Microvascular research
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Microvascular research · Mar 2001
Hyperthermic pretreatment decreases microvascular protein leakage and attenuates hypotension in anaphylactic shock in rats.
Systemic anaphylaxis is a life-threatening allergic reaction and its pathologic conditions, such as edema, bronchospasm, and hypotension, have been attributed to release of vasoactive mediators. Heat shock protein (HSP) is known to play a protective role in living cells under various stresses. In these studies, we investigated the protective role of heat shock response in anaphylactic shock, focusing on changes of blood pressure (BP) and vascular permeability. ⋯ BP in the heated rats was significantly higher than BP in the nonheated rats from 4 to 15 min during anaphylactic shock (P < 0.001). Inducible HSP72 appeared overexpressed in heart, lung, and liver tissue in the heated rats tested by Western immunoblotting. The results indicate that reduction of increased protein leakage and attenuation of hypotension may result from induction of HSP by whole-body hyperthermia.
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In this paper we quantitatively investigate the hypothesis proposed by Michel (Exp. Physiol. 82, 1-30, 1997) and Weinbaum (Ann. Biomed. ⋯ Physiol. 388, 421-435, 1987) on frog mesentery capillary, but a small positive filtration once a steady state is achieved. The new model also predicts that the local protein concentration behind the surface glycocalyx can differ greatly from the tissue protein concentration, since the convective flux of proteins through the orifice-like pores in the junction strand will greatly impede the back diffusion of the proteins into the lumen side of the cleft when the local Peclet number at the orifice is >1. The net result is that the filtration in the capillaries is far less than heretofore realized and there may be no need for venous reabsorption.
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Hepatic failure is one of the major problems developed during the posttransplantation period. A possible cause of hepatic failure is the prolonged ischemia induced during the implantation procedure. Hepatic ischemia leads to a reduction in oxygen supply, ATP level decline, liver metabolism impairment, and finally organ failure. ⋯ Also, it will allow us to determine of the coupling between tissue blood flow and oxidative phosphorylation. It is believed that the measurements of respiratory chain dysfunction might predict organ viability in clinical organ transplantation situations. Using this probe may also help to decrease the variability in liver blood flow monitoring since liver blood flow monitoring is supported simultaneously with the mitochondrial redox state, which supplies the information on liver metabolic and functional state.
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Microvascular research · Nov 1997
Venular oscillatory flow during hemorrhagic shock and NO inhibition in hamster cheek pouch microcirculation.
Blood flow oscillations (flowmotion) during hemorrhagic shock (HS) were recorded with laser Doppler perfusion monitoring (LDPM) and red blood cell (RBC) velocimetry in arterioles and venules in hamster cheek pouch microcirculation. Experiments were carried out after baroceptor denervation or inhibition of nitric oxide (NO) synthesis with NG-monomethyl-L-arginine prior to and during HS. Flowmotion was characterized by spectral analysis with fast Fourier transform and autoregressive modeling. ⋯ High frequency oscillations remained in arterioles during HS. In conclusion, LDPM low frequency flowmotion was not originated by variations in the diameter of vessels, but corresponded to RBC velocity changes. A compensatory higher blood flow and concomitant low frequency flowmotion in venules appeared to be related to NO production during HS, independently of neural mechanism.
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Microvascular research · Jul 1997
Comparative StudyEffects of hypoxia and hypercapnia on capillary flow velocity in the rat cerebral cortex.
The velocity of red blood cells (RBC) in individual capillaries of the rat cerebral cortex was assessed using direct, intravital video microscopy under normal conditions and during systemic hypoxia or hypercapnia. The movement of RBC in capillaries within 50-microm depth of the parietal cortex was visualized with the aid of fluorescent labeling of RBC in a closed cranial window preparation in pentobarbital-anesthetized, artificially ventilated adult rats. Hypoxia was produced by lowering the concentration of oxygen in the inspired gas from 30 to 15% for 5 min. ⋯ A significant negative correlation between the velocity change at 10% CO2 and the normocapnic resting velocity was found in a group of capillaries isolated by cluster analysis. These results suggest that the dominant component of cerebral hyperemic response to hypoxia and to moderate hypercapnia is an increase in capillary RBC flow velocity. A more complex change in the velocity distribution occurs during severe hypercapnia and results in increased homogeneity of RBC perfusion in the cerebrocortical capillary network.