Randomized, placebo-controlled trial of lazaroid effects on severe acute pancreatitis in rats

Schulz, Hans–Ulrich; Hoenl, Hanns; Schräder, Thomas; Kropf, Siegfried; Halangk, Walter; Ochmann, Christian; Matthias, R.; Letko, G; Roessner, Albert; Lippert, H.; Niederau, Claus

doi:10.1097/00003246-200104000-00035

Cited by 14 publications

(21 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…ROS scavenger therapy was also found effective in taurocholate- (Gough et al 1990;Schoenberg et al 1991Schoenberg et al , 1994, caerulein- (Guice et al 1986;Wisner et al 1988;Schoenberg et al 1994) and pancreatic duct obstruction (Sevillano et al 2003) induced AP in rats, as well as in caerulein-and cholinedeficient/ethionine-enriched diet induced AP in mice (Nonaka et al 1991(Nonaka et al , 1992Cuzzocrea et al 2004). However, in other studies of caerulein and cholinedeficient/ethionine-enriched diet models of pancreatitis in rodents, administration of ROS scavengers and suppression of ROS production was unable to reduce the degree of the acinar cell injury (Steer et al 1991;Schulz et al 2001). Antioxidants also inhibited caerulein-induced NF-kB activation in isolated rat pancreatic acinar cells (Yu et al 2002).…”

Section: Mechanisms Of Ros and Rns Induced Damage In Pancreatic Acinamentioning

confidence: 95%

Free radicals and the pancreatic acinar cells: role in physiology and pathology

Chvanov

Petersen

Tepikin

2005

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

Reactive oxygen and nitrogen species (ROS and RNS) play an important role in signal transduction and cell injury processes. Nitric oxide synthase (NOS)-the key enzyme producing nitric oxide (NO)-is found in neuronal structures, vascular endothelium and, possibly, in acinar and ductal epithelial cells in the pancreas. NO is known to regulate cell homeostasis, and its effects on the acinar cells are reviewed here. ROS are implicated in the early events within the acinar cells, leading to the development of acute pancreatitis. The available data on ROS/RNS involvement in the apoptotic and necrotic death of pancreatic acinar cells will be discussed.

show abstract

Section: Mechanisms Of Ros and Rns Induced Damage In Pancreatic Acinamentioning

confidence: 95%

Free radicals and the pancreatic acinar cells: role in physiology and pathology

Chvanov

Petersen

Tepikin

2005

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

show abstract

“…Macroscopic severity of pancreatitis was based on a previously described scoring system. 19 Up to three points are allocated for each of ascites, extrapancreatic fat necrosis, pancreatic edema, hemorrhage, and necrosis. The maximum score by this method was.…”

Section: Severity Scorementioning

confidence: 99%

“…Overall, relative water content of the lungs in Figure 1 a Mean macroscopic pancreatitis severity score (as per Schulz et al 19 ), comparing control animals with pancreatitis to those with pancreatitis undergoing HBO therapy. Subgroup analysis of animals surviving to 7 days is shown.…”

Section: Lung Edemamentioning

confidence: 99%

Hyperbaric Oxygen Therapy Reduces Severity and Improves Survival in Severe Acute Pancreatitis

Nikfarjam

Cuthbertson

Malcontenti‐Wilson

et al. 2007

Journal of Gastrointestinal Surgery

View full text Add to dashboard Cite

Severe acute pancreatitis is characterized by pancreatic necrosis, resulting in local and systemic inflammation. Hyperbaric oxygen (HBO) therapy modulates inflammation, but has not been extensively studied in pancreatitis. This study investigates the effects of HBO in a rat model of severe acute pancreatitis. Sixty-four rats were induced with severe pancreatitis using 4% sodium taurocholate and randomized to HBO treatment or control. HBO was commenced 6 h after induction (100% oxygen at 2.5 atmospheres for 90 min) and continued every 12 h for a maximum of eight treatment episodes. Surviving animals were killed at 7 days. Severity of pancreatitis was graded macroscopically and microscopically. Lung edema was calculated using wet and dry lung weights. Macroscopic and microscopic severity scores (mean +/- SE) of HBO-treated animals with pancreatitis (8.3 +/- 0.7; 9.6 +/- 0.4) were lower than those of controls (10.5 +/- 0.5; 11.1 +/- 0.4) (p = 0.02 and p = 0.03, respectively). The HBO-treated group had reduced pancreatic necrosis compared to controls (40 +/- 4% vs. 54 +/- 4%; p = 0.003). There was no difference in pulmonary edema between the groups. Median survival in the HBO-treatment group was 51 h, compared to 26 h in controls. Day-7 survival was significantly improved in the HBO-treated animals compared to controls (40% vs. 27%; p = 0.04). HBO therapy reduces overall severity, decreases the extent of necrosis, and improves survival in severe acute pancreatitis.

show abstract

“…Acute necrotizing pancreatitis was induced by intraductal injection of 0.6 ml of 3.5% sodium taurocholate (Sigma, Deisenhofen, Germany) with a pressure-controlled (25 cm H 2 O) infusion rate of 6 ml/h, as described elsewhere [4,12] .…”

Section: Methodsmentioning

confidence: 99%

Effect of Procainhydrochloride on Phospholipase A2 Catalytic Activity in Sodium Taurocholate-Induced Acute Experimental Pancreatitis in Rats

Kahl

Mayer²,

Schuette³

et al. 2010

Dig Dis

View full text Add to dashboard Cite

Background: In human acute pancreatitis (AP) the local anaesthetic procainhydrochloride (procain-HCl) is given intravenously for pain treatment. Procain has been shown to inhibit catalytic activity of pancreatic (group I) phospholipase A2 (PLA2) and non-pancreatic (group II) PLA2. Both enzymes are important mediators for the local and systemic inflammatory process in AP. To determine the effect of procain, we examined serum and tissue levels of both types of PLA2 activity in the experimental rodent taurocholate model of AP. Methods: In 60 rats, severe pancreatitis was induced by taurocholate. Forty rats were treated with procain-HCl intravenously at a dosage of 2 mg/kg body weight/h either at or 1 h after induction of pancreatitis. Twenty rats served as controls. We measured catalytic activities of group I and group II PLA2 in serum and tissue samples of lung and pancreas. Results: Serum group II PLA2 catalytic activity was significantly reduced 3 and 6 h after AP induction in rats treated with procain-HCl (p < 0.001) in both treatment groups. In pancreatic and lung tissue, group II PLA2 catalytic activity was significantly reduced compared with normal values (p < 0.001). Conclusion: Procain-HCl given intravenously either at or 1 h after induction of necrotizing pancreatitis significantly inhibits group II PLA2 catalytic activity in serum and tissues.

show abstract

Randomized, placebo-controlled trial of lazaroid effects on severe acute pancreatitis in rats

Cited by 14 publications

References 47 publications

Free radicals and the pancreatic acinar cells: role in physiology and pathology

Free radicals and the pancreatic acinar cells: role in physiology and pathology

Hyperbaric Oxygen Therapy Reduces Severity and Improves Survival in Severe Acute Pancreatitis

Effect of Procainhydrochloride on Phospholipase A2 Catalytic Activity in Sodium Taurocholate-Induced Acute Experimental Pancreatitis in Rats

Contact Info

Product

Resources

About