Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabbit kidney cortex tissue slices were made ischemic (37 degrees C) for 60 min and then either reperfused in warm (37 degrees C) oxygenated physiologic buffer for 210 min or placed in UW Na gluconate solution (+/- quinacrine; 100 micromol/L) for 18 h followed by warm aerobic reperfusion. Slices were sampled at intervals and analyzed for malondialdehyde (MDA) content by HPLC. Control (nonischemic) slices had no change in MDA content over the duration of the experiment. Hypothermic storage of nonischemic slices did not result in any increase in MDA during reperfusion. Ischemic slices showed significant increases in MDA content during the first 1.5 h of reperfusion and remained elevated for the remainder of the experiment. Hypothermic storage of warm ischemic kidney slices resulted in a significant decrease in MDA content during the storage period. However, MDA content in these slices increased during warm reperfusion and was significantly higher than that in nonischemic controls. Quinacrine added during hypothermic storage of warm ischemic slices significantly decreased slice MDA content during warm reperfusion, an effect which was lost by increasing the storage solution calcium content. This study shows that aerobic hypothermic storage can aid in reducing oxidative stress in warm ischemic kidney tissue during reperfusion. This study suggests that the effects of quinacrine are at the level of the mitochondrion and not as an antioxidant compound.
 ...
PMID:The effect of quinacrine on oxidative stress in kidney tissue stored at low temperature after warm ischemic injury. 1060 Feb 53

Hypothermia-rewarming of the heart results in contractile dysfunction under in vitro as well as in vivo conditions. Increase in reactive oxygen species (ROS), lipid peroxidation and calcium overload are proposed mechanisms. In the first protocol of this study, the effect of putative phospholipase and calcium channel modulator mepacrine during deep hypothermia (4 h 14 degrees C) plus rewarming was tested in an isolated perfused rat heart model previously reported not to involve increase in lipid peroxides. Contractile function was measured under isovolumetric conditions using an intra-ventricular balloon connected to a transducer and recording system. Mepacrine completely reversed hypothermia-rewarming induced contractile failure in this model (LV dP/dt(max): 3236+/-517 vs. 1058+/-185 mmHg/s in untreated hearts). In the second part of the study, lipid peroxidation of the heart was examined in vivo in anesthetized rats subjected to 4h of deep hypothermia followed by rewarming. In this model recovery of heart function judged by cardiac output is decreased whereas blood pressure and heart rate recover fully. Peroxy conjugated diene isomers of unsaturated fatty acids were measured in heart phospholipids. The composition of the non-esterified fatty acids and the phospholipid fatty acid pool was examined in order to reveal signs of membrane remodeling. The results demonstrated no significant changes in phospholipid peroxidation after rewarming (91.07+/-5.23 vs. 88.63+/-7.73 nmol/g dry wt. in control). There was significant relative reduction in the content of arachidonic acid in the phospholipid fraction (29.55+/-1.65 vs. 24.76+/-1.48%). There was marked decrease in non-esterified fatty acids in myocardial tissue (1992+/-291 vs. 1069+/-189 nmol/g dry wt.), but a significant relative increase in arachidonic acid (20:4) in this fraction (3.46+/-0.42 vs. 4.99+/-0.30%). In conclusion, rewarming from deep hypothermia is not associated with increased phospholipid peroxidation. There is, however, a significant remodeling of the phospholipid fraction of myocardial lipids in vivo probably as a result of receptor or calcium stimulated phospholipase activity. Calcium or calcium stimulated phospholipase activity could contribute to posthypothermic contractile dysfunction.
 ...
PMID:Loss of heart phospholipid arachidonic acid without phospholipid peroxidation in anaesthetized rats rewarmed after prolonged deep hypothermia. 1972 18