PMID- 10568188
OWN - NLM
STAT- MEDLINE
DCOM- 19991130
LR  - 20171027
IS  - 0039-6060 (Print)
IS  - 0039-6060 (Linking)
VI  - 126
IP  - 5
DP  - 1999 Nov
TI  - Surface cooling inhibits tumor necrosis factor-alpha-induced microvascular 
      perfusion failure, leukocyte adhesion, and apoptosis in the striated muscle.
PG  - 881-9
AB  - BACKGROUND: Surface cooling is frequently used in a number of conditions, 
      especially traumatic, ischemic, burn, and neurologic injury to reduce the tissue 
      damage. However, the protective mechanisms of cold therapy on traumatized tissues 
      remain unclear. Tumor necrosis factor-alpha (TNF-alpha) is a fundamental mediator 
      in inflammatory reactions and trauma-induced tissue injury. In the present study, 
      we examined the microvascular response to TNF-alpha challenge and the effects of 
      local cooling on the TNF-alpha-induced changes in the striated muscle of 
      hamsters. METHODS: By the use of the dorsal skinfold chamber preparation and in 
      vivo fluorescence microscopy in combination with computer-based image analysis, 
      we determined TNF-alpha-induced leukocyte rolling and adhesion to microvascular 
      endothelium, capillary perfusion, venular leakage, and cellular apoptosis with 
      and without surface cooling. RESULTS: We found that topical administration of 
      2000 units TNF-alpha caused a progressive impairment of microvascular perfusion 
      and increased leukocyte recruitment and vascular macromolecular leakage. Local 
      cooling to 10 degrees C for 60 minutes markedly (P < .05) inhibited the 
      TNF-alpha-induced capillary perfusion failure and leukocyte response and slightly 
      attenuated the increase of microvascular permeability after 180 minutes of 
      stimulation. Furthermore, it was observed that 24 hours of TNF-alpha stimulation 
      increased the number of apoptotic cells (i.e., nuclear condensation and 
      fragmentation) by 10-fold. This TNF-alpha-mediated effect was almost abolished by 
      treatment with local hypothermia. CONCLUSION: These data suggest that the 
      protective effect of surface cooling of traumatized tissue is due to its 
      attenuation of the microvascular inflammatory response associated with the 
      inhibition of the process of apoptosis.
FAU - Westermann, S
AU  - Westermann S
AD  - Institute for Clinical and Experimental Surgery, University of Saarland, 
      Homburg/Saar, Germany.
FAU - Vollmar, B
AU  - Vollmar B
FAU - Thorlacius, H
AU  - Thorlacius H
FAU - Menger, M D
AU  - Menger MD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Surgery
JT  - Surgery
JID - 0417347
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Cell Adhesion/drug effects/physiology
MH  - *Cold Temperature
MH  - Cricetinae
MH  - Endothelium, Vascular/physiology
MH  - Leukocytes/*physiology
MH  - Mesocricetus
MH  - Microcirculation/drug effects
MH  - Muscle, Skeletal/*blood supply
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors/*pharmacology
EDAT- 1999/11/24 00:00
MHDA- 1999/11/24 00:01
CRDT- 1999/11/24 00:00
PHST- 1999/11/24 00:00 [pubmed]
PHST- 1999/11/24 00:01 [medline]
PHST- 1999/11/24 00:00 [entrez]
AID - S0039606099700292 [pii]
PST - ppublish
SO  - Surgery. 1999 Nov;126(5):881-9.