1,720,963 research outputs found
Tyrosine kinase inhibition protects from ischemi reperfusion injury in hamstercheek pouch microcirculation
No full textL’insulina protegge il microcircolo della sacca buccale del criceto dal danno indotto dall’ischemia-riperfusione dopo inibizione della sintasi dell’ossido nitrico
No full textMicrovascular permeability and leukocyte adesion are not reduced by insulin during ischemia reperfusion injury in hamster cheek pouch microcirculation
No full textEffects of melatonin and luzindole during ischemia reperfusion injury in rat pial microcirculation
No full textThis study aimed to investigate the role of melatonin [MT] againstbrain ischemia-reperfusion injury after MT receptor inhibition byluzindole [LZ]. The pial microcirculation of male Wistar rats wasobserved by fluorescence microscopy through a cranial window, using fluorescent dextran [70 K] as a tracer. Vessel diameter, permeability increase [PI], leukocytes adhering to venular walls [LA], capillary red blood cell velocity [CVRBC] and perfused capillary length [PCL] were determined by computerized methods. MT [0.5-1-2 mg/Kg body wt.,i.v.] was infused 10 min before ischemia, induced by bilateral occlusion of common carotid arteries for 30 min, and at the beginning of reperfusion lasting 60 min. In the control group, ischemia caused constriction of arterioles, while reperfusion induced constriction, dilation andconstriction within 40 min. At the end of reperfusion vessel permeability and adhering leukocytes increased; CVRBC and PCL were reduced. MT dose-dependently decreased arteriolar constriction during ischemia and reperfusion. At 40 min of reperfusion MT highest dosage caused dilation of all arterioles. PI and LA were reduced, CVRBC and PCL increased compared to control [p<0.01]. LZ [2 mg/Kg body wt.] prior to MT [2mg/Kg body wt.] prevented arteriolar dilation observed at 40 min ofreperfusion, but did not influence the effects of MT against interstitial edema and leukocyte adhesion. CVRBC and PCL did not differ from baseline. In conclusion, MT appears to cause dilatation of pial arterioles through MT1 and MT2 receptors and protection against blood brain barrier disruption likely acting as a free radical scavenger
Lesion evolution in pial microcirculation after transient occlusion of the middle cerebral artery in rats
No full textAn endogenous protection of retinal photoreceptors against light-induced oxidative stress
No full textGeometric characteristics of arterial network of rat pial microcirculation
No full textOBJECTIVE: 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. Diameters and lengths of arterioles were measured with a computer-assisted method. Pial arterioles were classified according to a centripetal ordering scheme (Strahler method modified according to diameter) from the smallest order 1 to the largest order 5 arterioles in the preparation. A distinction between arteriolar segments and elements was used to express the series-parallel features of the pial arteriolar networks. A connectivity matrix was used to describe the connection of blood vessels from one order to another. RESULTS: The arterioles were assigned 5 orders of branching by Strahler's ordering scheme, from order 1 (diameter: 16.0 +/- 2.5 microm) to order 5 (62 +/- 5.0 microm). Order 1 arterioles gave origin to capillaries, assigned order 0. The diameter, length and branching of the 5 arteriolar orders grew as a geometric sequence with the order number in accordance with Horton's law. The segments/elements ratio was the highest in order 4 and 3 arterioles, indicating the greatest asymmetry of ramifications. Finally, the branching vessels in the networks were described in details by the connectivity matrix. Fractal dimensions of arteriolar length and diameter were 1.75 and 1.78, respectively. CONCLUSIONS: The geometric characteristics of rat pial microcirculation indicate that distribution of vessels is fractal. The connectivity matrix allowed us to describe the number of daughter vessels spreading from parent vessels. This ordering scheme may be useful to describe vessel function, according to diameter, length and branching
Pial microvascular responses to transient bilateral common carotid artery occlusion: effects of hypertonic glycerol
No full textOBJECTIVE: 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. METHODS: Pial microcirculation of male Wistar rats was visualized by a fluorescent microscopy technique through an open cranial window, using fluorescein isothiocyanate bound to dextran (molecular weight 70 kDa). BCCAO was induced for 30 min and reperfusion lasted 60 min. The arterioles were classified according to the Strahler ordering scheme. Permeability increase was quantified by normalized grey levels (NGL). Leucocytes were stained with rhodamine 6G. Perfused capillary length and capillary red blood cell (RBC) velocity were measured by computer-assisted methods. RESULTS: The arterioles were assigned 5 orders of branchings, from order 1 (diameter 16.0 +/- 2.5 microm) to order 5 (62.0 +/- 5.0 microm). BCCAO caused inhomogenous changes in diameter of arterioles and leakage of fluorescent dextran, that was further enhanced by reperfusion (0.45 +/- 0.05 NGL, p < 0.01). Adhesion of leukocytes to venules was marked and capillary perfusion was reduced by 39.2 +/- 6.0% of baseline as well as capillary RBC velocity. 10% glycerol solution caused an increase in diameter of all arterioles within 25 +/- 2 min of administration (by 20 +/- 5% in order 4, 25 +/- 4% in order 3 and 18 +/- 3% in order 2; p < 0.01). Leakage (0.19 +/- 0.03 NGL, p < 0.01), leukocyte adhesion (2.0 +/- 1.0/100 microm of venular length, p < 0.01) and capillary occlusion (reduction by 13.0 +/- 5.5% of baseline) were prevented compared with controls. Capillary RBC velocity increased compared with controls. N(G)-nitro-L-arginine-methyl ester or N(G)-nitro-L-arginine infused prior to glycerol caused vasoconstriction and reduced the protective effects of hypertonic glycerol on permeability increase. The number of adherent leukocytes and perfused capillary length decreased, while capillary RBC velocity was higher than baseline. Glibenclamide prior to 10% glycerol solution blunted glycerol-induced vasodilatation, but did not affect protection by hypertonic glycerol on blood-brain barrier disruption, leukocyte adhesion and capillary perfusion, preserving high capillary RBC velocity. Papaverine (20 mg/kg body weight) induced an increase in arteriolar diameter, enhancing interstitial edema; adhesion of leukocytes was marked as well as capillary occlusion, while capillary RBC velocity increased. CONCLUSIONS: 10% glycerol solution was able to prevent microvascular alterations due to BCCAO protecting cerebral tissue. The effects appear to be due to hyperosmolality causing stimulation of K(ATP) channels, increase in vessel wall shear stress and release of nitric oxide
Rhythmic diameter changes in rat pial arterioles after the transient occlusion of middle cerebral artery
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