The objective of the present study was to develop an experimental model suitable for studying the effects of a nonhemorrhagic soft tissue
trauma on plasma volume (PV) and microvascular permeability. Anesthetized Sprague-Dawley rats were exposed to a
sham procedure or a
laparotomy followed by a standardized
trauma to the abdominal rectus muscle. We evaluated the effects of
trauma on transcapillary escape rate and on PV (3 h after
trauma) using 125I-albumin as tracer and on
edema formation in the traumatized muscle with a wet- versus dry-weight method. The effects of the
trauma on the
cytokines IFN-gamma,
IL-4,
IL-6,
IL-10, and
TNF-alpha were investigated 1 and 3 h after
trauma in a separate group. Transcapillary escape rate was 13.9% per hour in the
sham animals compared with 18.5% per hour in the traumatized animals (P < 0.05). Because arterial and venous blood pressures were not altered by the
trauma, the change in transcapillary escape rate most likely reflects a change in microvascular permeability. Plasma volume decreased from 42 mL/kg at baseline to 31 mL/kg at the end of the experiments (P < 0.05) in the
trauma group, whereas PV remained unchanged in the
sham group. Only 15% of the PV loss could be referred to
edema in the traumatized muscle.
Trauma induced a significant increase in
IL-6 and
IL-10 after 1 h. We conclude that the present nonhemorrhagic
trauma induces an increase in microvascular permeability in the traumatized tissue and in other parts of the body, resulting in
hypovolemia. The model may be used for the evaluation of different therapeutic interventions aimed at the correction of
hypovolemia.