title: Changes in myocardial contractility and contractile proteins after four weeks of simulated [correction of simulate] weightlessness in rats.
abstract: The interaction between the gravitational field, the position of the body, and the functional characteristics of the blood vessels determines the distribution of intravascular volume. In turn, this distribution determines cardiac pump function. One of the most profound circulatory changes that occurs in man during exposure to weightlessness is a cephalad redistribution of fluid caused by the lack of hydrostatic pressure in this microgravitative environment. The cephalad redistribution of fluid results in a loss of blood volume and then induces a decrease in preload. Recently, a decrease in sensitivity of arteriole to catecholamine has reported in rats of simulated weightlessness. This change in arteriole may reduce afterload. As a result, cardiovascular system may be shifted to a hypokinetic state during weightlessness condition for long-term. Echocardiographic data from astronauts during space flight showed an increase in heart rate, a 12 % decrease in stroke volume, and a 16 % decrease in left end diastolic volume. Electron-microscopic studies have shown changes in cardiac morphology in rats after exposure to microgravity for 7-12.5 days. After the COSMOS 2044 flight for 14 days, the light-microscopic studies have shown an atrophy of papillary muscles in rats left cardiac ventricle. It is not clear whether the function of atrophic myocardium is impaired. The data in three aspects as mentioned above suggest that weightlessness or simulated weightlessness may decrease the myocardial function. However, definite changes in cardiac performance have been hard to prove due to many limits. This studies were to answer two questions: Is the myocardial contractility depressed in rats subjected to simulated weightlessness for four weeks? What are the underlying mechanisms of the changing contractility?
authors.affiliation: Department of Aerospace Physiology, The Fourth Military Medical University, Xi'an, P.R. China.
authors.forename: Z B
authors.initials: ZB
authors.lastname: Yu
authors.forename: J X
authors.initials: JX
authors.lastname: Bao
authors.forename: J
authors.initials: J
authors.lastname: Ma
authors.forename: L F
authors.initials: LF
authors.lastname: Zhang
authors.forename: J P
authors.initials: JP
authors.lastname: Jin
mesh_terms: D000818:Animals; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D019417:Hindlimb Suspension; D007537:Isometric Contraction / Q000502:physiology; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D009210:Myofibrils / Q000201:enzymology / Q000378:metabolism; D018995:Myosin Heavy Chains / Q000378:metabolism; D010210:Papillary Muscles / Q000201:enzymology / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D019210:Troponin I / Q000378:metabolism; D020107:Troponin T / Q000378:metabolism; D018474:Weightlessness Simulation
chemical_list: D019210:Troponin I; D020107:Troponin T; D018995:Myosin Heavy Chains; D000252:Calcium-Transporting ATPases