Sham-burned Rats Research Articles

Relationship between Energetic, Ionic, and Functional Status in the Perfused Rat Heart Following Thermal Injury: A31P and23Na NMR Study

To test the hypothesis that energy deficits and intracellular ion derangements may be the cellular basis for intrinsic myocardial dysfunction in rats after burn trauma, we examined ATP metabolism, intracellular pH, sodium, and mechanical performance simultaneously in perfused beating hearts from sham burn or burned rats (43% TBSA, 3° scald burn, resuscitated for 24 hr with lactated Ringer's solution, Parkland formula). Intracellular calcium was also measured in myocytes harvested from parallel groups of sham burn and burn resuscitated rats. Burn trauma caused a 46% decrease in left ventricular developed pressure, a 69% decrease in +dP/dtmax, and a 72% decrease in −dP/dtmax. Intracellular to external standard sodium ratio increased (+58%) from 0.318 ± 0.027 to 0.500 ± 0.048 (P< 0.05), and intracellular calcium increased (+67%) from 206 ± 13 to 445 ± 37 nM(P< 0.01). Burn hearts exhibited decreased functional response to isoproterenol challenge compared to sham burn controls, but energy metabolism was similar in all hearts, regardless of burn injury. Our data suggest that burn trauma alters intracellular cardiomyocyte calcium and sodium homeostasis, and ionic derangements are not related to either altered intracellular pH or high energy phosphate deficits.

Activity changes of ATP synthase and adenylate kinase in rat-liver mitochondria during the early phase after burn injury

Using succinate as a substrate, the activities of ATP synthase and adenylate kinase in liver mitochondria of male Sprague-Dawley rats 30 min after 20 per cent full skin thickness burns were increased in comparison with the sham burn rats, suggesting that these two enzymes might contribute to the increased rates of ATP formation and oxidative phosphorylation coupling during the early phase after burn injury.

Kinetics of nitrogen oxide production following experimental thermal injury in rats.

Nitric oxide is biosynthesized from the amino acid L-arginine by the enzyme nitric oxide synthase. Nitric oxide is a vasodilator, a neurotransmitter, and may modulate immune function. The experiments presented here were performed to determine whether the synthesis of nitric oxide is increased following experimental burn injury in rats. After a 30% total body surface area burn in 300-g Lewis rats, the urinary output of nitrate, a stable metabolite of nitric oxide, was significantly increased for 8 days postburn compared with that in sham-burned control rats. The origin of the urinary nitrate from L-arginine was demonstrated by administering the stable isotope 15N2-guanido-arginine to burned and sham-burned rats and observing an immediate enrichment of 15N in nitrate. The amount of administered 15N recovered as 15NO3 was < 1% of the administered arginine isotope in both the burned and unburned rats; the recovery of the isotope increased tenfold over baseline recovery in burned rats. The arginine analog N-monomethyl-arginine, an inhibitor of the enzyme nitric oxide synthase, blocked the postburn rise in urinary NO3 output in burned rats, but did not completely inhibit the output of NO3 in burn wound-infected rats. Experimental burn injury in rats results in an increase in L-arginine-dependent nitric oxide production and urinary nitrate output.

Hepatocellular membrane function during chronic burn injury

Hepatocellular membrane dysfunction, as indicated by depolarization of the membrane potential, occurs after acute injury and early bacteremia. To determine whether hepatocellular membrane dysfunction occurs in the setting of ongoing thermal injury and infection, Wistar rats were divided into four groups: (1) sham-burned, freely fed controls (FF); (2) rats sustaining ≈30% total body surface area dorsal full-thickness scald burn (Burn); (3) rats sustaining burns as in group 2 followed by immediate inoculation of 1 × 10 8 CFU Pseudomonas aeruginosa (Burn/Inf); and (4) sham-burned rats pair-fed to the food intake of the Burn/Inf group (PF). On the third and seventh days postburn, body and liver weights were determined. In vivo hepatocellular transmembrane potentials were measured and hepatic ATP, RNA, DNA, and protein contents were assayed. By Day 7, despite greater weight loss in the Burn/Inf group than due to starvation alone ( P < 0.01 Burn/Inf vs FF and PF), hepatic mass was conserved. This was associated with hyperpolarization of the hepatic transmembrane potential (−46.6 ± 1.5 vs −32.1 ± 0.6 mV, Burn/Inf vs FF, P < 0.01) and increases in RNA (141 ± 9 vs 91 ± 4 mg/liver, Burn/Inf vs FF, P < 0.01) and DNA (37 ± 5 vs 22 ± 2 mg/liver, Burn/Inf vs FF, P < 0.05) contents, with no change in ATP or hepatic protein contents. There was a significant hypercorticosteronemia observed in the Burn/Inf group (43 ± 9 vs 2.8 ± 0.7 μg/dl, Burn/Inf vs FF, P < 0.01). This hepatic membrane hyperpolarization and augmented RNA content were not secondary to burn or starvation alone as the response in these groups was significantly less than that of the Burn/Inf group. It is suggested that this hepatic membrane hyperpolarization is one mechanism by which hepatic function is maintained during ongoing burn infection in the rat.