The effect of nicardipine on the zone of stasis in burns: An experimental rat model.

Ramazan Deniz, Murat İğde, Nesrin Tan Başer, Numan Atılgan, Nihat Yumuşak, Nihat Birtane, Ufuk Zan
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Abstract

Background: The zone of stasis in burns is particularly vulnerable to progressive ischemia, making it a critical target for therapeutic interventions. Preventing damage in this zone is essential, as its viability can be preserved with adequate perfusion. Recognizing this, we aimed to investigate the systemic effects of nicardipine, a calcium channel blocker with vasodilatory properties, on the stasis zone in an experimentally induced burn model in rats. We hypothesized that nicardipine could mitigate ischemic progression in the stasis zone and thereby preserve tissue viability.

Methods: A total of 20 Wistar-Albino rats were included in this study and divided into two groups: a control group (n=10) and a treatment group (n=10). The experimental burn model described by Regas and Ehrlich was employed. Under anesthesia, a 1 x 2 cm metal comb, preheated in boiling water, was applied to the dorsal skin of the rats for 30 seconds to create burn wounds. No treatment was administered to the control group. The treatment group, however, received a daily systemic dose of nicardipine (5 mg/kg) via gastric lavage for three days. Wound healing was monitored daily using a digital camera for three consecutive days. One rat in the treatment group was excluded due to mortality. After three days, the burned areas were excised from the dorsal skin of all rats and subjected to histopathological examination. Additionally, photo analysis of the burn areas was conducted using data obtained from the digital images.

Results: Nicardipine treatment significantly improved burn healing parameters in the stasis zone. Compared to the control group, the treatment group demonstrated lower scores for edema (0.78 vs. 2.80, p<0.05), congestion (0.22 vs. 2.80, p<0.05), inflammation (0.67 vs. 2.90, p<0.05), vascularization (0.11 vs. 2.70, p<0.05), and fibrosis (0.22 vs. 2.90, p<0.05). Quantitative measurements also revealed a significant reduction in necrosis zone thickness (1079.75 µm vs. 2818.82 µm, p<0.05) and necrosis area (249.33 µm² vs. 400.13 µm², p<0.05). These findings indicate that nicardipine effectively mitigates ischemic progression and promotes tissue recovery in burn injuries.

Conclusion: Our experimental study demonstrated that nicardipine has the potential to prevent and treat damage in the burn stasis zone, suggesting its therapeutic role in burn injuries.

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