These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Heat shock improves ischemic tolerance of hypertrophied rat hearts. Author: Cornelussen R, Spiering W, Webers JH, De Bruin LG, Reneman RS, van der Vusse GJ, Snoeckx LH. Journal: Am J Physiol; 1994 Nov; 267(5 Pt 2):H1941-7. PubMed ID: 7977825. Abstract: The postischemic recovery of hypertrophied hearts was studied 24 h after total body hyperthermia. To this end, anesthetized aortic-banded and sham-operated rats were subjected to heat shock (AoBHS and ShamHS, respectively). Cardiac hypertrophy was induced 8 wk earlier. In isolated ejecting hearts, functional recovery after 45 min of global ischemia was poor and moderate in nonheated (control) hypertrophied (AoBC) and nonheated (control) nonhypertrophied (ShamC) hearts, respectively. Heat shock significantly improved postischemic recovery in both AoBHS and ShamHS hearts. This improvement of functional recovery was associated with a significant reduction of the duration of arrhythmias. In addition, coronary flow was significantly higher in both types of heat-shocked hearts than in the corresponding control hearts during the preischemic as well as the postischemic period. Postischemic endocardial flow, assessed using radioactive microspheres, was significantly improved in AoBHS hearts. Compared with the corresponding control hearts, the native endogenous catalase activity was not changed in AoBHS hearts but was significantly increased in ShamHS hearts. The present findings suggest that the postischemic functional improvement after total body hyperthermia can be explained by increased and more homogeneous myocardial perfusion, which may also reduce the duration of postischemic arrhythmias. This effect is especially beneficial for the hypertrophied heart, which is known to be extremely vulnerable to the ischemic insult probably caused by subendocardial underperfusion.[Abstract] [Full Text] [Related] [New Search]