Short-term hypobaric hypoxia enhances visual contrast sensitivity

The effect of hypoxia on early visual functions remains a controversial area of research. To explore this question, we measured static and dynamic visual contrast sensitivity in 14 healthy volunteers at a simulated altitude of 5500 m. In comparison with the baseline condition (mean arterial oxygen saturation: 98.4%), contrast sensitivity significantly increased after 5, 10 and 15 min of hypoxic exposure (saturation: 82.9%, 77.0%, 74.3%, respectively). After 10 min, this enhancement was markedly pronounced under dynamic conditions. Returning to the baseline altitude (saturation: 97.7%), contrast sensitivity recovered, mostly at the lower spatial frequencies. There was a significant negative relationship between arterial oxygen saturation and contrast sensitivity values at low and medium spatial frequencies (0.5-4.8 c/deg). These results suggest that early visual processing may be enhanced during short-term hypoxic challenge.     

Role of endothelium in hyperemia during cortical spreading depression (CSD) in the rat

The purpose of this study was to examine whether endothelium-mediated dilation is responsible for the cortical hyperemia that occurs during cortical spreading depression (CSD) in rats using three different approaches. The first approach taken was the acute pharmacological inhibition of the predominant endothelium-centered dilator systems, using indomethacin, a cyclooxygenase inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, and miconazole, a cytochrome P-450 epoxygenase inhibitor. The second approach used was the acute general pharmacological impairment of endothelial function by the intravascular administration of phorbol 12, 13-dibutyrate (PDBu). The third approach taken was the chronic impairment of endothelium-dependent dilator responses by diet in insulin resistant (IR) rats. Cerebral blood flow (CBF) was measured using laser Doppler flowmetry. CSD was elicited by the topical application of potassium chloride. Pharmacological inhibition of endothelium-dependent dilator factors did not affect CSD. For example, with 20 mg/kg L-NAME, CBF peak of the first series of CSDs was 377 +/- 67% of baseline CBF. After drug administration, CBF peaks of the second and the third series of CSDs were 451 +/- 67% and 390 +/- 69% (n=5, P=n.s.), respectively. Control and IR animals and those treated with indomethacin, miconazole and PDBu showed similar results. We also calculated the area under the CBF curve to fully represent the extent of hyperemia during CSD. However, there were no significant differences in the CBF area with any treatment compared to control animals. Thus, our results provide strong evidence that endothelium-mediated mechanisms have minimal effects on the CSD-associated hyperemia.     

Cerebrovascular dysfunction in Zucker obese rats is mediated by oxidative stress and protein kinase C

Insulin resistance (IR) impairs vascular function in the peripheral and coronary circulations, but its effects on cerebral arteries are virtually unexplored. We examined the vascular responses of the basilar artery (BA) and its side branches through a cranial window in Zucker lean (ZL) and IR Zucker obese (ZO) rats. Nitric oxide (NO) and K+ channel-mediated dilator responses, elicited by acetylcholine, iloprost, cromakalim, and elevated [K+], were greatly diminished in the ZO rats compared with ZL rats. In contrast, sodium nitroprusside induced similar relaxations in the two experimental groups. Expressions of the K+ channel pore-forming subunits were not affected by IR, while endothelial NO synthase was upregulated in the ZO arteries compared with ZL arteries. Protein kinase C (PKC) activity and production of superoxide anion were increased in the cerebral arteries of ZO rats, and pretreatment with superoxide dismutase restored all examined dilator responses. In contrast, application of PKC inhibitors improved only receptor-linked NO-mediated relaxation, but not K+ channel-dependent responses. Thus, IR induces in ZO rats cerebrovascular dysfunction, which is mediated by oxidative stress and partly by PKC activation. The revealed impairment of NO and K+ channel-dependent dilator responses may be responsible for the increased risk of cerebrovascular events and neurodegenerative disorders in IR.     

Severe nephrotic syndrome in a young man taking anabolic steroid and creatine long term

Anabolic steroids and creatine supplementation is one of the current abuse used by body builders. It is less known that this combination beside of many deleterious effects may also cause renal damage. Authors report a case of diffuse membranoproliferative glomerulonephritis type I in a 22-year-old man who had been taking continuously methandion in a large quantity and 200 grams of creatine daily, and was sent to the outpatient nephrologic unit with typical clinical signs of nephrosis syndrome. They also call attention to the role of the continuously consumed creatine in the renal failure.