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Biomedical subjects

Q W Mao

Publications and source records attributed to Q W Mao.

10 recordsLinked to original sources
PubMed2001

Peripheral effector mechanism hypothesis of postflight cardiovascular dysfunction.

Studies on the mechanisms of cardiovascular dysfunction after space-flight are important to illustrate the cardiovascular effect of microgravity and develop appropriate multi-system countermeasures for future long-duration spaceflights. Over the past 10 yr, we have systematically studied the adaptational changes in structure and function of both the heart and vessels, using the tail-suspension rat model to simulate microgravity effects. Our results indicate that simulated microgravity induced atrophic changes and reduced contractility of the heart muscle, and upward- and downward-regulation in structure, function, and innervation state of vessels in the brain and hind body of the rat. In addition, more recent advances in relevant ground-based and space-flight studies from different laboratories have also been reviewed. Based on these studies, it has been speculated that, in addition to hypovolemia, the microgravity-induced adaptational changes in the structure and function of the two main effectors of the cardiovascular system, i.e., the arterial smooth muscle and the cardiac muscle, might be among the most important mechanisms responsible for postflight cardiovascular dysfunction and orthostatic intolerance. In this paper we will review the available evidence with comments.

Adaptation, Physiological↗
PubMed2001

[Peripheral effector mechanism hypothesis on cardiovascular dysfunction after spaceflight].

In the years of 1990's, we systematically studied the adaptational changes in structure and function of both the heart and the vessels during simulated weightlessness. In our serial work, the tail-suspension rat model was used to simulate the microgravity-induced cephalad shift and redistribution of blood. On the basis of the facts we observed and the more recent advances in space and ground-based studies in 1990's, we put forward a hypothesis to offer a possible explanation for the frequent occurrence of postflight cardiovascular dysfunction. It states that, in addition to the factor of hypovolemia, the microgravity-induced adaptational changes in the structure and function of the two main effectors of the cardiovascular system, i.e., the arterial smooth muscle and the cardiac muscle might be one of the most important mechanisms accounting for postflight cardiovascular dysfunction.

Cardiovascular System↗
PubMed1999

[Ultrastructural changes of arterial wall from different body parts of rats during simulated weightlessness].

OBJECTIVE: To test the nature of remodeling of arteries in different body parts in adapting to local hemodynamic changes induced by tail-suspension. METHOD: Ultrastructural changes of hindlimb and cerebral arteries from 4-wk tail-suspended (SUS-4), 1-wk recovered (REC-1), and control (CON) rats were studied by transmission electron microscopy. RESULT: For the hindquarter arteries, like the femoral artery and anterior tibial artery, there were fewer smooth muscle layers, less myofilaments in the smooth muscle cell (SMC), and more intercellular substance in SUS-4 group than in CON group. After 1-wk recovery, the internal elastic lamina of the arteries thickened, the amount of myofilaments in SMC increased, the content of intercellular substance restored, and neoformative SMCs emerged under the endothelium. With respect to arteries in the neck region and the brain, like the common carotid artery and basilar artery, SMCs of contractile phenotype were converted to that of synthetic phenotype, and migration and hyperplasia of SMCs also happened. After 1-wk recovery all these alterations were somewhat restored. CONCLUSION: It provided further evidence that peripheral effector mechanism might play an important role in the genesis of postflight orthostatic intolerance.

Actin Cytoskeleton↗
PubMed1999

[Changes in lumen diameters of vessels in arteriolar network in rat soleus muscle after simulated weightlessness].

Objective. To elucidate whether simulated weightlessness can induce changes in lumen diameters of vessels in arteriolar networks in hindlimb muscles and whether these changes are reversible. Method. Changes in lumen diameters of the vessels in the arteriolar network in soleus muscle of 4 wk tail-suspended (SUS-4), 1 wk (REC-1) and 5 wk (REC-5) recovered rats were examined and compared with that of control (CON) rats by use of the method of intra-arterial infusion of a carbon suspension. Result. The lumen diameters of the feeding arteries and arcade arterioles, and the transverse arterioles of the order of both V and II in the SUS-4 group were reduced by 31%, 29%, 28%, and 41%, respectively, as compared with that of the CON group (P<0.01). The diameters of these arterioles in REC-1 group were partially restored but remained significantly less than that of the CON group (P<0.05, or P<0.01). In REC-5 group, except for the transverse arterioles of order II, the diameters of all the other arterioles were fully recovered. Conclusion. These findings indicate that a 4 wk simulated weightlessness might induce atrophic changes in the arterioles of the hindlimb muscles. It also suggests that structural changes in arteriolar network might be an important mechanism accounting for postflight orthostatic intolerance.

Animals↗
PubMed1999

[Differentiated remodeling changes of medium-sized arteries from different body parts in tail-suspended rats and their reversibility].

Objective. The aim of the present study was to test whether medium-sized arteries in different body parts are differentially directed to achieve stimulus-specific remodeling to adapt local hemodynamic changes induced by tail-suspension, and to examine whether these structural changes are reversible. Method. Morphological changes of femoral, anterior tibial, common carotid, and basilar arteries from 4 wk tail-suspended (SUS-4), 1 wk recovered (REC-1), and control (CON) rats were studied using van Gieson-Orcein staining method. Result. For the hindquarter arteries, like the femoral and anterior tibial arteries, the lumen diameter (d) and medial tissue area (A) of SUS-4 group were significantly decreased (P<0.05, P<0.01) as compared with that of CON group, and that of REC-1 group were not fully recovered though the differences were not significant. With respect to arteries in the neck region and the brain, the remodeling changes were just in an opposite direction. In SUS-4 group, the d and A of both common carotid and basilar arteries were significantly increased (P<0.05, P<0.01) as compared with that of CON, and not fully restored after 1 wk recovery. Conclusion. The structures of medium-sized arteries in different body parts remodel differentially in response to local hemodynamic changes during simulated weightlessness and these changes were reversible.

Adaptation, Physiological↗
PubMed1997

Plasticity of arterial vasculature during simulated weightlessness and its possible role in the genesis of postflight orthostatic intolerance.

Even after several decades of extensive research, the basic mechanism of postflight cardiovascular dysfunction has not yet been fully elucidated. It is now well recognized that multiple mechanisms might account for the frequent occurrence of significant postflight orthostatic intolerance. It has been found that all tissues adapt their design when exposed to sustained alteration in local activity and/or stress. The most obvious example is the musculo-skeletal system, structure and function of which might be severely affected during microgravity exposure. In an attempt to elucidate whether structure and function of cardiac and vascular smooth muscle might be affected by simulated by microgravity, a serial work was started several years ago. In this paper, we present our more recent findings on plasticity of arterial vasculature and its innervation state during and after simulated microgravity and its time course.

Adaptation, Physiological↗