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Biomedical subjects

C O Feddersen

Publications and source records attributed to C O Feddersen.

At least 19 recordsLinked to original sources
PubMed1995

[Spiroergometry].

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Cardiovascular Diseases↗
PubMed1993

[N-acetylcysteine decreases functional and structural, ARDS-typical lung changes in endotoxin-treated rats].

Oxygen radicals and oxygen radical mediators derived from activated granulocytes are important components in the development of acute lung injury, namely the adult respiratory distress syndrome ARDS. N-acetylcysteine (NAC) is one important substance for endogenous production of reduced glutathion, which is known to be an intra- and extracellular reducing agent also found in lung tissue. We evaluated the effect of exogenous NAC on the endotoxin induced development and course of ARDS in rats. ARDS-like injury was induced in rats via intraperitoneal injection of Salmonella enteritidis endotoxin 30 mg/kg body weight. NAC or solvent was injected intraperitoneally 30 min prior to, at the time of and 30 min after injection of endotoxin respectively with 150 mg/kg body weight each dose. Endotoxin injection in rats resulted in 80% mortality within 72 hours, increased lung wet weight, severe ultrastructural lung damage as measured by histological methods. In isolated, ventilated, with physiological salt solution perfused rat lungs vasocontractility was severely blunted, lung albumin leakage was increased, thromboxane B2 (TXB2) and 6-keto-prostaglandin-F1 alpha (6-keto-PGF1 alpha) perfusate levels were increased. NAC treatment significantly improved survival of endotoxin treated rats, ameliorated structural lung damage, diminished lung wet weight and lung albumin leakage, lowered lung perfusate TXB2 and 6-keto-PGF1 alpha levels and slightly improved vasocontractility in isolated perfused lungs. Therefore, NAC significantly ameliorates ARDS-like lung injury in rats, when given in vivo.

Acetylcysteine↗
PubMed1991

[Hyponatremia].

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Humans↗
PubMed1991

Lung injury in acute experimental pancreatitis in rats. I. Morphological studies.

The pathogenesis of pancreatitis-related pulmonary injury was studied at the light- and electronmicroscopic level. Experimental pancreatitis was induced in rats by infusion of supramaximal doses of cerulein for 12 h. Investigations were carried out 3, 6, and 12 h after the start of infusion and 12, 48, and 72 h after the end of pancreatitis induction. Initial manifestations of pancreatitis-associated lung injury revealed a pronounced clustering of polymorphonuclear leukocytes in pulmonary microvessels, followed by severe damage of alveolar endothelial cells. Consecutively, the increase in vascular permeability of the lung resulted in interstitial edema formation. Structural changes were maximal after 12 h and reversed completely after 84 h. In conclusion, the structural appearance of pulmonary injury in cerulein-induced pancreatitis was similar to that reported in early stages of the adult respiratory distress syndrome (ARDS). It is suggested that polymorphonuclear granulocytes play a crucial role in the pathogenesis of pancreatitis-related lung injury.

Acute Disease↗
PubMed1991

Lung injury in acute experimental pancreatitis in rats. II. Functional studies.

In this study we report the functional changes in isolated perfused lungs from rats with cerulein-induced experimental pancreatitis. Rat lungs isolated immediately after the cerulein infusion demonstrated decreased pressor responses to angiotensin II (A II) and acute hypoxia (FIO2: 0.0). The lung wet- to dry-weight ratio was increased, as was the lung-leak index, consistent with high-permeability edema formation in the lung. Neither saline-solution infusion for 12 h nor perfusion with cerulein of rat lungs isolated from untreated animals caused lung injury or functional alterations. The changes in pulmonary vascular reactivity were normalized 48-72 h after induction of pancreatitis. In conclusion, we describe an animal model of pancreatitis and reversible, ARDS-like lung injury.

Acute Disease↗
PubMed1991

[Allergic alveolitis].

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Alveolitis, Extrinsic Allergic↗
PubMed1990

[Central pontine myelinolysis following severe hyponatremia].

Central pontine myelinolysis is a process of demyelinisation with variable neurological symptoms related to the localization. Predisposing factors are alcoholism and malnutrition. Rapid correction of severe hyponatremia is suspected to be a primary cause for central pontine myelinolysis. We report a 43 year old chronic alcoholic and polytoxicomanic female patient, who was admitted comatose with a serum sodium level of 94 mmol/l, caused by a syndrome of inappropriate ADH secretion. After initial improvement under careful sodium correction, the patients neurologic condition degraded progressively and within 4 weeks she developed a "locked-in"-syndrome. Only then the suspected central pontine myelinolysis could be demonstrated in nuclear magnetic resonance and computer tomography. We presume that, although sodium correction was done relatively slowly in this patient, it probably contributed to her development of central pontine myelinolysis all the same. Due to this case we review the literature on correction of hyponatremia, which shows growing evidence that it should start early but be continued very slowly (rise in serum-Na: max. 0.6 mmol/l/h) and requires frequent laboratory controls.

Adult↗
PubMed1990

Disseminated tuberculosis after renal transplantation. A report of two cases.

