10 min of LAD ischemia with TEA. WTF was measured at baseline (BL) and predetermined time points until complete recovery from ischemic dysfunction occurred. LAD ischemia caused a significant decrease of LAD-WTF with (-28% +/- 5.1% versus BL) and without TEA (-15.5% +/- 5.3% versus BL). After 3 h of reperfusion, WTF as percent of BL values was significantly higher with TEA (P < 0.001). BL values of WTF were reached after 24 h with TEA and after more than 48 h without TEA (P < 0.05). There were no significant differences for mean arterial pressure (MAP), heart rate (HR), LVP, LAP, and LVdP/dtmax between the groups during ischemia and reperfusion. In nonischemic myocardium TEA caused an increase of subendocardial blood flow. During ischemia neither the subendocardial/subepicardial nor the occluded/ normal zone blood flow was affected by TEA. TEA attenuates myocardial stunning in conscious dogs. This finding is consistent with data regarding a reduction of infarct size due to TEA.
Department of Anesthesiology and Intensive Care Medicine, University Hospital Münster, Germany.
N
N
Rolf
M
M
Van de Velde
P F
PF
Wouters
T
T
Möllhoff
T P
TP
Weber
H K
HK
Van Aken
D000767:Anesthesia, Epidural; D000779:Anesthetics, Local / Q000008:administration & dosage; D000818:Animals; D016279:Atrial Function, Left / Q000502:physiology; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D002408:Catheters, Indwelling; D003243:Consciousness; D003326:Coronary Circulation; D018592:Cross-Over Studies; D004285:Dogs; D004699:Endocardium / Q000503:physiopathology; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D008012:Lidocaine / Q000008:administration & dosage; D008297:Male; D008863:Microspheres; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology; D015425:Myocardial Reperfusion; D017682:Myocardial Stunning / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D010496:Pericardium / Q000503:physiopathology; D013904:Thoracic Vertebrae; D016277:Ventricular Function, Left / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology
D000779:Anesthetics, Local; D008012:Lidocaine