RESUMEN

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Nitric oxide (NO) is a short-lived radical that functions as a neurotransmitter in the central nervous system and plays a physiological role in the regulation of hypothalamic–pituitary–adrenal axis and vasopressinergic axis. In the present study, we aimed to investigate the interaction between the generation of NO and vasopressin (AVP) and corticosterone release after 3 days of water deprivation in rats. Animals were previously treated with intraperitoneal (i.p.) saline or L-nitro-arginine methyl ester (L-NAME) injection. L-NAME is a nonspecific inhibitor of nitric oxide synthases. In control rats given i.p. saline or L-NAME, hypothalamic, pituitary, and plasma AVP levels and plasma corticosterone did not change from baseline levels (p > 0.05). Three days of water deprivation increased significantly the corticosterone levels in plasma (p < 0.01) and AVP levels in hypothalamus and plasma (p < 0.01), but not in pituitary, which showed a significant decrease. These variations were concomitant with the elevation of nitrates/nitrates in plasma. L-NAME injection abolished significantly (p < 0.01) the elevation of plasma corticosterone and hypothalamic AVP levels induced by water deprivation. These findings showed that in water-deprived rats, nitric oxide synthase inhibition by L-NAME inhibits corticosterone and vasopressin release, suggesting a potent stimulatory role of NO (AU)

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RESUMEN

Nitric oxide (NO) is a short-lived radical that functions as a neurotransmitter in the central nervous system and plays a physiological role in the regulation of hypothalamic-pituitary-adrenal axis and vasopressinergic axis. In the present study, we aimed to investigate the interaction between the generation of NO and vasopressin (AVP) and corticosterone release after 3 days of water deprivation in rats. Animals were previously treated with intraperitoneal (i.p.) saline or L-nitro-arginine methyl ester (L-NAME) injection. L-NAME is a nonspecific inhibitor of nitric oxide synthases. In control rats given i.p. saline or L-NAME, hypothalamic, pituitary, and plasma AVP levels and plasma corticosterone did not change from baseline levels (p>0.05). Three days of water deprivation increased significantly the corticosterone levels in plasma (p<0.01) and AVP levels in hypothalamus and plasma (p<0.01), but not in pituitary, which showed a significant decrease. These variations were concomitant with the elevation of nitrates/nitrates in plasma. L-NAME injection abolished significantly (p<0.01) the elevation of plasma corticosterone and hypothalamic AVP levels induced by water deprivation. These findings showed that in water-deprived rats, nitric oxide synthase inhibition by L-NAME inhibits corticosterone and vasopressin release, suggesting a potent stimulatory role of NO.

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In many clinical situations, it is crucial to determine circulating blood volume (BV) easily and to repeat this measurement. The Dye DensitoGram Analyzer (DDG, Nihon Kohden Corp) measures semi-automatically BV, using an injection of IndoCyanine Green (ICG, 10 mg), and avoiding intermittent blood samples. The DDG was used during a 90-day microgravity simulation by Head-Down-Tilt bed rest (HDT) to measure BV and compared with the calculation of the plasma volume (PV) variations according to Dill and Costill's formula (DC). Seventeen healthy volunteers were included: 8 control subjects (Co) and 9 subjects submitted to a resistive exercise counter-measure (CM). Measurements were performed, one day before HDT, on days 3 and 90 of HDT and on day 9 after HDT. A double measurement of the BV was performed to assess the repeatability of this method. On the last day of HDT a significant decrease (p < 0.05) in the PV was noted with the DDG (Co: -12.3+/-5.7%, CM: -9.0+/-5.3%) and DC; (Co: -4.7+/-1.8%, CM: -6.8+/-2.5%). A good repeatability of the technique was shown with a low intrasubjects coefficient of variation (4.95+/-0.95%) and an acceptable intersubjects coefficient of variation (15.30+/-1.13%). No correlation was noted between DDG and DC (r2 = 0.27). The DDG gives a good repeatability, not affected by the microgravity exposure. Thanks to its capacity to measure accurately the BV within 7-10 min, this device presents major advantages for clinical use and research purpose.

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Although various exercise regimens are commonly used as countermeasures to reduce the cardiovascular deconditioning induced by microgravity, the underlying mechanisms are not well understood. In this study we aimed to test whether lower limb resistance exercise with flywheel technology can prevent the fluid homeostasis alterations induced by 90-day head-down tilt bed-rest (HDT), and thus improve orthostatic tolerance. Total body water (TBW, measured by isotope dilution) and plasma volume (PV, calculated from the haemoglobin and the haematocrit) were measured in a control group (Co, n=9) and a countermeasure group (CM, n=9). Simultaneously, plasma atrial natriuretic peptide (ANP), renin (AR), and aldosterone (Aldo), as well as urinary anti-diuretic hormone (ADH), were measured. Orthostatic tolerance was evaluated with a 10 min +80 degrees tilt-test the first day of recovery. After HDT, both groups showed a comparable decrease in orthostatic tolerance [8.2 (0.9) min, Co; 8.0 (0.7) min, CM], PV [-4.7 (1.8)%, Co; -6.2 (2.5)%, CM, P<0.05] and TBW [-6.3 (5.4)%, Co; -3.7 (2.1)%, CM, P<0.05]. AR [97.4 (22.0)%, Co; 117.3 (26.4)%, CM] and Aldo [111.3 (58.4)%, Co; 100.6 (52.0)%, CM] increased significantly in both groups but the countermeasures produced no noticeable effects [data are expressed as mean (SE)]. The drop in ANP was also similar in both groups [-42.0 (15.2)%, Co; -51.1 (27.7)% for the CM]. Surprisingly, urinary ADH declined similarly in both groups during the basal data control period [-25.3 (5.2)%, Co; -26.1 (9.6)%, CM) and was sustained at this level during the 90-day HDT. These results show that, under the conditions described, the flywheel exercise device failed to improve characteristic manifestations of cardiovascular deconditioning and suggest that more frequent and powerful exercise, associated with another device (e.g. LBNP) might be a better countermeasure.

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Many factors are involved in the development of orthostatic intolerance after real or simulated weightlessness. The aim of our study was to compare the effects of 7-day head-down bed rest (HDBR) in eight women and eight men on the spontaneous baroreflex sensitivity (standard spectral method and new time-frequency algorithm) during lower body negative pressure (LBNP) tests. Results obtained before HDBR have shown in women, compared to men, higher heart rate, lower blood pressure, higher parasympathetic modulation at rest and greater decrease in baroreflex sensitivity with greater increase in sympathetic activity during LBNP. After HDBR, we observed in both men and women a dramatic decrease in orthostatic tolerance (7.0 min at R + 1 vs. 10.0 min, p<0.05, at BDC-1 in men; 5.4 vs. 9.0 min, p<0.05, in women) together with a decrease in plasma volume (-9.1 +/- 0.9% in men, -9.5 +/- 1.4% in women) and in spontaneous baroreflex sensitivity without gender effect. After HDBR, at the highest level of LBNP, diastolic blood pressure increased in men (+5.6 +/- 1.3 mm Hg) and decreased in women (-1.0 +/- 2.7 mm Hg) with a gender difference (p<0.05). This result suggests impaired vasoconstriction in women after HDBR. Neither endocrine response nor alterations to the cardiac baroreflex can explain gender differences in orthostatic tolerance after HDBR as reported by previous studies. Further studies need to be conducted in order to obtain a more precise analysis of gender difference in arteriolar vasoconstriction after HDBR. The time frequency method we developed to study changes in spontaneous baroreflex might be applied to the analysis of LBNP tests.

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