The effect of whole gut irrigation on contractile responses of guinea pig gallbladder, ileum, and tissue cholecystokinin levels.

AIM: An experimental study was performed to evaluate the effect of whole gut irrigation (WGI) solutions on contractile responses of the gallbladder and ileum and also on tissue cholecystokinin (CCK) levels. MATERIALS AND METHODS: Thirty guinea pigs were enrolled into five groups including control group (CG) and WGI group (saline physiologic [SP], Ringer lactated [RL], polyethylene glycol [PEG], and dibasic sodium phosphate [DNP]). After median laparotomy, the distal esophagus was ligated and SP, PEG, RL, and DNP infusions (2 mL/kg/min) were performed via gastric catheter until rectal discharge became clear in WGI groups. Ileum and gallbladder samples were obtained for in vitro and biochemical studies without irrigation in CG and after irrigation with different WGI solutions. Isolated ileum and gallbladder preparations were suspended in organ baths for contractile responses of carbachol and CCK. Also, biochemical analysis of tissue CCK levels was performed in ileum and gallbladder samples. RESULTS: In PEG group, gallbladder and ileum CCK levels were significantly higher than CG (p < 0.05). Also, DNP irrigation caused increased CCK levels in gallbladder samples (p < 0.05). In lower carbachol concentrations, PEG group showed increased contraction responses in gallbladder samples when compared with controls (p < 0.05). However, ileal responses to carbachol did not show any significant difference between groups, contraction responses to CCK was decreased in PEG group when compared with CG (p < 0.05). CONCLUSION: Among WGI solutions, PEG caused the highest CCK levels in gallbladder and ileum samples. Different WGI solutions affected the contractile responses of gallbladder and ileum smooth muscles divergently. Increased levels of CCK in PEG group support the decreased contractile responses in ileum. Therefore, our results confirm that the effect of WGI on gallbladder and ileum contractility may be CCK related.

Effect of SWL on renal hemodynamics: could a change in renal artery contraction-relaxation responses be the cause?

The aim of this study was to reveal the effect of shock wave lithotripsy (SWL) on renal artery contraction-relaxation responses and the relation of this effect with renal hemodynamics. Twenty-four rabbits are divided into six different groups. The first two groups evaluated as the control groups. After isolating the kidneys, we applied phenylephrine (Ph) and acetylcholine (Ach) in the first group and sodium nitroprusside (SNP) and histamine (H) in the second group. In the third, fourth, fifth and sixth groups, 14.5 kV shock wave (SW) was focused on the left kidneys. We adjusted the number of shocks to a total of 500, 1,500, and 3,000 SW, in the third, fourth and fifth groups, respectively. After isolating the kidneys, Ph, Ach was given in groups 3, 4 and 5. In the sixth group, to get the SNP and the H responses, 3,000 shocks modality was utilized. Marked contractile responses were obtained by phenylephrine in the control group. In kidneys that were exposed to 500 shocks SWL procedures, a decrease in contractile responses and hence, in perfusion pressures in different concentrations of phenylephrine was noted. However, a notable change in relaxation responses occurred after 3,000-shock applications. No difference in relaxation responses to nitroprusside, a direct vasodilating agent, was observed in any group, compared to the control group. Another cause of deterioration of renal hemodynamics after SWL can be attributed to the reduction in renal artery contraction-relaxation responses that result in the vascular smooth muscle and endothelial damage.

In vitro sensitivity of mouse esophagus to agonists in different pH medium values.

AIM: The aim of this study is to determine the in vitro sensitivity of mouse esophagus to contracting and relaxing agonists in different pH medium values. MATERIALS AND METHODS: Forty-eight Swiss albino mice (30-40 g) of both sexes were anesthetized with tiopental sodium (30 mg/kg). After exsanguinations from abdominal artery, esophagi were removed and suspended under 0.6 g of resting tension in a tissue bath containing 10 mL of Krebs solution at 37 degrees C. The experiments were performed in different pH mediums 7.4, 6.4, 4, and 2. Carbachol and acetylcholine were used as contractile agonists, and noradrenalin and isoproterenol to evaluate relaxation responses. Data concerning similar concentrations of contractile agonists obtained from different pH mediums were analyzed using Kruskal-Wallis nonparametric analysis of variance and post hoc Dunn test. Relaxation responses were compared with Student t test. A P value less than .05 was considered significant. The study was approved by Local Ethical Committee of Kirikkale University. RESULTS: Carbachol and acetylcholine caused concentration-dependent contractility in pH 7.4, 6.4, and 4, but contractile responses were inhibited in pH 2. In carbachol and acetylcholine experiments, there was a significant decrease in contractile responses to all concentrations in conjunction with a decreased in pH value. Relaxation responses in pH 2 and 4 could not be obtained because precontraction of tissues was not possible. Noradrenalin and isoproterenol produced concentration-dependent relaxations in pH 7.4 and 6.4. Although noradrenalin responses showed no significant difference according to pH, isoproterenol caused better relaxations in pH 6.4 (between 10(-8) and 10(-6) mol/L) when compared to pH 7.4 studies. CONCLUSION: The mouse esophagus has impaired contractile responses to carbachol and acetylcholine in decreased pH values. Contraction responses did not occur in pH medium of 2. In contrast, esophagus segments showed better relaxations in lower pH values with isoproterenol.

Pentylenetetrazol-induced seizures are not altered by pre- or post-drug exposure to a 50 Hz magnetic field.

PURPOSE: To investigate whether pre- and post-drug magnetic field (MF) exposure of 50 Hz, 0.2 mT has any significant effect on pentylenetetrazol (PTZ)-induced seizures in mice. MATERIAL AND METHODS: MF was generated by a pair of Helmholtz coils. Seizures were induced by PTZ injection intraperitoneally (i.p.) at a dose of 60 mg/kg. A total of 48 locally bred adult female mice 25-35 g in weight were used. Latency to seizure, total seizure duration, and mortality were recorded for each mouse. RESULTS: Neither pre- nor post-drug exposure to a 50 Hz, 0.2 mT MF was found to have any effect on PTZ-induced epileptic seizures or mortality rates in mice. CONCLUSION: The present study failed to provide any support for a therapeutic potential of a 50 Hz, 0.2 mT MF for epilepsy.

Ultrastructural damage in vascular endothelium in rats treated with paclitaxel and doxorubicin.

Endothelium is the first physiological barrier between blood and tissues and can be injured by physical or chemical stress, particularly by the drugs used in the cancer therapy. Paclitaxel and doxorubicin are frequently used anticancer drugs and their cardiac side effects are well observed in clinical setting. Their side effects on the endothelium are still not clear enough. There are few investigations assessing the damages elicited by the combination use of chemotherapy agents in animal experimental models. The purpose of this study was to examine and compare the side effects of doxorubicin and paclitaxel on endothelium in vivo. The drugs were administered weekly to rats via intraperitoneal injections singly or in combinations. Lastly, aorta endothelium was examined. The most familiar parts of the aorta endothelium are the nucleus, free ribosomes, Weibel-Palada granules, plasmalemmal vesicles, and clear basement membrane. Examination of the endothelium and the related structures revealed some clear degenerative findings. Notably, administration of a paclitaxel and doxorubicin combinations caused the most dramatic change in ultrastructure, which may disrupt many functions of the endothelium.

Effects of probucol in hyperlipidemic rabbit liver: a preliminary ultrastructural study.

Probucol is a lipid-lowering agent with an antioxidant effect; however, its influence on the liver remains unclear. The effects of probucol on hyperlipidemic rabbit liver are investigated to add a structural data on its therapeutical profile. Local albino rabbits were divided into three groups. 1) Hyperlipidemic group: fed with 1% cholesterol (150 g/kg/day) enriched chow for 2 months. 2) Probucol treated group: group 1 + intraperitoneal probucol (10 mg/kg/day) administration for 15 days. 3) Control group fed with normal chow. The blood lipid profile was investigated biochemically. Liver samples were examined electronmicroscopically. Within the parenchymal cells of group 1, the amount of rough surfaced endoplasmic reticulum was increased, its cisterna was dilated displaying a moderately electron dense substance in it and showed close apposition with the condensed mitochondria. In group 2, smooth surfaced endoplasmic reticulum was in extensive amounts filling almost all of the cytoplasm, displayed a reticular, degenerated appearance and was in close relation with the condensed, degenerated mitochondria. Probucol may cause degenerative changes on the liver parenchyme at the subcellular level. It alters the structure of these cells mainly acting on the smooth surfaced endoplasmic reticulum and the mitochondria that are known to be involved in cellular detoxification.

Effects of vasoconstriction on the acute anterior pituitary hormonal response to head injury.

Since cerebral vasoconstriction alone may impair the hypothalamic and pituitary circulation, we planned to investigate whether the hormonal response to the vasoconstriction that may be induced by the head injury is a significant component of the general acute hormonal response to head injury. Although diffuse adrenocorticotropic hormone immunohistochemical staining of the adenohypophysis of rabbits was observed in the head trauma administered group, only mild positive staining was present in the Endothelin-1 administered group. However, decreased prolactin staining was found in both of the groups. It is postulated that trauma induced vasoconstriction may not be an important manipulating factor in the corticotrophic hormone response to injury, while it may be responsible for the decreased prolactin response.

Effect of glycerol on endothelium-derived factors in the vasculature of the rabbit kidney.

1. In the present study, endothelium-derived relaxing factor (EDRF/nitric oxide (NO)), conversion of big endothelin (ET)-1 to endothelin-1 (ET-1) and the role of reactive oxygen species were investigated in kidneys isolated from glycerol (GLY)-pretreated rabbits. 2. Acetylcholine (ACh)-induced vasodilation that is due to the release of EDRF/NO is significantly decreased, whereas big ET-1-induced vasoconstriction was increased in kidneys isolated from GLY-pretreated rabbits. 3. Pretreatment of rabbits with the xanthine oxidase inhibitor allopurinol and the NO precursor L-arginine reversed the inhibition of ACh-induced vasodilation due to GLY and protects the kidney vasculature. 4. Big ET-1, but not ET-1, responses were found to be significantly increased in kidneys isolated from GLY-pretreated rabbits. This increase is attributed to the higher conversion rate of big ET-1 to ET-1 because the ET-converting enzyme (ECE) inhibitor phosphoramidon, at a concentration of 10(-6) mol/L, causes an inhibition in the response to big ET-1 by 52.6% in normal kidneys, whereas this inhibition with the same concentration of phosphoramidon was found to be significantly decreased in kidneys isolated from GLY-pretreated rabbits. 5. The non-selective NO synthase inhibitor N(G)-nitro-L- arginine methyl ester (L-NAME) caused a significant potentiation in the vasoconstrictor response to ET-1 in normal isolated perfused rabbit kidneys. However, L-NAME did not alter the responses to ET-1 in GLY-pretreated kidneys. 6. These results indicate that accumulation of reactive oxygen species causes an inhibition in NO bioavailability. Increased conversion of big ET-1 to ET-1 may also contribute to the mechanism of vascular damage due to GLY.