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B H Pannen

Publications and source records attributed to B H Pannen.

20 records · Page 2Linked to original sources

The acute-phase response.

Inflammation and tissue injury elicit profound changes in the concentrations of several plasma proteins. These proteins are predominantly synthesized in the liver and named acute-phase proteins. The regulatory mechanisms that control this response are highly complex and include the release of various mediators affecting specific subsets of acute-phase genes. Individual mediators can either synergistically enhance or inhibit the effects of other mediators. Binding of mediators to their respective receptors on hepatocytes and transduction of this signal induce changes in acute-phase protein gene expression that are primarily regulated on a transcriptional level. However, under certain conditions post-transcriptional mechanisms may also be involved in this process. Although some acute-phase proteins have been shown to minimize tissue damage, as well as to participate in hemostasis, tissue repair, and regeneration in response to injury, the actual in vivo functions of several acute-phase reactants remain speculative. Measurements of acute-phase protein plasma concentrations can be of diagnostic or prognostic value under certain clinical conditions. Further characterization of the regulatory mechanisms that govern the acute-phase response in vivo could lead to the development of new therapeutic strategies aimed at improving the organism's integrated response to injury.

Acute-Phase Proteins↗

Chronic ethanol consumption increases hepatic sinusoidal contractile response to endothelin-1 in the rat.

Recent evidence suggests that hepatic stellate cells function as liver-specific pericytes that are highly contractile in response to endothelin-1 (ET-1). Liver injury has been shown to lead to "activation" of stellate cells producing a phenotypic change to a more myofibroblastic cell type including loss of vitamin A and increased contractility. The present study was undertaken to test the effects of short-term chronic ethanol consumption (36% of total calories for 5 weeks according to the Lieber-DeCarli protocol) on hepatic vitamin A storage, expression of smooth muscle alpha-actin, and sinusoidal contractility in Sprague-Dawley rats. Using in vivo epifluorescence video microscopy, we quantified the number of sites of vitamin A fluorescence (purportedly stellate cells) and assessed sinusoidal microhemodynamics at baseline and during a 20-minute infusion period of ET-1 (1 pmol * 100 g body weight [bw]*1*min-1). Retinol and retinyl palmitate were measured after the experiment by means of high-pressure liquid chromatography (HPLC). A highly significant decrease in liver retinyl palmitate level (control: 622.5 +/- 50.9; ethanol: 273.0 +/- 38.0 microgram/g liver; P< .001) was found that correlated with a decrease in sites of vitamin A fluorescence (control: 531.4 +/- 76.1; ethanol: 141.1 +/- 30.2* mm-2; r = .82, P <.001). Concomitantly scattered expression of smooth muscle alpha-actin in sinusoids was observed. Although sinusoidal hemodynamics were not affected at baseline, a significant increase in sinusoidal contractility on endothelin-1 infusion (e.g., sinusoidal resistance [% of baseline value]: control: 10 minutes: 288.7 +/- 71.7, 20 minutes: 200.5 +/- 46.9; ethanol: 10 minutes: 1,916.0 +/- 701.7, 20 minutes: 656.8 +/- 103.3; P < .05 and .01, respectively) was observed. These data indicate that chronic ethanol consumption in this moderate model initiates stellate cell activation. Increased sinusoidal responsiveness to the vasoconstrictor ET-1 in vivo may contribute to the increased susceptibility of ethanol-fed rats to secondary stresses that increase ET-1 expression, such as endotoxemia.

Actins↗