Pial microvascular responses to transient bilateral common carotid artery occlusion: effects of hypertonic glycerol.

Objective: The aim of the study was to assess the rat pial microvessel alterations due to transient bilateral common carotid artery occlusion (BCCAO) and to investigate the mechanism of 10% hypertonic glycerol neuroprotection. Our suggestion was that 10% glycerol solution infusion could dilate pial arterioles through nitric oxide release and/or stimulation of ATP-sensitive potassium (K(ATP)) channels. Therefore, we studied the effects of hypertonic glycerol after inhibition of nitric oxide synthase, with N(G)-nitro-L-arginine-methyl ester or N(G)-nitro-L-arginine, or K(ATP) channels with glibenclamide.

Geometric characteristics of arterial network of rat pial microcirculation.

Objective: The aim of the study was to assess the geometric characteristics of rat pial microcirculation and describe the vessel bifurcation patterns by 'connectivity matrix'.

Methods: Male Wistar rats were used to visualize pial microcirculation by a fluorescent microscopy technique through an open cranial window, using fluorescein isothiocyanate bound to dextran (molecular weight 70 kDa). The arteriolar network was mapped by stop-frame images.

Protective effects of insulin during ischemia-reperfusion injury in hamster cheek pouch microcirculation.

Objective: The effects of insulin (0.18 nM-0.18 microM) on reduced capillary perfusion, microvascular permeability increase and leukocyte adhesion induced by ischemia-reperfusion injury were investigated in the hamster cheek pouch microcirculation.

Effects of tetraiodothyronine and triiodothyronine on hamster cheek pouch microcirculation.

The aim of the present study was to assess the effects of topically applied triiodothyronine (T(3)) and thyroxine (T(4)) on the arterioles of hamster cheek pouch microcirculation in vivo. Microvessels were visualized using a fluorescent microscopy technique. Topical application of T(3) (3.

Molecular steps involved in light-induced oxidative damage to retinal rods.

Purpose: To define the molecular mechanism underlying light-induced oxidative damage to retinal photoreceptors.

Methods: Oxidative stress was induced in isolated rod photoreceptors by bright 470- to 490-nm light and monitored by measuring the conversion of dihydrorhodamine 123 to rhodamine, with fluorescence microscopy. The effect of the wavelength on oxidant generation was investigated by applying prebleaching stimuli of either 485- or 520-nm light before the bright 470- to 490-nm light.