Effect of sildenafil on intestinal adaptation parameters in a rat model of short bowel syndrome.

OBJECTIVE: We aimed to evaluate the effect of sildenafil on the intestinal adaptation in short bowel syndrome (SBS). MATERIALS AND METHODS: Forty-eight male Wistar-albino rats (weight, 231-390 g) were randomly divided into four groups with 12 rats in each. Group TA had only ileal transection+anastomosis, Group TA+S was given sildenafil after ileal transection+anastomosis, Group RA had a resection of 75% of the small bowel+anastomosis, Group RA+S was given sildenafil after small bowel resection+anastomosis. Sildenafil was injected subcutaneously at 60 mg/kg/day dose throughout 3-21 days postoperatively. Bowel and mucosal weights, villus height, crypt depth, DNA and protein concentrations were determined. RESULTS: Jejunal bowel weight was lower in TA and TA+S groups than RA and RA+S groups (p < 0.05). RA+S group had higher ileal and jejunal mucosal weights than RA and TA+S groups (p < 0.05). Villus height was highest in RA+S group both in ileum and jejunum (466.1 ± 38.6 µm and 648.1 ± 65.7 µm, respectively). Jejunal crypt depth was highest in RA+S group (255.1 ± 21.9 µm) compared to other groups (p < 0.05). There was no significant difference in ileal and jejunal protein concentration between TA and TA+S groups and in ileal protein concentration between RA ve RA+S groups (p > 0.05). Ileal DNA concentration was higher in TA+S group, and jejunal DNA concentration was higher in RA and RA+S groups than TA and TA+S groups (p < 0.05). CONCLUSIONS: Sildenafil has a positive effect on intestinal adaptation parameters, particularly in jejunum in a rat SBS model. Thus, its role in the treatment of SBS should be further investigated with clinical studies.

Founding the first hernia center in Turkey.

For years, centers dedicated to hernia surgery have been operating in North America and Europe. However, such centers have not been available to patients in most other countries, including Turkey. In 2006, the first Turkish center devoted to hernia surgery, the "Ankara Hernia Center", was opened. In this paper, we present general information about the center's construction, staff, practice, patient profiles, and future goals.

Effects of intravenous and intracerebroventricular theophylline on hypoxic ventilatory depression in anesthetized cats.

OBJECTIVE: The present study was undertaken to investigate the ventilatory response due to sustained isocapnic moderate hypoxia and the possible role of adenosine in hypoxic depression in anesthetized cats. MATERIALS AND METHODS: Cats anesthetized with pentothal sodium (30 mg kg(-1) i.p.) were divided into two groups: treated (n = 11) and control (n = 15). Respiratory frequency (f), tidal volume (VT), minute volume (VE) and systemic arterial blood pressure were recorded during air and 20 min of breathing hypoxic gas mixture (14% O2-86% N2). Isocapnia was maintained by adding fractions of 1% CO2 to the inspired hypoxic gas mixture. The PaO2 and PaCO2 were determined. RESULTS: On hypoxic gas mixture breathing, VT and VE values of the control animals increased significantly, at 5 min to 50 +/- 6 and 53 +/- 6%, respectively, above the prehypoxic air phase value (p < 0.001). After that, the magnitude of increase in VT and VE declined gradually. At 20 min of hypoxia, VT and VE were less than those in prehypoxic air phase (17 +/- 7, 16 +/- 7%, respectively). In cats injected with an adenosine antagonist (theophylline 13.6 mg kg(-1) i.v.), f, VT and VE increased significantly at 5 min of hypoxia (p < 0.001). At 20 min of hypoxia, f, VT and VE were 8 +/- 2, 30 +/- 8, and 39 +/- 8%, respectively, higher than corresponding values of the prehypoxic stage. In cats injected with theophylline (0.5 mg kg(-1)) by cisternal puncture VT and VE increased significantly at 5 min of hypoxia. At 20 min of hypoxia, VT and VE were 27 +/- 7 and 31 +/- 8% higher than those in the prehypoxic air phase. CONCLUSION: The results of this study show that accumulation of adenosine in the brain during hypoxia seems to reduce the response of the central mechanisms to chemoreceptor impulses.

Chemical control of laryngeal vascular resistance in anesthetized dogs.

