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  • 1
    Electronic Resource
    Electronic Resource
    The nitric oxide donor sodium nitroprusside protects against hepatic microcirculatory dysfunction in early endotoxaemia (1998)
    Springer
    Intensive care medicine 24 (1998), S. 1257-1263 
    Details
    ISSN: 1432-1238
    Keywords: Key words Sepsis ; Nitric oxide ; Sodium nitroprusside ; Liver ; Microcirculation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: Endotoxin rapidly inhibits the activity of the constitutive endothelial nitric oxide synthase (ecNOS); this precedes the production of NO from inducible NOS (iNOS). This leaves a period in early endotoxaemia with a supposed scarcity of NO. The present study was conducted to examine the effects of external supplementation of NO on liver microcirculation and function. Material: 13 male Sprague Dawley rats. Interventions: The rats underwent laparotomy, and the left liver lobe was exteriorised. All animals were given a bolus dose of endotoxin (LPS) 5 mg/kg intraportally. One group (n = 6) had a continuous infusion of sodium nitroprusside (SNP) 1.4 μg/kg per min started concurrently, the other group (n = 7) was treated with normal saline. The study was terminated after 3 h LPS. Measurements and results: Intravital microscopy was performed at baseline, at 2 h and 3 h LPS. Hepatic function was assessed by arterial ketone body ratio, acid base values, and bile flow. At baseline 1 % of the sinusoids were without perfusion. After 2 h LPS this figure had risen to 9.8 ± 1.5 % in the SNP group versus 16.9 ± 1.4 % in the controls (p 〈 0.05 vs controls). The corresponding values after 3 h LPS were 13.5 ± 1.5 versus 19.3 ± 1.5 % (p 〈 0.05 vs controls). The leukocyte count in sinusoids and venules had a similar development. Functional parameters were all slightly better preserved in the SNP group, but with no individual significance versus controls. Conclusions: Infusion of the NO donor SNP in early endotoxaemia attenuates the detrimental effects of LPS on liver microcirculation, most probably by alleviating a relative deficit of NO at the microcirculatory level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340050759
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  • 2
    Electronic Resource
    Electronic Resource
    Impact of brain death on hormonal homeostasis and hepatic microcirculation of transplant organ donors (1998)
    Springer
    Transplant international 11 (1998), S. S404 
    Details
    ISSN: 1432-2277
    Keywords: Key words Brain death ; Organ donor ; Liver transplantation ; Graft viability ; Hepatic microcirculation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To elucidate the pathophysiological mechanisms involved in the deterioration of hepatic graft viability in brain-dead organ donors, the impact of brain death on hepatic microcirculation was investigated with respect to hormonal homeostasis and graft viability. Rats were assigned to two groups: group I (n = 6) served as sham controls, and in group II (n = 6), brain death was induced through insufflation of an intracranial balloon. Mean arterial pressure was elevated significantly within 5 min after the induction of brain death and then decreased significantly to below the control value. Urine osmolality was significantly lower and serum osmolality significantly higher than the control values. Antidiuretic hormone level was significantly lower than the control value. Bile secretion also decreased significantly. Furthermore, in group II there were significantly higher numbers of nonperfused sinusoids (15.9 % vs 6.2 % in group I), and sinusoidal stagnant and postsinusoidal venular adherent leukocytes (53.9/lobule and 258.6/mm2 versus 25.2/lobule and 124.8/mm2 in group I, respectively). In summary, sinusoidal perfusion is compromised after brain death, possibly, in part, through an increased leukocyte activation and accumulation in the hepatic microvasculature, leading to the deterioration of hepatic function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001470050509
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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