Adenosine instead of supranormal potassium in cardioplegic solution preserves endothelium-derived hyperpolarization factor-dependent vasodilation☆
| Autor: | Sveinung Ekse, Dag Sørlie, Lars M. Ytrebø, Thor Allan Stenberg, Øyvind Jakobsen, Ole Kristian Losvik |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Male
Pulmonary and Respiratory Medicine medicine.medical_specialty Adenosine Endothelium Hyperkalemia Vasodilator Agents Hemodynamics Myocardial Reperfusion Injury Vasodilation Biological Factors Random Allocation Coronary circulation Coronary Circulation Internal medicine medicine Animals Cardioplegic Solutions Cardioprotection Cardiopulmonary Bypass business.industry General Medicine Treatment Outcome medicine.anatomical_structure Anesthesia Heart Arrest Induced Potassium Cardiology Female Surgery medicine.symptom Cardiology and Cardiovascular Medicine business medicine.drug Blood vessel |
| Zdroj: | European Journal of Cardio-Thoracic Surgery. 33:18-24 |
| ISSN: | 1010-7940 |
| Popis: | Objective: We have recently shown that adenosine instead of supranormal potassium in cold crystalloid cardioplegia improves cardioprotection. Studies indicate that hyperkalemia has unfavorable effects on vascular endothelial function. Three pathways have been identified as major vasodilatory pathways: thenitricoxide(NO)pathway,thecyclooxygenase (COX)pathway, andtheendothelium-derivedhyperpolarization(EDHF) pathway, where the EDHF pathway, in particular, seems susceptible to hyperkalemia. We hypothesized that adenosine cardioplegia improves postcardioplegic endothelial function. Methods: Sixteen pigs were randomized to receive either cold (6 8C) hyperkalemic cardioplegia (n =8 ) or cardioplegia where hyperkalemia was substituted with 1.2 mM adenosine (n = 8). After 1 h of cold ischemic arrest, coronary blood flow was monitored for the following 2 h. The LAD artery was then explanted, and cylindrical rings were mounted for isometric tension recordings in organ chambers. Vessels were preconstricted with U46610 (Thromboxane A2 analog) and then bradykinin-mediated relaxation was investigated. To differentiate between the vasodilatory pathways the relaxation was assessed in the absence and presence of inhibitors of the COX (indomethacin), NO (L-NAME + carboxy-PTIO), and EDHF (apamin + charybdotoxin) pathways. Results: In vivo: The adenosine group had, as distinct from the hyperkalemic group, a significantly increased coronary blood flow index 1 h after cross-clamp release (from (ml/min/100 g, mean SD) 50.9 13.9 to 72.8 21.9, p = 0.010). The difference was, however, not statistically significant between groups. In vitro: Maximal relaxation without blockers was 27.4 10.1% of maximal tension in the adenosine group and 22.2 7.5% in the hyperkalemic group. To investigate EDHFdependent vasodilation the vessel rings were simultaneously treated with indomethacin, L-NAME, and carboxy-PTIO. Maximal relaxation in the hyperkalemic group was then reduced to 47.4 17.4% of maximal tension, which was a significant reduction compared to the adenosine group with a maximal relaxation of 20.6 8.7% (p = 0.028). Conclusion: Adenosine instead of supranormal potassium in cold crystalloid cardioplegia increases postcardioplegic myocardial blood flow and preserves EDHF-dependent vasodilation. # 2007 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|