Title: INJURY OF HEAT-STRESS TO RAT CARDIOMYOCYTES
Abstract: Aim:To observe the injury and its mechanism of heat-stress to rat cardiomyocytes. Methods:Rat cardiomyocytes were cultured with Typsin digestion method and stressed in water at 39℃、41℃and 43℃ repectively. The variation of lactate dehydrogenase (LDH) in medium was biochemistry method, the apoptosis rate of cardiomyocytes with Flow Cytometry (FCM) mthod,the necrosis rate of cardiomyocytes with trypan blue dying method and the intensity of reactive oxygene species(ROS) in cardiomyocytes and medium with fluorescence spectrophotometer method. Results:After heat stress at 39℃、41℃ and 43℃, the activation of LDH in medium increasd significantly , and the apoptosis rate (%) of cardiomyocytes increased from 4.74(37℃) to 5.12、16.31 and 28.97 respectively. The necrosis rate(%) of cardiomyocytes increased from 3.52 to 3.61 after heat stress at 39℃,from 3.55 to 5.81 at 41℃,from 3.53 to 10.80 at 43℃.The apoptosis rate of cardiomyocytes changed with cultured time after stress and it was highest at the sixth hour after stress.The necrosis rate of cardiomyocytes after heat stress decreased with time. The intensity of ROS in heat stressed cardiomyocytes and medium increased significantly than that in normal cardiomyocytes and medium. Conclution: Cardiomyocytes can be injured by heat stress and apoptosis is the main way of the death of cardiomyocytes caused by heat stress. Increased ROS in cardiomyocytes is one of important mechanisms leading to injury of cardiomyocytes caused by heat-stress.
Publication Year: 2000
Publication Date: 2000-01-01
Language: en
Type: article
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Cited By Count: 12
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