Abstract
BackgroundIntestinal ischemia-reperfusion (IR) is an important clinical occurrence seen in common diseases, such as gastric dilatation-volvulus in dogs or colic in horses. Limited data is available on the use of methylene blue in veterinary medicine for intestinal ischemia-reperfusion. The present study aimed to compare the hemodynamic, histopathological, and immunohistochemical effects of two doses of methylene blue in two rabbit model groups In one group, 5 mg/kg IV was administered, and in another, 20 mg/kg IV was administered following a constant rate infusion (CRI) of 2 mg/kg/h that lasted 6 h. All the groups, including a control group had intestinal ischemia-reperfusion. Immunohistochemical analysis was performed using caspase-3.ResultsDuring ischemia, hemodynamic depression with reduced perfusion and elevated lactate were observed. During reperfusion, methylene blue (MB) infusion generated an increase in cardiac output due to a positive chronotropic effect, an elevation of preload, and an intense positive inotropic effect. The changes in heart rate and blood pressure were significantly greater in the group in which methylene blue 5 mg/kg IV was administered (MB5) than in the group in which methylene blue 20 mg/kg IV dose was administered (MB20). In addition, lactate and stroke volume variations were significantly reduced, and vascular resistance was significantly elevated in the MB5 group compared with the control group and MB20 group. The MB5 group showed a significant decrease in the intensity of histopathological lesion scores in the intestines and a decrease in caspase-3 areas, in comparison with other groups.ConclusionsMB infusion produced improvements in hemodynamic parameters in rabbits subjected to intestinal IR, with increased cardiac output and blood pressure. An MB dosage of 5 mg/kg IV administered at a CRI of 2 mg/kg/h exhibited the most protective effect against histopathological damage caused by intestinal ischemia-reperfusion. Further studies with MB in clinical veterinary pathologies are recommended to fully evaluate these findings.
Highlights
Intestinal ischemia-reperfusion (IR) is an important clinical occurrence seen in common diseases, such as gastric dilatation-volvulus in dogs or colic in horses
A significant hemodynamic depression with a drop in cardic index (CI) (− 86 mL/min/ kg: CI 95% -105/− 67 mL/min/kg; p = 0.001) was observed due to a reduction of preload (stroke volume index (SVI): − 0.35 mL/beat/kg: CI 95% -0.37/− 0.24 mL/beat/kg; p = 0.001), contractility, and elevation of afterload (systemic vascular resistance index (SVRI): 0.09 mmHg/mL/ min/kg: CI 95% 0.02/0.15 mmHg/mL/min/kg; p = 0.005)
During the reperfusion period in the control group, no significant changes were detected in hemodynamic parameters such as heart rate (HR) (p = 0.999), mean arterial pressure (MAP) (p = 0.998), cardiac index (CI) (p = 0.999), dPmx (p = 0.372), Stroke volume index (SVI) (p = 0.998) or Delivery of oxygen (DO2) (p = 0.999)
Summary
Intestinal ischemia-reperfusion (IR) is an important clinical occurrence seen in common diseases, such as gastric dilatation-volvulus in dogs or colic in horses. Limited data is available on the use of methylene blue in veterinary medicine for intestinal ischemia-reperfusion. The present study aimed to compare the hemodynamic, histopathological, and immunohistochemical effects of two doses of methylene blue in two rabbit model groups In one group, 5 mg/kg IV was administered, and in another, 20 mg/kg IV was administered following a constant rate infusion (CRI) of 2 mg/kg/h that lasted 6 h. Ischemia can lead to intestinal lesions such as edema, hemorrhages, or mucosal damage. Delivery of oxygen is reduced in the splanchnic compartment and results in depleted adenosine triphosphate levels. This leads to an increase in intracellular calcium levels, initiates anaerobic glycolysis, and activates xanthine oxidase and cell death [1]. Depending on the duration of the ischemic period, reperfusion may result in delivery of toxic oxygen metabolites and free radicals created from hypoxanthine and ß-actin, which may be more severe than those during the ischemic period [1, 3, 4]
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