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Local cooling restores microcirculatory hemodynamics after closed soft-tissue trauma in rats


Schaser, K D; Stover, J F; Melcher, I; Lauffer, A; Haas, N P; Bail, H J; Stöckle, U; Puhl, G; Mittlmeier, T W (2006). Local cooling restores microcirculatory hemodynamics after closed soft-tissue trauma in rats. Journal of Trauma - Injury Infection & Critical Care, 61(3):642-649.

Abstract

BACKGROUND: Severe closed soft-tissue injury (CSTI) results in progressively developing microvascular dysfunction and local inflammation. Cooling reduces swelling, pain, cellular oxygen demand, and metabolic activity. However, effects of cooling on posttraumatic microcirculation are not yet fully understood. Thus, we assessed effects of local cooling on microcirculation, regional inflammatory response including leukocyte-endothelial cell interaction, and edema formation after CSTI. METHODS: Standardized CSTI was induced by means of controlled impact injury in the left tibial compartment of 14 male Sprague-Dawley rats. Rats were assigned to four groups (n = 7 per group) as follows: group I, no trauma/no cooling; group II, no trauma/20 minutes of cooling; group III, 1.5 hours posttrauma/no cooling; and group IV, 1.5 hours posttrauma/20 minutes of cooling. RESULTS: CSTI resulted in a significant decrease in functional capillary density, a marked increase in microvascular permeability, and granulocyte infiltration (HIS48) as revealed by intravital microscopy and immunohistochemistry of the left extensor digitorum longus muscle. After 20 minutes of local cooling, these microvascular derangements were restored to the level of controls (group I). Edema (extensor digitorum longus muscle wet-to-dry weight ratio) was less pronounced compared with noncooling conditions (group III). Immunoreactivity for HIS48 (neutrophilic granulocytes) in injured rats subjected to local cooling (group IV) was markedly decreased compared with noncooling conditions (group III). CONCLUSION: These results provide in vivo evidence that cooling affords protection of posttraumatic microcirculation through sustained inhibition of microvascular and endothelial dysfunction leading to less granulocyte-dependent inflammation and skeletal muscle edema. Local cooling appears to reduce propagation of acute microvascular injury, preventing leukocyte-dependent tissue destruction and escalation of secondary tissue damage after musculoskeletal soft-tissue trauma.

Abstract

BACKGROUND: Severe closed soft-tissue injury (CSTI) results in progressively developing microvascular dysfunction and local inflammation. Cooling reduces swelling, pain, cellular oxygen demand, and metabolic activity. However, effects of cooling on posttraumatic microcirculation are not yet fully understood. Thus, we assessed effects of local cooling on microcirculation, regional inflammatory response including leukocyte-endothelial cell interaction, and edema formation after CSTI. METHODS: Standardized CSTI was induced by means of controlled impact injury in the left tibial compartment of 14 male Sprague-Dawley rats. Rats were assigned to four groups (n = 7 per group) as follows: group I, no trauma/no cooling; group II, no trauma/20 minutes of cooling; group III, 1.5 hours posttrauma/no cooling; and group IV, 1.5 hours posttrauma/20 minutes of cooling. RESULTS: CSTI resulted in a significant decrease in functional capillary density, a marked increase in microvascular permeability, and granulocyte infiltration (HIS48) as revealed by intravital microscopy and immunohistochemistry of the left extensor digitorum longus muscle. After 20 minutes of local cooling, these microvascular derangements were restored to the level of controls (group I). Edema (extensor digitorum longus muscle wet-to-dry weight ratio) was less pronounced compared with noncooling conditions (group III). Immunoreactivity for HIS48 (neutrophilic granulocytes) in injured rats subjected to local cooling (group IV) was markedly decreased compared with noncooling conditions (group III). CONCLUSION: These results provide in vivo evidence that cooling affords protection of posttraumatic microcirculation through sustained inhibition of microvascular and endothelial dysfunction leading to less granulocyte-dependent inflammation and skeletal muscle edema. Local cooling appears to reduce propagation of acute microvascular injury, preventing leukocyte-dependent tissue destruction and escalation of secondary tissue damage after musculoskeletal soft-tissue trauma.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Division of Surgical Intensive Care Medicine
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2006
Deposited On:19 Mar 2009 08:41
Last Modified:05 Apr 2016 12:50
Publisher:Lippincott Wiliams & Wilkins
ISSN:0022-5282
Publisher DOI:https://doi.org/10.1097/01.ta.0000174922.08781.2f
PubMed ID:16967001

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