Intravital pathophysiological comparison of acid- and alkali-burn injuries in a murine model

The breakdown of skin microcirculation plays a key role in the pathophysiology of chemical burns. Available data for alkali and acid injuries are rare. To determine the pathophysiological similarities and differences, two comparable in vivo acid and alkali burn models were developed.

Deep partial-thickness acid burns (32% hydrochloric acid) or alkali burns (11% sodium hydroxide solution) were inflicted to the ears of hairless mice (n = 17). Intravital fluorescent microscopy was used to assess microcirculation, angiogenesis, and leukocyte-endothelium interaction over a 21-d period.

The angiogenesis occurred significantly faster after acid burns than after alkali burns in the first 3 days (nonperfused area day 3, 80% ± 9% [acid] versus 94% ± 17% [alkali]; P = 0.045) and then a significant acceleration occurs in the alkali group: nonperfused area day 14, 27% (alkali) versus 57% (acid), P = 0.004. The loss of functional vessel density was more pronounced after acid burns (directly after trauma, 87% [alkali] versus 79% [acid], P = 0.049). The other parameters such as rolling and sticking leukocytes, edema formation, and arteriolar and venular red blood cell velocities and diameters showed similar results.

The comparison of analogous intravital acid and alkali burns shows that despite many similarities in the microcirculatory parameters, there was a marked difference particularly in the course of the tissue regeneration by angiogenesis. The longer lasting destruction by alkali burns stands in contrast to the later onset but faster regeneration by angiogenesis compared with that by acid burns.