Linked Life Data

15183455

Source:http://linkedlifedata.com/resource/pubmed/id/15183455

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-6-8
pubmed:abstractText
The primary purpose of this study was to evaluate ischemic-preconditioning (IPC) as a means of improving tolerance to ischemia-reperfusion (IR) stress on neuromuscular function. A secondary objective was to isolate the area of injury within the neuromuscular unit responsible for contractile dysfunction after IR injury. Twenty-eight male rabbits were randomly assigned to four groups (sham, IPC only, sustained ischemia only, IPC and sustained ischemia). The IPC protocol consisted of three cycles of 10 min of tourniquet-induced ischemia (125 mmHg) followed by 10 min of reperfusion. Sustained ischemia was induced by 350 mmHg external compression for 2 h. Peak tetanic tension of the tibialis anterior (TA) muscle was evaluated 48 h after the tourniquet protocol by both peroneal nerve and direct muscle stimulation, with and without pharmacologic neuromuscular junction blockade. Animals subjected to combined IPC and sustained ischemia had an equivalent loss of contractile force to those undergoing sustained ischemia alone. Two hours of tourniquet-induced ischemia resulted in marked dysfunction of the TA neuromuscular unit when evaluated by peroneal nerve stimulation (p < 0.0001). Isolation of the TA muscle from the peroneal nerve with direct muscle stimulation and neuromuscular junction blockade preserved muscle function after 3 h of ischemia. In our model, these results clearly demonstrate that IPC provides no significant protective effect from IR injury to either nerve or muscle function in our model. In addition, nerve or neuromuscular junction injury, rather than muscle damage, is identified as primarily responsible for IR-related muscle dysfunction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0736-0266
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
918-23
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Ischemic-preconditioning does not prevent neuromuscular dysfunction after ischemia-reperfusion injury.
pubmed:affiliation
Department of Orthopaedic Surgery, University of California, 200 W. Arbor Drive, San Diego, CA 92103-8894, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't