Disseminated mycobacterial infections occurred in two female renal graft recipients late after transplantation. In the first patient, initially presenting with fever, diagnosis was made at autopsy. Temporary defervescence following antibiotic therapy with ofloxacin possibly contributed to the fatal diagnostic delay. In the second case, body temperature was normal throughout the protracted course of the patient's illness. Her presenting symptom was rapidly increasing ascites, attributed initially to chronic liver disease. These cases demonstrate that tuberculosis remains a serious complication after renal transplantation, in particular due to its sometimes atypical clinical manifestations. Response to antibacterial therapy has to be critically evaluated in order to avoid fatal diagnostic delay.

Adult↗
PubMed1990

Arachidonic acid causes cyclooxygenase-dependent and -independent pulmonary vasodilation.

In this study we examined the action of arachidonic acid in the isolated rat lung perfused with a cell- and protein-free physiological salt solution. When pulmonary vascular tone was elevated by hypoxia, bolus injection of a large dose of arachidonic acid (75 micrograms) caused transient vasoconstriction followed by vasodilation. When arachidonic acid (100 micrograms) was injected during normoxia and at base-line perfusion pressure (low vascular tone) or when vascular tone was elevated by KCl, arachidonic acid (50 micrograms) caused only vasoconstriction. Doses less than 7.5 micrograms caused vasodilation only when injected during hypoxic vasoconstriction and subsequent blunting of either angiotensin II- or hypoxia-induced pulmonary vasoconstriction. The higher doses of arachidonic acid (7.5 and 75 micrograms), but not the lower doses (7.5-750 ng), caused increases in effluent 6-ketoprostaglandin F1 alpha, thromboxane B2, and prostaglandin E2 and F2 alpha. 6-Ketoprostaglandin F1 alpha was the major cyclooxygenase product. Meclofenamate (10(-5) M) blocked the increased metabolite synthesis over the entire dose range of arachidonic acid tested (7.5 ng-75 micrograms). Because vasodilation immediately after arachidonic acid was cyclooxygenase-independent, we investigated whether this effect was due to the unsaturated fatty acid properties of arachidonic acid and compared its action with that of oleic acid and docosahexaenoic acid. Because neither compound mimicked the vasodilation observed with arachidonic acid, we concluded that the cyclooxygenase-independent action of arachidonic acid could not be explained by unsaturated fatty acid properties per se. Because 1-aminobenzotriazole, a cytochrome P-450 inhibitor, partially inhibited the immediate arachidonic acid-induced pulmonary vasodilation, we concluded that cytochrome P-450-dependent metabolites can account for some of the cyclooxygenase-independent vasodilation of arachidonic acid.

Animals↗
PubMed1987

Platelet-activating factor mediates hemodynamic changes and lung injury in endotoxin-treated rats.

Within 20 min after intraperitoneal injection of Salmonella enteritidis endotoxin in rats, blood platelet-activating factor (PAF) increased from 4.3 +/- 1.3 to 13.7 +/- 2.0 ng/ml (P less than 0.01) and lung PAF from 32.3 +/- 4.9 to 312.3 +/- 19.6 ng (P less than 0.01), but not lung lavage PAF. We tested the effect of PAF receptor antagonists, CV 3988 and SRI 63-441, on endotoxin-induced hemodynamic changes and lung vascular injury. Pretreatment with CV 3988 attenuated systemic hypotension, preserved hypoxic pulmonary vasoconstriction, and prolonged survival of awake catheter-implanted endotoxin-treated (20 mg/kg) rats. Pretreatment with SRI 63-441 prevented the depressed hypoxic pulmonary vasoconstriction after low dose (2 mg/kg) endotoxin. Both CV 3988 and SRI 63-441 blocked the increased extravascular accumulation of 125I-albumin and water in perfused lungs isolated from endotoxin-treated rats. We conclude that PAF is produced in the lung during endotoxemia and may be an important mediator of the systemic and pulmonary hemodynamic changes as well as the acute lung vascular injury after endotoxemia.

Animals↗
PubMed1986

Acetylcholine induces vasodilation and prostacyclin synthesis in rat lungs.

Acetylcholine causes pulmonary vasodilation, but its mechanism of action is unclear. We hypothesized that acetylcholine-induced pulmonary vasodilation might be associated with prostacyclin formation. Therefore, we used isolated rat lungs perfused with a recirculating cell- and plasma-free physiological salt solution to study the effect of acetylcholine infusion on pulmonary perfusion pressure, vascular responsiveness and lung prostacyclin production. Acetylcholine (20 micrograms infused over 1 minute) caused immediate vasodilation during ongoing hypoxic vasoconstriction and prolonged depression of subsequent hypoxic and angiotensin II-induced vasoconstrictions. Both effects of acetylcholine were abolished by atropine pretreatment. The prolonged acetylcholine effect, but not the immediate response, was blocked by meclofenamate, an inhibitor of cyclooxygenase. The prolonged effect, but not the immediate response, of acetylcholine was associated with an increase in perfusate 6-keto-PGF1 alpha concentration. The acetylcholine stimulated increase in 6-keto-PGF1 alpha production was inhibited by meclofenamate and by atropine. Thus, blockade of prostacyclin production corresponded with blockade of the prolonged acetylcholine effect. In conclusion, acetylcholine caused in isolated rat lungs an immediate vasodilation and a prolonged, time-dependent depression of vascular responsiveness. Whereas both acetylcholine effects were under muscarinic receptor control, only the prolonged effect depended on the cyclooxygenase pathway and, presumably, prostacyclin synthesis.

6-Ketoprostaglandin F1 alpha↗