Beneficial effects of sevoflurane and desflurane against myocardial reperfusion injury after cardioplegic arrest

• Published in: Canadian journal of anesthesia Vol. 46; no. 11; pp. 1076 - 1081
• Main Authors: PRECKEL, B, THÄMER, V, SCHLACK, W
• Format: Journal Article
• Language: English
• Published: Toronto, ON Canadian Anesthesiologists' Society 01.11.1999; Springer Nature B.V
• Subjects: Anesthetics, Inhalation - pharmacology; Animals; Biological and medical sciences; Cardiovascular system; Creatine Kinase - secretion; Diastole - drug effects; Glucose - pharmacology; Heart Arrest, Induced; Heart attacks; Isoflurane - analogs & derivatives; Isoflurane - pharmacology; Male; Mannitol - pharmacology; Medical sciences; Methyl Ethers - pharmacology; Miscellaneous; Myocardial Reperfusion Injury - prevention & control; Pharmacology. Drug treatments; Potassium Chloride - pharmacology; Procaine - pharmacology; Rats; Rats, Wistar; Rodents; Ventricular Function, Left - drug effects; Volatile compound; Rat; Rodentia; Cardioprotective agent; Cardiovascular disease; Cardioplegia; Coronary heart disease; Myocardial disease; Vascular disease; Sevoflurane; Vertebrata; Chemotherapy; Mammalia; Reperfusion; Treatment; General anesthetic; Ischemia; Desflurane; Animal; Myocardium; Halogen Organic compounds
• ISSN: 0832-610X; 1496-8975
• DOI: 10.1007/bf03013206

To determine whether sevoflurane or desflurane offer additional protective effects against myocardial reperfusion injury after protecting the heart against the ischemic injury by cardioplegic arrest. Isolated rat hearts in a Langendorff-preparation (n = 9) were arrested by infusion of HTK cardioplegic solution and subjected to 30 min global ischemia followed by 60 min reperfusion (controls). An additional 18 hearts were subjected to the same protocol, and sevoflurane (n = 9) or desflurane (n = 9) was added to the perfusion medium during the first 30 min of reperfusion in a concentration corresponding to 1.5 MAC in rats. Left ventricular (LV) developed pressure and creatine kinase (CK) release were determined as indices of myocardial performance and cellular injury, respectively. The LV developed pressure recovered to 46+/-7% of baseline in controls. Functional recovery during reperfusion was improved by inhalational anesthetics to 67+/-3% (sevoflurane, P<0.05) and 61+/-5% of baseline (desflurane, P<0.05), respectively. Peak CK release during early reperfusion was reduced from 52+/-11 U x min(-1) x g(-1) in controls to 34+/-7 and 26+/-7 U x min(-1) x g(-1) in sevoflurane and desflurane treated hearts, respectively. The CK release during the first 30 min of reperfusion was reduced from 312+/-41 U x g(-1) in control hearts to 195+/-40 and 206+/-37 U x g(-1) in sevoflurane and desflurane treated hearts. After ischemic protection by cardioplegia, sevoflurane and desflurane given during the early reperfusion period offer additional protection against myocardial reperfusion injury.