Hypothermia preserves myocardial function and mitochondrial protein gene expression during hypoxia
| Autor: | Shi Han Chen, Cheng Su Xu, Kun Qian, Michael A. Portman, Julia J. Krueger, Outi M. Hyyti, Xue Han Ning |
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| Rok vydání: | 2003 |
| Předmět: |
Male
Physiology Ischemia Myocardial Reperfusion Hypothermia In Vitro Techniques Biology Mitochondrion Mitochondria Heart Body Temperature Oxygen Consumption Coronary Circulation Physiology (medical) Gene expression medicine Animals HSP70 Heat-Shock Proteins Lactic Acid Inner mitochondrial membrane Adenosine Triphosphatases Myocardium Hemodynamics Adenine Nucleotide Translocator 1 Anatomy Carbon Dioxide Hypoxia (medical) Blotting Northern medicine.disease Cell biology Membrane protein Mitochondrial Membrane Protein Protein Biosynthesis Heart Function Tests RNA Female Rabbits medicine.symptom Cardiology and Cardiovascular Medicine |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 285:H212-H219 |
| ISSN: | 1522-1539 0363-6135 |
| DOI: | 10.1152/ajpheart.01149.2002 |
| Popis: | Hypothermia before and/or during no-flow ischemia promotes cardiac functional recovery and maintains mRNA expression for stress proteins and mitochondrial membrane proteins (MMP) during reperfusion. Adaptation and protection may occur through cold-induced change in anaerobic metabolism. Accordingly, the principal objective of this study was to test the hypothesis that hypothermia preserves myocardial function during hypoxia and reoxygenation. Hypoxic conditions in these experiments were created by reducing O2concentration in perfusate, thereby maintaining or elevating coronary flow (CF). Isolated Langendorff-perfused rabbit hearts were subjected to perfusate (Po2= 38 mmHg) with glucose (11.5 mM) and perfusion pressure (90 mmHg). The control (C) group was at 37°C for 30 min before and 45 min during hypoxia, whereas the hypothermia (H) group was at 29.5°C for 30 min before and 45 min during hypoxia. Reoxygenation occurred at 37°C for 45 min for both groups. CF increased during hypoxia. The H group markedly improved functional recovery during reoxygenation, including left ventricular developed pressure (DP), the product of DP and heart rate, dP/d tmax, and O2consumption (MVo2) ( P < 0.05 vs. control). MVo2decreased during hypothermia. Lactate and CO2gradients across the coronary bed were the same in C and H groups during hypoxia, implying similar anaerobic metabolic rates. Hypothermia preserved MMP βF1-ATPase mRNA levels but did not alter adenine nucleotide translocator-1 or heat shock protein-70 mRNA levels. In conclusion, hypothermia preserves cardiac function after hypoxia in the hypoxic high-CF model. Thus hypothermic protection does not occur exclusively through cold-induced alterations in anaerobic metabolism. |
| Databáze: | OpenAIRE |
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