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Exercise-caused metabolic changes can be followed by monitoring exhaled volatiles; however it has not been previously reported if a spectrum of exhaled gases is modified after physical challenge. We have hypothesized that changes in volatile molecules assessed by an electronic nose may be the reason for the alkalization of the exhaled breath condensate (EBC) fluid following physical exercise.Ten healthy young subjects performed a 6-minute running test. Exhaled breath samples pre-exercise and post-exercise (0 min, 15 min, 30 min and 60 min) were collected for volatile pattern (“smellprint”) determination and pH measurements (at 5.33 kPa CO2), respectively. Exhaled breath smellprints were analyzed using principal component analysis and were related to EBC pH.Smellprints (p=0.04) and EBC pH (p=0.01) were altered during exercise challenge. Compared to pre-exercise values, smellprints and pH differed at 15 min, 30 min and 60 min following exercise (p<0.05), while no difference was found at 0 min post-exercise. In addition, a significant correlation was found between volatile pattern of exhaled breath and EBC pH (p=0.01, r=−0.34).Physical exercise changes the pattern of exhaled volatiles together with an increase in pH of breath. Changes in volatiles may be responsible for increase in EBC pH.

Some of the maternal symptoms of preeclampsia can be produced by uterine ischemia, although no quadriped spontaneously exhibits this disease. It may be that the combination of upright posture and uteroplacental ischemia are necessary for manifestation of the full syndrome. Chronic nitric oxide synthase inhibition in rats produces a pattern of change that resembles the symptoms of preeclampsia, and the preeclamptic-like response of rats with adriamycin nephropathy and hyperinsulinemia is associated with endothelial dysfunction. These models are definitely of use in preeclampsia research, but because this disease only occurs spontaneously in primates, the definitive studies on preeclampsia will, of necessity, be clinical.

We have previously reported that acute systemic nitric oxide (NO) blockade in the conscious rat leads to increases in blood pressure and a profound renal vasoconstriction. In the present studies, we investigated the effect on renal vascular resistance of normalization of blood pressure (BP) during acute, i.v. NO blockade with nitro-L-arginine methyl ester (NAME). We found that two separate pharmacologic maneuvers which normalized BP after a transient period of hypertension, namely the NO donor sodium nitroprusside (SNP) or the calcium entry blocker verapamil (VER), did not reverse the increased renal vascular resistance (RVR) produced by acute NAME. In further studies, we prevented the transient increase in BP with the same combination of NAME and VER but with simultaneous administration of the drugs and in this situation, where the kidney was never exposed to a transient rise in renal perfusion pressure, RVR was unchanged compared to control. When we used angiotensin II (AII) as an alternative method of producing acute increases in BP and RVR, we found that VER reversed both the hypertension and the renal vasoconstriction, despite exposure of the kidney to a transient increase in BP. These data suggest that acute, transient exposure of the kidney to an increased BP during NO inhibition produces a sustained increase in RVR that is not reversible with either SNP or VER. The urinary data suggest that the combination of NAME and VER have a synergistic effection the renal tubule to produce a massive natriuretic and diuretic response.

Infrarenal aortic constriction was performed on pregnant rabbits on the 21st day of gestation, and the ensuing responses to uteroplacental ischemia were compared to sham-operated pregnant and constricted nonpregnant rabbits. Aortic constriction in pregnant animals induced hypertension (25-41% rise), proteinuria, thrombocytopenia (40% decrease), hypovolemia, decreased packed cell volume and fetal growth retardation. Renal fibrin deposition was demonstrated in the glomerular mesangium. In addition, pressor responsiveness to the administration of both angiotensin II and norepinephrine was increased. Correlation of higher plasma norepinephrine content with blood pressure suggests that an α-adrenergic mechanism is activated by the ischemia of the pregnant uterus. Veins draining ischemic uteroplacental tissues contained 2.5 and 2 fold higher amounts of angiotensin II and PGE2 respectively. Because arterial levels of these substances either decreased or remained unchanged, it is suggested that they may have induced local vasodilation rather than having exerted an influence on systemic hemodynamics