Microcirculatory disturbance of the gastric wall is a crucial factor in the development of gastric mucosal lesions induced by Helicobacter pylori, anti-inflammatory drugs and stress. Opening of the arteriovenous shunting channel after thermal injury is one of the possible mechanisms to reduce mucosal blood flow. However, no in vivo observation of arteriovenous shunting blood flow in the stomach has been reported. To assess gastric microcirculatory disturbance, especially arteriovenous shunting blood flow after thermal injury by in vivo microsciopy, male Wistar rats were anesthetized and thermal injury was inflicted on the back skin. Gastric microvascular images were observed by in vivo microscopy. Rolling of leukocytes labelled with carboxyfluorescein diacetate, succinimidyl ester were counted and blood flow dynamics were observed by flow of a micro dye, monastral blue B (MBB). The endothelial damage was assessed by deposits of MBB 5 min after the administration. Arteriovenous shunting blood flow is difficult to detect by normal methods, but it could be observed by How of MBB after thermal injury. Statistical analysis showed a significant difference in the ratio of arteriovenous shunting blood flow detection between the control (no injury) (0%; n = 15) and thermal injury (5 hrs after thermal injury) (28.6%; n = 14) groups. In the thermal injury group, the percentage of rolling leukocytes and the area of monastral blue B deposits increased, and the venular walls tended to be irregular. The total length of erosion increased time-dependently after thermal injury, and the length at 5 hrs was approximately 2 times larger than that at 2 hrs. Arteriovenous shunting blood flow is intravitally observed after thermal injury. A-V shunting blood flow can be a cause of mucosal hypoperfusion. It is suggested that the microcirculatory disturbance seen 5 hrs after thermal injury is contributed to the final step of erosion formation.