Myocardial injury is decreased by late remote ischaemic preconditioning and aggravated by tramadol in patients undergoing cardiac surgery: a randomised controlled trial.
The purpose of this study was to test, whether the late phase of remote ischaemic preconditioning (L-RIPC) improves myocardial protection in coronary artery bypass grafting (CABG) with cold-crystalloid cardioplegia and whether preoperative tramadol modifies myocardial ischaemia-reperfusion injury using the same group of patients in a single-blinded randomized controlled study. One hundred and one adult patients were randomly assigned to either the L-RIPC, control or tramadol group. L-RIPC consisted of three five-minute cycles of upper limb ischaemia and three five-minute pauses using blood pressure cuff inflation 18 hours prior to the operation. Patients in the tramadol group received 200 mg tramadol retard at 19:00 hours, the day before the operation and at 06:00 hours. Serum troponin I levels were measured at eight, 16 and 24 hours after surgery. Myocardial samples for inducible and endothelial nitric oxide synthases (iNOS, eNOS) estimation were drawn twice: before and after cannulation for cardiopulmonary bypass from the auricle of the right atrium. We found that L-RIPC can reduce injury beyond the myocardial protection provided by cold-crystalloid cardioplegia, and tramadol worsened myocardial injury after CABG. Expressions of iNOS were increased in the control (significantly) and L-RIPC groups and dampened in the tramadol group.
Wagner
Robert
R
Department of Cardiac Anaesthesia, Centre for Cardiovascular and Transplant Surgery (CKTCH), St. Anne's University Hospital, Brno, Czech Republic. robert.wagner@cktch.cz
Piler
Pavel
P
Bedanova
Helena
H
Adamek
Petr
P
Grodecka
Lucie
L
Freiberger
Tomas
T
D000368:Aged; D000369:Aged, 80 and over; D000701:Analgesics, Opioid / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D001026:Coronary Artery Bypass / Q000009:adverse effects*; D018153:Czech Republic; D005260:Female; D006324:Heart Arrest, Induced; D006331:Heart Diseases / Q000139:chemically induced / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control*; D006801:Humans; D007036:Hypothermia, Induced; D019194:Ischemic Preconditioning; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000201:enzymology; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D017680:Potassium Compounds / Q000008:administration & dosage; D016037:Single-Blind Method; D013997:Time Factors; D014147:Tramadol / Q000009:adverse effects*; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood
D000701:Analgesics, Opioid; D015415:Biomarkers; D017680:Potassium Compounds; D019210:Troponin I; C018369:potassium cardioplegic solution; D014147:Tramadol; C496319:NOS2 protein, human; C496314:NOS3 protein, human; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III