Accommodation of skeletal muscle in rats under hypoxic conditions induced by tourniquet

Quevedo, L; Cárdenas, Hernán; Iturriaga, Rodrigo

doi:10.1007/bf01851711

Cited by 3 publications

(1 citation statement)

References 25 publications

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“…The use of direct electrical stimulation of muscle has been well described both in vivo and in vitro, but controversy exists with regards to its ability to isolate muscle tissue functionally from its smaller neural elements [4][5][6]19,21,37]. Baraka argues that direct stimulation of muscle without neuromuscular junction blockade results in transmission through neural elements [4].…”

Section: Discussionmentioning

confidence: 99%

Ischemic‐preconditioning does not prevent neuromuscular dysfunction after ischemia–reperfusion injury

Eastlack

Groppo

Hargens

et al. 2004

Journal Orthopaedic Research

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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 ishemia 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. © 2003 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.

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