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The experimental model of acute gastritis such as water immersion restraint (WRS) stress-induced gastric injury is useful tool in examination of pathomechanism of acute gastritis. Nitric oxide (NO) plays an important role in the maintenance of gastric barrier, however, the interaction between reactive oxygen species (ROS) and NO on gastric mucosal integrity has been little studied. The purpose of our present study was to explain the participation of ROS in healing of WRS-induced gastric lesions accelerated by NO. Experiments were carrying out on 120 male Wistar rats. To assess gastric blood flow (GBF) laser Doppler flowmeter was used and the number of gastric lesions was counted in each stomach. The colorimetric assays were used to determine gastric tissue level of malondialdehyde (MDA) and 4- hydroxynonenal (4-HNE), the products of lipid peroxidation by ROS, as well as superoxide dismutase (SOD) activity, the enzyme scavanger of ROS. We demonstrated that 3.5 h of WRS resulted in appearance of acute gastric lesions accompanied by a significant decrease of GBF. Biological effects of ROS were estimated by measuring tissue levels of MDA and 4-HNE, as well as the SOD activity. It was demonstrated that 3.5 h of WRS led to significant increase of mucosal levels of MDA and 4-HNE, and it was accompanied by a decrease of SOD activity. Pretreatment with NO-donors (SIN-1, SNAP, nitroglycerin, NO-ASA) resulted in reduction in gastric lesion number, increment of GBF, decrease of MDA and 4-HNE tissue level and increase of SOD activity. Suppression of ROS plays an important role in the action of NO-donors on healing of acute gastric lesions induced by 3.5 h of WRS. NO-donors caused an attenuation of lipid peroxidation as documented by a decrease of MDA and 4-HNE levels and enhancement of antioxidative properties as evidenced by an increase of SOD activity.
Acute gastric mucosal lesions represent an important clinical problem. The experimental model of acute gastritis such as water immersion restraint (WRS) stress is useful tool in examination of pathomechanism of acute gastric damage. Nitric oxide (NO) plays an important role in the maintenance of gastric barrier, however the role of reactive oxygen species (ROS) in the interaction between NO and gastric mucosa integrity has been little studied. The purpose of our present study was to explain the participation of ROS in healing of WRS-induced gastric lesions accelerated by NO. Experiments were carrying out on 120 male Wistar rats. To assess gastric blood flow (GBF) laser Doppler flowmeter was used. The number of gastric lesions was established by planimetry. The colorimetric assays were used to determine gastric tissue level of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), the products of lipid peroxidation by ROS, as well as superoxide dismutase (SOD) activity, the enzyme scavanger of ROS. We demonstrated that 3.5 h of WRS resulted in appearance of acute gastric mucosal lesions accompanied by a significant decrease of GBF. Biological effects of ROS were estimated by measuring tissue level of MDA and 4-HNE, as well as the SOD activity. It was demonstrated that 3.5 h of WRS led to significant increase of MDA and 4-HNE mucosal level, that was accompanied by a decrease of SOD activity. Pretreatment with NO-donors (SIN-1, SNAP, nitroglycerin, NO-ASA) resulted in reduction of gastric lesions number, increment of GBF, decrease of MDA and 4-HNE tissue level and increase of SOD activity. Suppression of ROS play an important role in NO-donors action in gastroprotection against gastric acute lesions induced by 3.5 h of WRS. NO-donors cause an attenuation of lipid peroxidation as documented by a decrease of MDA and 4-HNE levels and enhancement of antioxidative properties as evidenced by increase of SOD activity.
The relationship between gastrin levels and presence of Helicobacter-like organisms (HLO) in dogs with acute or chronic gastritis was investigated. For this purpose, a total of 52 crossbred Kangal Dogs aging 2-5 years were used; including 12 dogs with acute gastritis, 25 dogs with chronic gastritis, and 15 healthy dogs. Blood samples were collected from the vena cephalica. Serum gastrin levels were measured using commercial competitive binding radioimmunoassay. HLO were found in 64%, 58.3%, and 60% of animals with chronic gastritis or acute gastritis, and controls, respectively. The gastrin levels in dogs with chronic gastritis were higher than in those with acute gastritis and controls. There were no significant differences between the gastrin levels in all groups, with regard to HLO positive versus HLO negative dogs. In conclusion, HLO incidence was generally found in high levels in all the dogs. However, HLO did not primarily affect the stomach mucosal damage. In the mean time, there was no relation between the levels of serum gastrin in dogs with gastritis, either being HLO positive or negative. The results of the study showed that higher gastrin levels in dogs with gastritis were related to severe gastric lesions and mucosal damage.
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