Prompt Myocardial Damage Contributes to Hepatic, Renal, and Intestinal Injuries Soon After a Severe Burn in Rats

Abstract

The prompt cardiac dysfunction has some initiating effects on ischemic/hypoxic injury to organs such as the liver, kidneys, and intestines soon after a severe burn.

Captopril protects against burn-induced cardiopulmonary injury in rats

“…Numerous experimental studies have been performed to identify the molecular mechanisms involved in burn-related cardiac dysfunction with the end goal of creating novel therapeutic interventions and agents to reduce the incidence of life-threatening complications. [37,38] In our study, by improving cardiac function, captopril protected cardiac and lung tissues since oxidative injury observed through MDA and GSH levels and MPO, Na + , K + -ATPase and caspase activities were reversed in both tissues. One of the causative agents accountable for the development of burn shock and distant organ damage in animal models of burn injury are oxygen radicals.…”

Electroacupuncturing At Zusanli Point (St36) Attenuates Pro-Inflammatory Cytokine Release And Organ Dysfunction By Activating Cholinergic Anti-Inflammatory Pathway In Rat With Endotoxin Challenge

“…ALT, and CK-MB were determined with automatic biochemical analyzer (HITACHI 7170, Japan). Serum diamine oxidase (DAO), activity was determined according to the method described by Xiao R，et al (Xiao et al, 2011). All reagents were purchased from Sigma (Aldrich, St. Louis, MO, USA).…”

Alcohol Modulation of the Postburn Hepatic Response

“…Decreased cardiac output in the early phases post burn [39] worsens circulating blood flow, leading to intestinal damage and a loss of barrier function [40,41] in rodents. A single intoxication event with alcohol prior to a burn injury in mice enhances intestinal damage leading to greater dissociation of tight junction complexes in the intestinal epithelium [42,43,44] and resultant permeability [45,46] compared to either insult alone.…”

“…Recent evidence revealed that alcohol given as a single oral gavage (1.1 g/kg) potentiates post burn bradykinin signaling in mice, leading to greater extravasation of fluid from the vascular compartment [47]. This adds a degree of hypovolemia into a scenario in which organs supplied by the splanchnic vasculature are already at risk for ischemic injury [41]. Likewise, clinical data demonstrate intoxicated burn patients require more aggressive fluid resuscitation than do their non-intoxicated counterparts [6], also indicating a shift in fluid compartments.…”