To explain several fortuitous observations, we hypothesized that there
is a naturally occurring lipid 'barrier' to HF injury in guinea-pig s
kin and sought to characterize both the barrier and its role in the na
tural history of such injuries. Under anaesthesia, the dorsal trunk sk
in of groups of guinea-pigs was gently clipped of hair, washed with ch
loroform, soap and water, acetone or nothing (controls), and examined
histologically for the presence of neutral lipid. Thereafter, in anima
l groups similarly washed, 1.5 in x 1.5 in (38 mm x 38 mm)areas were e
xposed to 40 percent HF for up to 50 min and. (a) mean percentages of
exposed areas with gross necrosis 5 days postinjury plotted on dose-re
sponse curves; or (b) more than 4 h after exposure to HF, intra-aortic
India ink was injected and skin specimens examined to discern depth o
f ischaemia and necrosis. In contrast to controls, washing reduced neu
tral lipid in epidermis and significantly (at P < 0.001) increased sus
ceptibility to injury by HF. With very rare (but interesting) exceptio
ns, HF injury was found to be full thickness in depth with ischaemia a
nd coagulative necrosis. In this study, development of guinea-pig skin
necrosis due to HF was typically an 'all-or-nothing' 'barrier-penetra
tion' phenomenon relating as much to the integrity of an epidermal lip
id barrier as to the duration and intensity of noxious exposure.