Email this article CHANGES OF THE ULTRASTRUCTURE OF HISTO-HEMATIC BARRIER IN RAT RIGHT ATRIUM AFTER SHORT-TERM AND PROLONGED HEAT STRESS
- Authors: Lapsha VI1, Gurin VN1, Lapsha VI2, Gurin VN2
-
Affiliations:
- National Academy of Sciences
- Issue: Vol 129, No 1 (2006)
- Pages: 49-53
- Section: Articles
- URL: https://j-morphology.com/1026-3543/article/view/398988
- DOI: https://doi.org/10.17816/morph.398988
- ID: 398988
Cite item
Open Access
Access granted
Subscription or Fee Access
Abstract
In experiments on rats, changes of the ultrastructure of myocardial histo-hematic barriers in the right atrium during short-term and prolonged heat stress were studied. Short-term heat exposure (40°C, 30 and 60 min) increased the rectal temperature by 3.0-3.5°C. Immediately after heat exposure and 24 and 48 h following the exposure, the destructive and compensatory adaptive alterations in the microcirculatory bed were detected, accompanied by an edema of the pericapillary space and the changes in the size of mitochondria under the cardiomyocyte sarcolemma. Prolonged heating (40°C, 4 h daily for
led to an increase in the rectal temperature by 0.4-1.6°C. Changes in the microcirculatory bed had both dystrophic and compensatory adaptive nature. Erythrocyte and thrombocyte sludge and erythrocyte lysis were found in the lumen of microvessels. The number of endocytotic vesicles in endotheliocytes was variable; endotheliocyte nuclei had increased electron density and irregular outline. Myelin-like structures and apoptotic bodies were found in the pericapillary spaces. Under the cardiomyocyte sarcolemma the accumulation of mitochondria and sarcoplasmic vacuolization were noted. Comparison of short- and long-term effects of heat on histohematic barriers in the right atrium shows more significant changes after prolonged heat stress.
led to an increase in the rectal temperature by 0.4-1.6°C. Changes in the microcirculatory bed had both dystrophic and compensatory adaptive nature. Erythrocyte and thrombocyte sludge and erythrocyte lysis were found in the lumen of microvessels. The number of endocytotic vesicles in endotheliocytes was variable; endotheliocyte nuclei had increased electron density and irregular outline. Myelin-like structures and apoptotic bodies were found in the pericapillary spaces. Under the cardiomyocyte sarcolemma the accumulation of mitochondria and sarcoplasmic vacuolization were noted. Comparison of short- and long-term effects of heat on histohematic barriers in the right atrium shows more significant changes after prolonged heat stress.
Keywords
About the authors
V I Lapsha
V N Gurin
V I Lapsha
National Academy of Sciences; National Academy of Sciences
V N Gurin
National Academy of Sciences; National Academy of Sciences
References
- Бардахчьян Э.А. и Харланова Н.Г. Морфологические изменения эритроцитов и содержания железа в крови крыс при действии эндотоксина кишечной палочки. Бюл. экспер. биол., 1992, т. 114, № 10, с. 439-442.
- Володина А.В., Гурко Н.С., Кипренский Ю.В. и Поздняков О.М. Патоморфологические признаки повреждения эндотелия капилляров при травме и реплантации скелетной мышцы. Бюл. экспер. биол., 1994, т. 118, № 10, с. 378-384.
- Гурин В.Н. Терморегуляция и симпатическая нервная система. Минск, Наука и техника, 1989.
- Ескунов П.Н. и Семченко В.В. Структурно-функциональные изменения гистогематического барьера миокарда крыс в постишемическом периоде. Морфология, 2003, т. 123, вып. 2, с. 60-64.
- Лапша В.И., Бочарова В.Н., Савчина Е.Н. и Гурин В.Н. Морфофункциональные изменения в сердце при тепловом стрессе. В кн.: Проблемы интеграции функций в физиологии и медицине (к 100-летнему юбилею присуждения Нобелевской премии акад. И.П. Павлову). Минск, ПЧУП Бизнес- офсет, 2004, с. 209-211.
- Шахламов В.А. Капилляры. М., Медицина, 1971.
- Hales J., Hubbard R. and Gaffin S. Limitation of heat tolerance. Am. Physiol. New York, Soc / Oxford Univ. Press, 1996, p. 285-355.
- Hayakawa K., Takemura G., Kanoh M. et al. Inhibition of granulation tissue cell apoptosis during the subacute stage of myocardial infarction improves cardiac remodeling and dysfunction at the chronic stage. Circulation, 2003, v.108, № 1, p. 104.
- Magbool H. Apoptosis and cardiovascular disease. Focus on heart failure. Pak J. Med. Sci., 2001, v. 17, № 4, p. 193-196.
- Okonski P., Banach M., Szram S. et al. L-arginine in reperfusion solution as a heart protecting factor. Pol. Merkuriusz Lek., 2004, v. 17, № 102, p. 550-554.
- Okonski P., Szram S., Banach M. et al. Effect of - arginine on overhydration and ultrastructure preservation of rat's heart exposed to cold cardioplegic ischaemia. Ann. Transplant., 2003, v. 8, № 2, p. 57-62.
- Takemura G., Ohno M., Hayakawa Y. et al. Role of apoptosis in the disappearance of infiltrated and proliferated interstitial cells after myocardial infarction. Circ. Res., 1998, v. 82, p. 1130-1138.
- Ward B.J. and McCarthy. Endothelial cell «swelling» in ischemia and reperfusion. J. Molec. Cell. Cardiol., 1995, v. 27, № 6, p. 1293-1800.
Supplementary files
СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).