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U Rauen

Publications and source records attributed to U Rauen.

43 records · Page 3Linked to original sources
PubMed1994

The potential role of reactive oxygen species in liver ischemia/reperfusion injury following liver surgery.

Reperfusion of a previously ischemic tissue may lead to an aggravation of injury. The liver has been shown to be susceptible to this reperfusion injury in several experimental systems. Reactive oxygen species appear to play an important role in the development of such injury, as has been demonstrated by direct measurements of their release, and by the protective effects of antioxidants. Upon reperfusion, reactive oxygen species may be released by hepatocytes, Kupffer cells and neutrophils. The relative contribution of the various liver cell types to the release of reactive oxygen species depends on several factors, including the duration and condition of ischemia and the time elapsed after reperfusion. There is only limited evidence for the occurrence of reperfusion injury in humans following liver surgery. The role of reactive oxygen species in this injury in humans remains to be shown.

Animals↗
PubMed1994

[Differences in the mechanisms of damage to Kupffer cells and liver endothelial cells during preservation in UW solution].

AIM OF THE STUDY: The predominant injury during cold preservation of the liver appears to affect the non-parenchymal cells. Therefore we studied the contribution of hypoxia and the effect of the University of Wisconsin (UW) solution on the injury to cultured liver endothelial and Kupffer cells. METHODS: Cultured endothelial cells and Kupffer cells of the rat liver were incubated in Krebs-Henseleit buffer at 37 degrees C and in both, Krebs-Henseleit buffer and UW solution, at 4 degrees C. Hypoxic conditions were simulated by the addition of cyanide (1 mM), to some of the cultures glucose (10 mM) was added. Cell injury was assessed by the uptake of the vital dye trypan blue and by the release of cytosolic lactate dehydrogenase. RESULTS: Kupffer cells as well as endothelial cells exhibited a high hypoxia tolerance in Krebs-Henseleit buffer at both 37 degrees C and 4 degrees C. A large difference between both cell types, however, was seen during cold incubation in UW solution: whereas only 35 +/- 10% of Kupffer cells lost viability during 24 hrs under aerobic control conditions, the loss of viability of liver endothelial cells was already 83 +/- 12% under the same conditions. The addition of KCN increased the Kupffer cell injury to 75 +/- 8% but strongly decreased the endothelial cell injury to 3 +/- 2%. The addition of glucose to the cyanide-containing UW solution decreased the injury to Kupffer cells but increased the injury to endothelial cells. CONCLUSION: During cold incubation in UW solution cultured liver endothelial cells are affected by an energy-dependent injury. This type of injury is not detectable in Kupffer cells.

Adenosine↗
PubMed1993

Injury to cultured liver endothelial cells during cold preservation: energy-dependent versus energy-deficiency injury.

Previously, we demonstrated an energy-dependent injury to cultured liver endothelial cells during cold incubation in University of Wisconsin (UW) solution. Here, the effects of Histidine-Tryptophan-Ketoglutarate (HTK) and Euro-Collins (EC) solutions on these cells were studied. In HTK solution, 83% +/- 4% of the cells had lost viability after 9 h of incubation at 4 degrees C. The addition of cyanide (1 mM) to simulate hypoxic conditions protected the cells to the extent that only 9% +/- 1% of the cells lost viability over the same period; the addition of glucose (10 mM) led to increased cell injury. ATP levels were highest in the incubations with the most rapid loss of viability. In Krebs-Henseleit buffer and EC solution, in contrast, cell injury increased upon addition of cyanide; the addition of glucose to Krebs-Henseleit buffer decreased injury. We conclude that the injury to cultured liver endothelial cells during cold incubation in HTK solution is energy-dependent, as it is in UW solution, whereas cells behave differently in EC solution and Krebs-Henseleit buffer.

Adenosine Triphosphate↗
PubMed1993

Energy-dependent injury to cultured sinusoidal endothelial cells of the rat liver in UW solution.

The critical injury to liver during cold preservation is believed to occur to the sinusoidal endothelium. In this study the viability of cultured sinusoidal endothelial cells from rat liver was assessed during storage in University of Wisconsin solution at 4 degrees C. The vast majority of cells (83 +/- 12%) died within 24 hr of storage. Addition of KCN (1 mM) to the solution to simulate hypoxia markedly increased survival: only 3 +/- 2% of cells had lost viability after 24 hr in the presence of cyanide. Further experiments showed that other inhibitors of mitochondrial ATP formation (antimycin A 1 microM, rotenone 1 microM, oligomycin 10 microM, carbonyl cyanide m-chlorophenylhydrazone 1 microM) were protective as well, whereas glucose (10 mM) greatly diminished the protective effect of cyanide (loss of viability 38 +/- 7% after 24 hr). ATP measurements confirmed the correlation between the energy state of the cells and cell death: ATP levels after 6 hr of incubation were 19.9 +/- 4.0 nmol/10(6) cells in UW solution, 13.7 +/- 2.9 nmol/10(6) cells in UW + glucose, 6.9 +/- 1.9 nmol/10(6) cells in UW + KCN + glucose and 1.9 +/- 1.5 nmol/10(6) cells in UW + KCN. In contrast to the protective effect observed in UW solution, addition of KCN to Krebs-Henseleit buffer led to increased endothelial cell damage upon cold storage. We therefore conclude that in UW solution damage to the sinusoidal endothelium is energy-dependent.

Adenosine↗
PubMed1992

Acute cholecystitis: a complication in severely injured intensive care patients.

Acute cholecystitis is an often unrecognized and potentially life-threatening complication seen among ICU patients with multiple injury. To investigate the epidemiology of this entity and to evaluate significant etiologic precursors, a prospective clinical and sonographic study was performed in 45 consecutive patients (mean age, 29 years) treated for multiple trauma (mean ISS, 27) in the ICU. Eight of 45 patients developed a cholecystitis during intensive care treatment (18%). Six patients recovered with conservative therapy; in two instances a cholecystectomy was necessary. There was no mortality as a result of cholecystitis. A significant relationship between the severity of the initial trauma (p less than 0.05), the number of blood transfusions (p less than 0.01), and the incidence of acute cholecystitis was found. Other factors such as prolonged shock, respiratory failure, or parenteral alimentation were less prevalent and were not temporally related to the onset of the disease. All patients had large amounts of narcotics administered over a prolonged period, so that narcotic-induced biliary stasis appeared to be another eminent factor involved in the genesis of posttraumatic cholecystitis. Our results lead to the conclusion that acute cholecystitis occurs with an unexpectedly high incidence and that a high remission rate can be expected following conservative treatment provided that appropriate serial ultrasound examinations are performed.

Acute Disease↗
PubMedDate not supplied

Acute acalculous cholecystitis in severely traumatized patients: a prospective sonographic study.

Acute acalculous cholecystitis is a well known complication in severely traumatized patients. Existing data originate from retrospective analyses and episodic case reports. In a prospective ultrasonographic study 25 polytraumatized patients admitted to our intensive care unit between January 1, 1989, and December 31, 1989, were examined in daily intervals for this condition. Trauma scoring was performed according to the injury severity score (ISS) and polytrauma score (PTS). "Stress cholecystitis" was defined as a combination of hydrops of the gallbladder, an increased mural thickness (> 3.5 mm), and the demonstration of "sludge." We were able to demonstrate this diagnostic triad in four out of 25 patients (= 16%). As a consequence early elective cholecystectomy was done in one patient. The remaining patients were treated conservatively. The incidence of stress cholecystitis in severely traumatized patients is probably higher than figures so far published suggest. Ultrasonography is a reliable method of early detection and follow-up for this complication.

Acute Disease↗