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Biomedical subjects

C Reboul

Publications and source records attributed to C Reboul.

7 recordsLinked to original sources
PubMed2006

Chronic exercise does not prevent hypoxia-induced increased aortic sensitivity to endothelin in rats.

OBJECTIVES: We report in the present study the effect of regular exercise on vascular reactivity alterations to endothelin (ET-1) following prolonged exposure to hypoxic stress. METHODS: Male Dark Agouti rats were randomly assigned to N (sedentary rats), NCE (normoxic exercised rats), CH (chronic hypoxic sedentary rats) and CHCE (chronic hypoxic exercised rats) groups. The effects of ET-1 in the presence or not of the endothelium and/or of the specific inhibitor, bosentan, have been investigated in an isolated model of rat thoracic aorta. RESULTS: Prolonged exposure to hypoxia induced a significant increase in aortic sensitivity to ET-1 (-log ED50 in CH = 8.15 +/- 0.01 vs in N = 7.98 +/- 0.02, p < 0.05). Despite exercise training reduced the sensitivity to ET-1 in normoxic rats, it has no effects in hypoxic rats (-log ED50 in CH = 8.15 +/- 0.01 vs in CHCE = 8.19 +/- 0.01, NS). Moreover, although the removal of endothelium has no effect in N rats, it leads, in NCE rats, to a significant increase in sensitivity to ET-1 (-log ED50 in endothelium intact rings = 7.89 +/- 0.04 vs in denuded rings = 8.04 +/- 0.02, p < 0.05). The implication of ET-1 receptors on both endothelial and smooth muscle cells is confirmed by the significant reduced sensitivity to ET-1 in the four groups when bosentan is present in organ bath. CONCLUSION: Our study clearly suggests that part of the beneficial effect of chronic exercise could be mediated by enhancing endothelial function associated with endothelin reactivity in peripheric vessels. However, chronic exercise training does not seem to be able to limit the increased vasoconstriction to ET-1 stimulation induced by chronic hypoxia exposure.

Animals↗
PubMed2006

Protection against reactive oxygen species injuries in rat isolated perfused hearts: effect of LPBNAH, a new amphiphilic spin-trap derived from PBN.

Numerous strategies have been designed to protect the myocardium against reactive oxygen species (ROS). The present study was designed to test wether LPBNAH, a new amphiphilic spin-trap derived from PBN is able to protect isolated perfused rat hearts against ROS injuries. Following total glola ischemia (30 min), hearts were reperfused in the presence or not of LPBNAH (10 micromol/l), and left ventricular function was continuously monitored. The addition of LPBNAH led to a significant recovery in left ventricular developped pressure (LVDevP, control: 16.5+/- 7.5, p < 0.05). To conclude, the present results strongly suggest that the modification of previous wellknown molecules in order to facilitate their access to intracellular site of ROS production might be of interest to limit oxidative stresses.

Animals↗
PubMed2005

Chronic hypoxia exposure depresses aortic endothelium-dependent vasorelaxation in both sedentary and trained rats: involvement of L-arginine.

This study was designed to test the hypothesis that the previously demonstrated training-induced improvement of the endothelium vasodilator function would be blunted under conditions of chronic hypoxia exposure as a result of deleterious effects of hypoxia per se on the nitric oxide pathway. Sea-level-native rats were randomly assigned to N (living in normoxia), NT (living and training 5 days/wk for 5 wk in normoxia), CH (living in hypoxia, 2,800 m), and CHT (living and training 5 days/wk for 5 wk in hypoxia, 2,800 m) groups. Concentration-response curves to acetylcholine (ACh; 10(-9) to 10(-4) M) with or without L-arginine (10(-3) to 10(-5) M) and/or nitro-L-arginine methyl ester (10(-5) M) were assessed on aortic isolated rings. The main finding was that chronic hypoxia severely depressed maximal ACh-responses of aortic rings in both sedentary and trained groups. However, chronic hypoxia did not interfere with training-induced increases in maximal ACh responses, considering that maximal ACh vasorelaxation was improved in CHT rats to the same extent as in NT rats when both groups were directly compared with their sedentary counterparts. It should be pointed out that the vasodilator response to ACh was restored in CH and CHT rats to the level obtained in N and NT rats, respectively, by an in vitro L-arginine addition. A hypoxia-induced decrease in L-arginine bioavailability resulting from acclimatization at altitude may be involved in this limitation of the NO pathway in CH and CHT rats. These results are of importance for aerobic performance as the specific vascular adaptations to training at altitude could contribute to limit peripheral vasodilatation and subsequently blood flow during exercise.

Adaptation, Physiological↗
PubMed2004

Cardiac remodeling and functional adaptations consecutive to altitude training in rats: implications for sea level aerobic performance.

This study questioned the effect of living and training at moderate altitude on cardiac morphological and functional adaptations and tested the incidences of potential specific adaptations compared with aerobic sea level training on maximal left ventricular performance. Sea level-native rats were randomly assigned to N (living in normoxia), NT (living and training 5 days/wk for 5 wk in normoxia), CH (living in hypoxia, 2,800 m), and CHT (living and training 5 days/wk for 5 wk in hypoxia, 2,800 m) groups. Cardiac adaptations were evaluated throughout the study period by Doppler echocardiography. Maximal stroke volume (LV(SVmax)) was measured during volume overloading before and after the study period. Finally, at the end of the study period, passive pressure-volume relationships on isolated heart and cardiac weighing were obtained. Altitude training resulted in a specific left ventricular (LV) remodeling compared with NT, characterized by an increase in wall thicknesses without any alteration in internal dimensions. These morphological adaptations associated with hypoxia-induced alterations in pulmonary outflow and preload conditions led to a decrease in LV filling and subsequently no improvement in LV performance during resting physiological conditions in CHT compared with NT. Such a lack of improvement was confirmed during volume overloading that simulated maximal effort (LV(SVmax) pretest: NT = 0.58 +/- 0.05, CHT = 0.57 +/- 0.08 ml; posttest: NT = 0.72 +/- 0.06, CHT = 0.58 +/- 0.07 ml; NT vs. CHT in posttest session, P < 0.05). Maximal aerobic velocities increased to the same extent in NT and CHT rats despite marked polycythemia in the latter. The lack of LV(SVmax) improvement resulting from altitude training-induced cardiac morphological and functional adaptations could be responsible for this phenomenon.

Adaptation, Physiological↗
PubMed1983

[Intramedullary locking nailing. Experimental study. Surgical technic. Results].

The authors describe a new type of intramedullary nail used mainly in the femur and or tibia. This nail can be locked by the provision of holes into which screws can be driven transversely. The technique of insertion is described and the use of ancillary devices. The advantages are that weight-bearing can be commenced early even in comminuted fractures. The method includes open reduction of the fracture and allows some compression of the fracture site. The results of a biomechanical study are given. One hundred and forty six patients have been operated on with only 2 non-unions. The authors consider that their method is superior to plating and can be applied in cases that could not be fixed by conventional nails.

Biomechanical Phenomena↗