[Reactivity of pulmonary arteries and thoracic aortae in rats under tail-suspension and the effects of NOS inhibitor].
OBJECTIVE
To further disclose mechanisms in adaptation of pulmonary and systemic arteries to simulated microgravity (SM), so as to elucidate the mechanisms accounting for orthostatic intolerance after SM, and to explore a new kind of countermeasure for orthostatic intolerance.


METHODS
300 tail suspended (TS) rats were used as the model to simulate the physiological effects of microgravity. Vasoreactivity changes of rings sectioned from pulmonary artery (PA) and thoracic aorta (TA) to 68 mmoles/L KCl, plus phenylephrine (PE) and acetylcholine (ACh) were observed after 7 d and 14 d tail-suspension. After preconditioning with 10(-5) moles/L N-nitro-L-arginine methyl ester (L-NAME) for 20 min, vasoreactivity changes of PA and TA to PE and ACh were respectively repeated.


RESULTS
The contractile responsiveness of PA and TA to KCl and PE decreased significantly or very significantly after TS7 d and TSI4 d. The dilatory reactivity of PA and TA to ACh after TS7 d had a significant or very significant increase, but reactivity of PA showed no change and TA showed only a tendency to increase after TS14 d. After preconditioning with 10(-5) moles/L L-NAME, responsiveness of PA to PE after TS7 d and TS14 d had no difference among the three groups, but responsiveness of TA to PE after TS7 d and TS14 d had a significant decrease. The dilatory reactivity of PA after TS7 d decreased significantly or very significantly, and the remains showed no significant change.


CONCLUSIONS
The decrease of contractile responsiveness of PA and TA might be due to the increased dilatory function of the endothelial cells. The fact that 10(-5) moles/L L-NAME reversed the decrease of contractile responsiveness of PA and partly of TA after tail suspension implicates that there might be an inhibitory action on the dilatory function of the endothelial cells. The NOS inhibitors may be helpful in preventing orthostatic intolerance.
Wang
De-sheng
DS
Institute of Space Medico-Engineering, Beijing, China.
Yuan
Min
M
Li
Zhi-li
ZL
Yuan
Ming
M
Liu
Zhao-xia
ZX
Cao
Yi
Y
Tong
Fei-zhou
FZ
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D019417:Hindlimb Suspension; D007024:Hypotension, Orthostatic / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D019001:Nitric Oxide Synthase / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011651:Pulmonary Artery / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D018544:Weightlessness Countermeasures; D018474:Weightlessness Simulation
D004791:Enzyme Inhibitors; D010656:Phenylephrine; D019001:Nitric Oxide Synthase; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester