Quercetin associated with dimethylsulfoxide has a curative effect on experimental colon anastomosis injury.

Purpose To examine the effects of quercetin on healing of experimental colon anastomosis injury in early and late period. Methods Eighty male Wistar-Albino rats were divided into 8 groups. For all groups, left colons of the rats were resected and for the rest end-to-end anastomosis was performed. Two of the groups for which the experiment protocol was ended on the 3rd and 7th day following the anastomosis were not administered with either quercetin or dimethylsulfoxide DMSO, whereas two other groups were administered with DMSO only, and four other groups were administered with quercetin dissolved in DMSO in doses of 20 and 100 mg/kg during the protocol. At the end of the study, anastomosis line was resected, histopathological evaluation was performed and bursting pressure, malondialdehyde, superoxide dismutase, catalase, and hydroxyproline levels were measured. Results Quercetin significantly increased hydroxyproline, superoxide dismutase, catalase levels, histopathological healing score, bursting pressure values and decreased malondialdehyde level in early period. It also significantly increased superoxide dismutase, catalase, and hydroxyproline levels and decreased malondialdehyde level in late period. Conclusion It was seen that quercetin speeds up the injury healing process and reveals an antioxidant effect, specifically in early period.

Effect of carnitine on cutaneous wound healing in immunosuppressed rats.

BACKGROUND: The wound is ischemic in nature. Chronic steroid administration impairs wound healing by changing enzymes in the glycolytic pathway. Carnitine supplementation may help to restore the energy deficiency caused by chronic steroid administration in the wound. The aim of this study was to evaluate the effect of carnitine on impaired wound healing. METHODS: The study was conducted in three groups. Surgical intervention was a 4 cm long midline skin incision at the back. In Group A, eight rats received methylprednisolone for 7 d prior to surgical intervention, and it was continued until the end of the experiment. In Group B, 12 rats received methylprednisolone for 7 d prior to surgical intervention. After surgery, methylprednisolone injection was continued and carnitine was supplemented until the end of the experiment. In Group C, eight rats received no medication. The wound of half of the animals in each group was harvested on the seventh day after surgical intervention and the remaining on the 14th d. Tensile strength and hydroxyproline content were measured in all groups. RESULTS: There was no significant difference in parameters in any of the groups on day seven. On day 14, all parameters were statistically different between methylprednisolone and control groups (P < 0.05). Values for tensile strength were higher in the methylprednisolone/carnitine group compared with methylprednisolone group (P < 0.05). Carnitine administration had also increased hydroxyproline levels in the methylprednisolone/carnitine group compared with the control group (P < 0.05). CONCLUSIONS: Carnitine is shown to increase tensile strength of the wound when supplemented to immunosuppressed rats in which wound healing is impaired by methylprednisolone.

Mild hypothermia improves survival during hemorrhagic shock without affecting bacterial translocation.

BACKGROUND: Accidental hypothermia in patients with hemorrhagic shock (HS) is associated with increased mortality. However, experimental mild and moderate hypothermia has beneficial effects. The mechanisms for beneficial effects of hypothermia have not been completely understood. Therefore, the aim of this study was to investigate the effect of hypothermia on survival, bacterial translocation (BT), and remote pulmonary injury in a controlled HS model in rats. METHODS: HS was achieved by blood withdrawal through femoral vein. Rats in the normothermia group (group I) were maintained at 37 degrees C. Mild hypothermia group (group II) was observed at 32 degrees C that was spontaneously induced by exposure to ambient temperature. Moderate hypothermia of 28 degrees C was actively induced by external cooling in group III for 90 min. Survival and neurological deficit scores (NDS) were recorded at 24th hr. Mesenteric lymph nodes, liver and spleen samples were collected. Myeloperoxidase (MPO) and malondialdehyde (MDA) levels were measured in lung tissue. RESULTS: Blood pressure significantly increased in hypothermia groups. Mild hypothermia significantly increased survival. No difference was found in BT rates in groups. Hypothermia was found to significantly decrease the NDS points in group III, compared to group I. There was no difference in lung tissue MPO levels among groups. Lung tissue MDA levels increased significantly in groups II and III. CONCLUSIONS: Mild hypothermia improved blood pressure, survival, and neurological outcome with a possible detrimental effect on pulmonary ROS production during HS in rats. These effects of hypothermia are not associated with BT.

The effect of hyperbaric oxygen treatment on the renal functions in septic rats: relation to oxidative damage.

PURPOSE: To investigate the effects of hyperbaric oxygen (HBO) treatment on renal functions and damage in septic rats. METHODS: The animals were divided into four groups, each containing ten animals: control, hyperbaric oxygen, sepsis, and sepsis/hyperbaric oxygen. One milliliter of saline containing live Escherichia coli cells (2.1 x 10(9)) was injected intraperitoneally to induce sepsis. The groups treated with HBO were given five sessions of 2 atmospheres absolute of 100% oxygen at intervals of 6 h. Blood, urine, and tissue samples were then collected, and the functional renal parameters, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) and catalase activities were examined. RESULTS: The reduced glomerular filtration rate and urine flow returned to normal levels after HBO treatment; however, the increase in fractionated sodium excretion continued. The increased MDA levels in the renal cortex and medulla also decreased to the level of the control group. In the sepsis group, both the SOD and catalase activities decreased in the renal cortex, while a reduction was observed only in the catalase activity in the medulla. The reduced enzyme activities significantly increased in the sepsis/hyperbaric oxygen group. CONCLUSION: HBO treatment has a beneficial effect on renal dysfunction in sepsis. The probable reason for this effect is the reduction in oxidative damage because of the increase in antioxidative capacity.

Effects of hyperbaric oxygen treatment on liver functions, oxidative status and histology in septic rats.

OBJECTIVE: The liver is thought to be responsible for multiple organ failure during sepsis. Increase in tissue oxygen consumption is a major component of the septic response. Hyperbaric oxygen (HBO) therapy provides more oxygenation in the whole body. This study examined the effect of HBO alone or in combination with cefepime (CEF) on the liver in septic rats. DESIGN AND INTERVENTIONS: We divided 90 male rats into six groups; control, HBO, sepsis (SEP), SEP+HBO, SEP+CEF, and SEP+CEF+HBO. Sepsis was induced with an intraperitoneal injection of Escherichia coli (2.1 x 10(9) cfu). A total of six HBO sessions were performed at 2 atm absolute for 90 min at 6-h intervals. CEF was administered intraperitoneally at a dose of 50 mg/kg twice daily. Animals were killed 48 h after sepsis induction. Their liver and blood were removed for biochemical and histopathological analysis. MEASUREMENTS AND RESULTS: Liver thiobarbituric acid reactive substances as well as serum alanine transaminase, aspartate transaminase and alkaline phosphatase levels increased while the activity of the antioxidant enzymes superoxide dismutase and catalase decreased significantly in septic rats. These parameters returned to nearly control levels in the SEP+CEF+HBO group. Histological observations supported these findings: Hepatocellular degeneration was observed and intensive polymorphonuclear cell infiltration appeared in all fields of septic animal livers. HBO alone could not sufficiently reverse these histopathological changes, but most liver sections presented normal histology when it was combined with CEF. CONCLUSIONS: HBO may be a useful adjuvant therapy modality to improve the efficacy of sepsis treatment.

Involvement of cholinoceptors in cadmium-induced endothelial dysfunction.

Cadmium (Cd) toxicity was produced in male rats to study the role of cholinoceptors in Cd-induced endothelial dysfunction. The changes in the tension of the aortic rings to constrictor and dilator agonists were compared with those of controls. A Cd-induced significant increase in phenylephrine response was associated with a decrease in basal dilator prostanoid release. In Cd-exposed rings, despite an obvious depression in the acetylcholine (ACh) response, the receptor-independent dilation to the calcium ionophore A23187, which elicits a receptor-independent endothelial relaxation, was slightly elevated (p<0.01), but the smooth muscle cell response to the NO donor, sodium nitroprusside (SNP) remained unaltered. Cadmium decreased both the maximal response to ACh (10(-5) M) and its pirenzepine (Prz) sensitive component. The M1 type cholinoceptor-mediated response to ACh decreased in Cd-exposed rings to 10.30 +/- 5.00% from 38.40 +/- 6.90% (p<0.001). Cadmium also reduced the share of indomethacin 1.64% to 13.92 +/- 2.89% (p<0.01), which correlated well with the changes in the M1-mediated response (r=0.991, p<0.0001). Most of the deleterious effect of Cd appears to be restricted to the M1-dependent ACh response. These findings suggest that Cd produces an endothelial dysfunction by impairing the M1 type cholinoceptor mediated response, which seems to be involved in prostanoid release.

Dietary zinc modifies the characteristics of endothelial dilation in normozincemic rats.

Because zinc attenuates endothelial cell dysfunction that proceeds atherosclerosis, depressed zinc status may be involved in the initiation of endothelial dysfunction. However, before recommending a zinc-enriched diet to reduce the risks for atherosclerosis, the effect of excess zinc on endothelial cell functions in normozincemic status should be known. Therefore, in this study, the effect of dietary zinc on normal endothelial cell functions in animals subjected to a diet containing 334 +/- 58 ppm zinc for 30 d was studied to see whether supplemented zinc has an effect on endothelial cells. Despite a slight increase in blood zinc, unaltered aortic and kidney zinc contents were associated with unchanged blood pressure in rats subjected to a zinc-enriched diet. Increased basal nitric oxide and prostacyclin were accompanied by a normal response to phenylephrine. Dietary zinc influenced neither endothelial-dependent nor endothelial-independent relaxations significantly. However, it elevated the share of M1-type cholinoceptor response as well as dilator prostaglandin release, which seems to be nitric oxide dependent. There was a strong correlation (r=0.826, p<0.05) between M1-type cholinoceptor response and prostacyclin release in zinc-treated rings. These results suggested that zinc ions increases M1-mediated prostacyclin release in normal endothelial cells without altering intracellular pathways.

The role of cholesterol on the pressure sensing ability of kidneys in rats.

We studied the effect of hypercholesterolemia on the pressure-sensing and regulating ability of the kidneys, using an acute hemorrhage model to provide 40% and 60% reduction in the blood pressure of hypercholesterolemic and control rats. The control group (n = 22) was fed a normal rat pellet diet and tap water; the experimental group (n = 22) received a diet containing 2% cholesterol/0.2% thaurocholate. Half the animals were subjected to 6 mL/kg bw and the others to 12 mL/kg bw of bleeding for 1 min. Blood pressure recording and proper samplings were done before bleeding and during the 20 min post-hemorrhagic period for analysis. Despite a finding of hypercholesterolemia in the experimental group, kidney cholesterol content as well as its function remained unchanged. Following an initial 40% decrease in rats bled 6 mL/kg bw, 20 min later the mean blood pressure returned to 90% of its initial value in control rats and to 70% of its basal level in hypercholesterolemic rats. A similar delay in pressure normalization occurred in rats subjected to 12 mL/kg of bleeding. Plasma renin activity remained unaffected. We conclude that dietary hypercholesterolemia delays the normalization of blood pressure after hemorrhage without affecting the sensing ability of kidneys, and that the kidneys are less sensitive than other organs to plasma cholesterol levels.