The branch of the cranial superior thyroid artery that supplies the larynx was perfused unilaterally at a constant flow rate in dogs anesthetized with pentobarbitone sodium (30 mg.kg-1, i.v.). Laryngeal vascular resistance (RLv) was calculated. Intraluminal laryngeal pressure (PL) was determined. Asphyxia caused a diminution in PL (-27.7 +/- 4.2%) (p < 0.01) and an initial decrease followed by an increase in RLv (-10.9 +/- 2.3% and +12.8 + 2.8%) (p < 0.001). Following vagotomy, asphyxia decreased PL (-17.1 +/- 4.2%) and increased RLv (+45.5 +/- 11.0%). Systemic hypoxia induced by breathing 8% O2-N2 increased RLv (+8.4 +/- 1.3%) (p < 0.001) and decreased PL (-24.9 +/- 3.7%) (p < 0.001). In chemodenervated dogs, the response of PL to hypoxia was abolished while that of RLv was similar to that in intact animals. Breathing of 7% CO2 in air caused an increase in RLv (+6.1 +/- 1.6%) (p < 0.001) and a decrease in PL (-20.9 +/- 3.2%) (p < 0.001). Following chemodenervation, hypercapnia still increased RLv (+11.3 +/- 3.2%) (p < 0.01) and diminished PL (-29.9 +/- 2.5%). Bilateral vagotomy reduced the response of PL to hypercapnia (-13.3 +/- 6.9%) (p < 0.05). Local intra-arterial injection of KCN produced an increase in RLv and PL (+7.0 +/- 1.2%, +9.0 +/- 1.0%). After peripheral chemodenervation KCN injection slightly increased PL (+2.0 +/- 0.9%). The response of RLv was almost abolished. In conclusion, laryngeal vasoconstriction in response to systemic hypoxia after chemodenervation is probably mediated by increased sympathetic discharge to the larynx due to hypoxia of the CNS. Laryngeal responses to hypercapnia may be due to the action of central chemoreceptors.

The effect of central and peripheral administration of acetylcholine and epinephrine on respiration.

The experiments were conducted in dogs anesthetized with Na-pentobarbital i.v. tidal volume (VT) and respiratory frequency (f min-1) were recorded. The central effects of acetylcholine (Ach) and epinephrine on respiration were investigated after injections of these substances directly into the cerebrospinal fluid by atlanto-occipital punction. The peripheral effects of Ach and epinephrine on respiration were studied after i.v. injections. Both central and peripheral administration of epinephrine caused significant increase in f min-1 and VT. After vagotomy the effects of centrally and peripherally administered epinephrine on f min-1 were abolished. The effect of central injection of epinephrine on VT persisted after vagotomy. The increase in VT in response to peripheral epinephrine administration was abolished by vagotomy. Both central and peripheral injection of Ach increased f min-1. In VT an initial decrease was followed by an increase. The initial decrease in VT was abolished by atropine. After vagotomy the effects of central and peripheral administration of Ach on f min-1 were abolished. The effects of central injection of Ach on VT persisted after vagotomy. Vagotomy abolished the effects of peripheral administration of Ach on VT.

Central and peripheral effects of the non-neural substances on respiration before and after vagotomy.

The central effects of capsaicin, veratrine, histamine and bradykinin were studied by injecting them directly into the oerebrospinal fluid and their peripheral effects were examined by injecting into femoral vein. Our experiments were performed in Na-pentobarbital-anaesthetized dogs. Tidal volume (VT), respiratory frequency (f/min), systemic arterial pressure (BP) were recorded. A significant increase in f, and an initial apnea or hypoventilation followed by a significant increase in VT were observed with central and peripheral capsaicin. Vagotomy removed the peripheral VT response, but not the central one. While central capsaicin administration increased BP, peripheral administration decreased. After vagotomy, a significant increase was observed in BP for both administrations. Respiratory responses to central and peripheral administrations of veratrine were similar to those of capsaicin. Significant increases were observed in f and VT of the intact group in response to central and peripheral administration of histamine. Response to peripheral administration disappeared after vagotomy. While central and peripheral bradykinin increased VT significantly, there was no significant change in f. Vagotomy only removed the increase in VT in response to peripheral administration. In conclusion, respiratory responses to central administration of capsaicin and veratrine are due to direct effects of these substances on respiratory neurons. In peripheral administration, disappearance of the responses after vagotomy indicate that the responses are brought about by stimulation of the lung receptors.