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Biomedical subjects

D Inthorn

Publications and source records attributed to D Inthorn.

At least 37 records · Page 2Linked to original sources
PubMed1988

Enzymatically active cathepsin B dissociating from its inhibitor complexes is elevated in blood plasma of patients with septic shock and some malignant tumors.

Using fluorogenic substrates and the specific inhibitor E-64, cysteine proteinase (CP) activity was measured in blood plasma of healthy controls (mean = 35.0 mU/l) and patients with cancer and severe septic shock. Whereas moderately elevated activity was observed in some kinds of cancer (mean = 63.9 mU/l), 10-fold increased CP activity was found in septic shock. The plasma CP activity of sepsis patients paralleled the immunologically determined concentration of elastase-alpha 1-proteinase inhibitor complex. On the basis of its substrate specificity and its Michaelis constant for Z-Phe-Arg-NMec the plasma CP was identified as cathepsin B or a cathepsin B-like proteinase (CBP). Kinetic studies revealed that dilution and competition with substrate effects reversible dissociation of CBP from complexes with plasma inhibitors that are most probably the kininogens. The dissociation of CBP was confirmed by gel chromatographic fractionation of the plasma proteins. The results suggest that active CBP can easily dissociate from its plasma inhibitor complexes in vivo and may be involved in pathogenetic extracellular proteolysis.

Cathepsin B↗
PubMed1988

Reactive hyperemia in patients with septic conditions.

In a prospective study microvascular reactivity was examined in 12 patients with septic conditions by means of the provocation of reactive hyperemia (RH) for evaluation of microcirculatory function. Data were compared with data from 10 nonseptic, postsurgical patients. At the time of the initial measurement, an adequate hyperemic response could be produced in all patients. In the further course of the disease, in nine of the 12 patients severe multiple organ failure developed. In spite of sufficient values for arterial blood pressure, oxygenation, and the clotting system, RH was absent in these patients (8 +/- 2 days after the initial measurement). Subsequently, seven of these nine patients died (4 +/- 2 days after the onset of microvascular nonreactivity). Until death, RH was absent in each patient, and at this time therapy-resistant hypoxemia, hypotension, and severe disturbances of the clotting system were present. In the two surviving patients RH was restored completely. These results indicate that (1) the septic state per se is not necessarily combined with impaired microvascular reactivity (rather, the absence of RH may be a sign of generally poor clinical conditions); (2) the absence of RH is not related to therapy-resistant hypotension, hypoxia, and severe clotting disorders but precedes these changes; and (3) provocation of RH may be of clinical use for early detection of microcirculatory malfunction in high-risk patients.

Age Factors↗
PubMed1987

D-erythro-neopterin plasma levels in intensive care patients with and without septic complications.

The activation of macrophages is accompanied by release of 2-amino-4-oxo-6(D-erythro-1',2',3'-trihydroxypropyl)-dihydropterid ine (D-erythro-neopterin). The neopterin levels of 21 patients were measured with radioimmunoassay. The patients were classified according to the clinical course and outcome. We found highly significant differences between survivors and nonsurvivors for each of the evaluated days of the observation period. In addition to a sustained increase, patients with fatal outcome always showed a higher percentage of neopterin levels (88.2 +/- 28 [SD]%) exceeding the upper confidence limit (27.4 nmol/L) than survivors (31.8 +/- 29.9%). We conclude that the assessment of D-erythro-neopterin might be an easily available aid for an early evaluation of the immunologic status of a patient at risk for septic complications.

Adult↗
PubMed1986

Pathobiochemistry of sepsis: role of proteinases, proteinase inhibitors and oxidizing agents.

Degradation of structural elements and excessive consumption of humoral factors, especially of plasma proteinase inhibitors, by proteolysis and/or oxidation is a major cause of multiple organ failure in sepsis or septic shock. Such pathobiochemical reactions seem to be induced primarily by extracellularly liberated lysosomal proteins from PMN granulocytes (e.g. elastase, cathepsin G, myeloperoxidase, lactoferrin) as well as oxygen radicals produced during extensive phagocytosis. In clinical studies on septicemia and septic shock the consumption of plasma proteins including proteinase inhibitors was inversely correlated to the liberation of lysosomal factors, especially the granulocytic elastase. Administration of relatively specific elastase-cathepsin G-inhibitors (Bowman-Birk inhibitor, eglin) in experimental septicemia proved to be a promising therapeutic approach to reduce consumption of plasma proteinase inhibitors and development of interstitial lung edema in severe inflammation.

Animals↗
PubMed1985

[Comparison between cimetidine-pirenzepine and antacids for the prevention of stress hemorrhage in intensive care patients. A controlled clinical study on 125 patients].

In a controlled clinical trial, the efficacy of an intravenous combination of cimetidine and pirenzepine (group A: 62 patients) was compared with that of an intragastric administration of a magnesium-aluminium-hydroxide concentrate (group B: 58 patients) in preventing visible and occult upper gastrointestinal tract bleeding in intensive-care patients. It was found that both forms of therapy had the same favourable effect on the extent and incidence rate of visible and occult gastric bleeding. The antacid was more effective than the cimetidine-pirenzepine combination in raising the pH level to 4 or higher (P less than 0.05). Intensive-care patients should, therefore, be treated with the antacid whenever possible, since it is equally effective as the cimetidine-pirenzepine combination in preventing bleeding from the upper gastrointestinal tract, whereas it is superior in elevating the gastric pH. Besides, the use of the antacid is also less costly.

Adult↗
PubMed1980

[Prevention and therapy of gastroduodenal stress bleeding with cimetidine].

In our intensive care unit we were able to prevent almost all bleedings from stress ulcerations in patients with insufficiency of various organs (1,6%) by administering the H2-receptor blocker cimetidine in doses of 8 X 200 mg per day. However, stress ulcer bleedings occurred in 14% of those patients also suffering from a sepsis. At lower doses of cimetidine, the rate of bleeding was comparable to that encountered in patients treated with antacids, i.e. 12,5% patients with multiple organ insufficiency and 42,7% with sepsis. Cimetidine was able to stop less extensive bleedings, but did not show any therapeutic effect in case of bleeding which led to a significant fall in hemoglobin concentration.

Cimetidine↗
PubMed1979

[Prevention and therapy of gastroduodenal stress hemorrhage in intensive care patients using the histamine H2-receptor antagonist cimetidine].

In our intensive care unit we were able to prevent almost all bleedings from stress ulcerations in patients with insufficiency of various organs by administering the H2-receptor blocker, cimetidine, in doses of 200 mg eight times per day. However, stres ulcer bleedings occurred in 14% of those patients also suffering from a sepsis. At lower doses of cimetidine, the rate of bleeding was comparable to that encountered in patients treated with antacids, i.e. 12.5% patients with multiple organ insufficiency and 42.7% with sepsis. Cimetidine did not show any therapeutic effect in case of bleeding which led to a significant fall in hemoglobin concentration.

Cimetidine↗
PubMed1975

[Prophylaxis of acute gastric erosions with vitamin A in the rat (author's transl)].

The protective effect of Vitamin A against stress-induced ulcerations of the gastric mucosa was investigated by the hypoxic stress model of the rat. The incidence of acute mucosal erosions in the main stomach was significantly reduced by intramuscular application of 125 000 - 500 000 U Vitamin A/kg body weight prior to or immediately after the onset of stress. A dosage smaller than that or an application 2 hours after the onset of stress had no influence on the development of the acute mucosal erosions.

Animals↗