Pathophysiological Characteristics of Cutaneous Microcirculation in Patients with Liver Cirrhosis: Relationships to Cardiovascular Hemodynamics and Plasma Neurohormonal Factors

Seino, Yoshihiko; Ohki, Kiyoshi; Nakamura, Tatsuo; Tsukamoto, Hiroshi; Takano, Teruo; Aramaki, Takumi; Okumura, Hidemasa; Hayakawa, Hirokazu

doi:10.1006/mvre.1993.1047

Cited by 21 publications

(20 citation statements)

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“…This has been considered as a suitable technique for the estimation of hepatic microvascular perfusion [16][17][18][19]. In each animal the probe of the flowmeter was placed at the same position on the surface of the median and the left lobe of the liver.…”

Section: Hepatic Tissue Blood Flowmentioning

confidence: 99%

Mouse livers with macrosteatosis are more susceptible to normothermic ischemic injury than those with microsteatosis

Selzner

Jochum

et al. 2006

Journal of Hepatology

119

147

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Section: Hepatic Tissue Blood Flowmentioning

confidence: 99%

Mouse livers with macrosteatosis are more susceptible to normothermic ischemic injury than those with microsteatosis

Selzner

Jochum

et al. 2006

Journal of Hepatology

119

147

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“…The laser-Doppler flowmeter provides continuous measurement of relative changes in microcirculatory blood flow in various tissues. 34 …”

Section: Hepatic Blood Perfusion Measurementmentioning

confidence: 99%

Preconditioning Protects Against Systemic Disorders Associated With Hepatic Ischemia–Reperfusion Through Blockade of Tumor Necrosis Factor-Induced P–Selectin Up–Regulation in the Rat

et al. 2001

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Previous studies indicate that ischemic preconditioning protects against lung injury resulting from hepatic ischemiareperfusion (I/R) through inhibition of tumor necrosis factor (TNF) release from Kupffer cells. The present study investigated whether this effect is limited to the lung or is a generalized systemic response and explores the molecular mechanisms involved. Hepatic I/R led to an increase in neutrophil accumulation in liver, lung, and splanchnic organs. Although preconditioning did not modify neutrophil infiltration in liver during reperfusion, it conferred protection against hepatic injury associated with I/R. In remote organs, preconditioning abrogated the increase in P-selectin up-regulation, preventing neutrophil infiltration and thus reducing the oxidative stress and microvascular disorders following hepatic I/R in these organs. Administration of Abs against P-selectin or TNF previous to ischemia had the same effects as preconditioning. The effects of preconditioning on the blockade of P-selectin up-regulation probably results from inhibition of systemic TNF release from Kupffer cells. Supplementation of TNF abolished the benefits of preconditioning, whereas the injurious effects of TNF were prevented by previous blockade of P-selectin. The results of the present study suggest that ischemic preconditioning protects the liver against I/R injury by a mechanism independent of adhesion molecule expression and neutrophil accumulation. In remote organs, however, hepatic preconditioning prevents inflammatory damage by reducing the systemic TNF release from the liver and thus preventing P-selectin up-regulation. (HEPATOLOGY 2001;33:100-113.)

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“…The laser-Doppler flowmeter provides continuous measurement of relative changes in microcirculatory blood flow in various tissues. 10 …”

Section: Hepatic Blood Perfusion Measurementmentioning

confidence: 99%

The Protective Role of Adenosine in Inducing Nitric Oxide Synthesis in Rat Liver Ischemia Preconditioning Is Mediated by Activation of Adenosine A2 Receptors

et al. 1999

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This study aims to determine if the protective role of adenosine in liver ischemic preconditioning is mediated by the activation of adenosine receptors and to ascertain which of these receptors is implicated in the process. Administration of adenosine A 1 and A 2 receptor antagonists to preconditioned animals indicates that hepatic preconditioning is mediated by the activation of adenosine A 2 receptors. Propentofylline (an inhibitor of adenosine transport into cells) in the preconditioned group, subjected to previous administration of an adenosine A 2 receptor antagonist, prevented the negative effect of the latter on the protection offered by preconditioning. An increase of NO production was detected just immediately after hepatic preconditioning, and the administration of an adenosine A 2 receptor antagonist to the preconditioning group prevented this increase, thus abolishing the protective effect of preconditioning. However, the administration of a NO donor to the preconditioned group subjected to previous administration of the adenosine A 2 receptor antagonist was able to maintain the preconditioning effects. In conclusion, these results indicate that, in preconditioning, the protective effect of adenosine could be a result of an increase in extracellular adenosine. This in turn would induce the activation of adenosine A 2 receptors, which, by eliciting an increase in NO generation, would protect against the injury associated with hepatic ischemia-reperfusion. (HEPATOLOGY 1999;29: 126-132.)Ischemic preconditioning, first shown in the myocardium has become a phenomenon described in the intestine, 1 brain, 2 and liver. 3 We have previously shown that ischemic preconditioning, induced by brief ischemia and reperfusion periods, renders the liver more tolerant to subsequent sustained ischemia-reperfusion. 4 We have also shown that the administration of adenosine mimics the effect of preconditioning in ischemic livers, and that the metabolization of endogenous adenosine by adenosine deaminase abolished the protective effect of preconditioning. We have further shown the beneficial effect of adenosine in inducing NO synthesis in ischemic tissue, 4 although the exact mechanism by which adenosine offered protection was not determined in that study. Recent work in heart preconditioning has shown that preconditioning-induced protection may require the activation of adenosine receptors. Thus, an adenosine receptor agonist can simulate the preconditioning whereas an adenosine receptor antagonist blocks its beneficial effect. 5 Also, recent studies in cerebral ischemia, have obtained evidence that the response to adenosine persists or is enhanced by nucleoside transport inhibitors such as propentofylline. Inhibition of adenosine uptake would increase its concentration in the extracellular space and hence potentiate its effects, particularly if adenosine binds to a specific receptor site on the external surface of the membrane. 6 Adenosine receptors have been divided into three major subclasses: A 1 , A 2 , and A 3 , 5,7 ...

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Pathophysiological Characteristics of Cutaneous Microcirculation in Patients with Liver Cirrhosis: Relationships to Cardiovascular Hemodynamics and Plasma Neurohormonal Factors

Cited by 21 publications

References 0 publications

Mouse livers with macrosteatosis are more susceptible to normothermic ischemic injury than those with microsteatosis

Mouse livers with macrosteatosis are more susceptible to normothermic ischemic injury than those with microsteatosis

Preconditioning Protects Against Systemic Disorders Associated With Hepatic Ischemia–Reperfusion Through Blockade of Tumor Necrosis Factor-Induced P–Selectin Up–Regulation in the Rat

The Protective Role of Adenosine in Inducing Nitric Oxide Synthesis in Rat Liver Ischemia Preconditioning Is Mediated by Activation of Adenosine A2 Receptors

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