Mesenteric Complications After Hypothermic Cardiopulmonary Bypass with Cardiac Arrest: Underlying Mechanisms
| Autor: | Gábor Szabó, Pál Soós, Alexander Juhász-Nagy, Terézia B. Andrási, Volker Buhmann |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
medicine.medical_specialty
Time Factors Biomedical Engineering Medicine (miscellaneous) Blood Pressure Bioengineering Peritoneal Diseases law.invention Biomaterials Dogs Hypothermia Induced law medicine.artery Internal medicine medicine Cardiopulmonary bypass Animals Mesentery Splanchnic Circulation Superior mesenteric artery Endothelial dysfunction Reactive hyperemia Cardiopulmonary Bypass biology business.industry Extracorporeal circulation General Medicine medicine.disease Heart Arrest Vasodilation Disease Models Animal Oxidative Stress surgical procedures operative medicine.anatomical_structure Anesthesia Cardiology biology.protein Vascular resistance Vascular Resistance Creatine kinase Sodium nitroprusside business circulatory and respiratory physiology medicine.drug |
| Zdroj: | Artificial Organs. 26:943-946 |
| ISSN: | 1525-1594 0160-564X |
| DOI: | 10.1046/j.1525-1594.2002.07116.x |
| Popis: | The aim of this study was to determine the pathophysiological mechanisms of postcardiopulmonary bypass (CPB) intestinal dysfunction using an in vivo canine model of extracorporeal circulation. Six dogs underwent a 90 min hypothermic CPB with continuous monitoring of mean arterial blood pressure (MAP) and mesenteric blood flow (MBF). Reactive hyperemia and vasodilator responses of the superior mesenteric artery to acetylcholine and sodium nitroprusside were determined before and after CPB. Mesenteric lactate production, glucose consumption, creatine kinase (CK) release and venous free radicals were determined. CPB induced a significant fall (p < 0.05) in MAP and MBF. After CPB, reactive hyperemia (-26 +/- 15% versus -53 +/- 2%, p < 0.05) and the response to acetylcholine (-42 +/- 9 versus -55 +/- 6%, p < 0.05) were significantly decreased. Reperfusion increased lactate production (0.8 +/- 0.09 mmol/L versus 0.4 +/- 0.18, p < 0.05) and the CK release (446 +/- 98 U/L versus 5 +/- 19 U/L, p < 0.01). Endothelial dysfunction, conversion from aerobic to anaerobic metabolism, and intestinal cell necrosis seem to be responsible for intestinal complications associated with CPB. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|