In the present study, coumarin and some coumarin derivatives (esculetin, scoparone, and 4-methylumbelliferone) were investigated for their lipid-lowering effect in rats. Male Sprague–Dawley rats (150–200 g) were divided into six groups and each group comprised of five rats. Hepatic injury-dependent hyperlipidemia was induced by carbon tetrachloride (CCl4, 1.25 ml/kg). Coumarin and coumarin derivatives esculetin (35 mg/kg), scoparone (35 mg/kg), 4-methylumbelliferone (35 mg/kg), or coumarin (30 mg/kg) were administered to experimental groups at 12-h intervals. Animals received the derivatives esculetin, scoparone or 4-methylumbelliferone prior to the administration of a single toxic dose of CCl4. Serum total cholesterol (TC), triglyceride (TG), very low-density lipoprotein cholesterol (VLDL-C), and low-density lipoprotein cholesterol (LDL-C) levels significantly increased in CCl4-treated group ( p < 0.05, p < 0.01, p < 0.01, and p < 0.05, respectively), while levels of serum high-density lipoprotein cholesterol (HDL-C) decreased ( p < 0.01). 4-Methylumbelliferone had no recovery effects on serum TC levels, however, significantly prevented CCl4-induced hyperlipidemia by reducing TG and VLDL-C levels ( p < 0.05 and p < 0.05, respectively). In addition, coumarin had no recovery effect on any of the serum lipid parameters against CCl4-induced hyperlipidemia. Among the coumarin derivatives only esculetin and scoparone significantly prevented serum HDL-C in CCl4-induced dyslipidemia. The results from this study indicate that the chemical structure of coumarins plays an important role on the regulation of serum lipid profiles.

In vivo somatostatin inhibits exocrine pancreatic secretion. In in vitro experiments, such as the isolated perfused pancreas, somatostatin fails to inhibit exocrine pancreatic secretion. This suggests an indirect action of somatostatin, such as modulation of neural regulation. In the anesthetized rat we tested the inhibitory capacity of somatostatin in the presence of neural blockade in vivo. Neither the drugs given intravenously – phentolamine, propanolol, atropine and naloxone – nor vagotomy were able to prevent somatostatin-induced inhibition of exocrine pancreatic secretion. We conclude that somatostatin-induced inhibition of exocrine pancreatic secretion is not dependent on intact extrinsic innervation.

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The objective of the study is to investigate the effects of ketamine and propofol on cytokines, antioxidant defense system, and neutrophil functions in dogs. A total of 24 dogs were used. Dogs were divided into two groups as ketamine and propofol. The ketamine group received ketamine (5 mg/kg) intravenously while the propofol group received propofol (4 mg/kg) intravenously. Blood samples were collected before sedation and 30 minutes after induction. Serum antioxidant and cytokine levels were analyzed and neutrophil functions were determined. Respiration rate, serum malondialdehyde, IL-4, IL-6 levels, and phagocytic and chemotaxic activity of neutrophils were decreased (P=0.001, P=0.010, P=0.014, P=0.039, P=0.008, and P=0.037, respectively), oxygen saturation were increased (P=0.025) in the ketamine group. Serum IL-6 and IFN-γ level were decreased (P=0.015 and P=0.032 respectively), chemotactic activity of neutrophils were increased (P=0.049) in propofol group. The administration of ketamine was found to have a positive effect both on the antioxidant system and the neutrophil. On the other hand, positive and negative effects of propofol on different parts of the immune system were observed. Therefore, the results should should be taken into account when designing an anesthesia protocol for dogs to predict possible defense system reactions during the postoperative period.

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