Abstract
This study aims to examine microcirculation and systemic hemodynamic disturbances in severe heat stroke (HS). A total of 147 rats were divided into HS group (HS), pretreated with superoxide dismutase (SOD+HS) group, and pretreated with normal saline (NS+HS) group. Heat stress was induced by incubating the animals in certain temperatures. Blood flow and vascular reactivity were monitored dynamically with intravital microscopy. Pulmonary permeability was reflected by wet-to-dry weight ratio, the concentration of Evans Blue (EB), and histopathology of lung. The results showed that heat stress could induce blood flow rate reduced, and SOD exhibited better protective role in blood flow rate. The arteriolar reactivity threshold to norepinephrine was markedly reduced at core temperature of 41°C, but no significant decrease occurred in SOD+HS group. Water content and EB concentration in lung tissue in HS group were increased along with temperature rise. SOD treatment could attenuate those changes. The pathological lung injury caused by heat stress was also milder in SOD+HS group than that in other two groups. Mean arterial pressure decreased at early stages of heat stress, but there was no decrease in SOD+HS group. There was a significant body weight loss during heat stress in all groups. Survival time in SOD+HS group was longer than that in other two groups. These results suggest that microcirculation disturbance occurs not only at the early stage but also before systemic hemodynamic disorder, monitoring microcirculation following HS is of prognostic value, and intervention with antioxidative agents may have certain protecting effects in severe HS.
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