Ischemic pain can be viewed as a part of protective mechanisms used to alert the central neural system about impending or actual tissue injury and prompt a living system to respond to this injury. Ischemic pain is different from other types of pain so far that tissue hypoxia, rather than direct tissue or nerve damage, is a main cause of this pain. Namely, tissue hypoxia secondary to decreased blood supply, and resultant tissue acidosis, seems to be the main trigger of the complex pathophysiological reaction to this damage, part of which is pain. Ischemic pain is thought to be mediated by protons. An acid sensing ion channel (ASIC) that may be responsible for the detection and sensing of ischemia has been cloned about 10 years ago. It is expressed in dorsal root ganglia and is also distributed widely throughout the brain (Dube et al. 2009). Not specific to the etiology of pain, some inflammatory and pain mediators, such as bradykinin, histamine, serotonin, acetylcholine, potassium ions, and adenosine, participate in pain triggering and conduction mechanisms. Additionally, studies of molecular mechanisms of ischemic pain led to the discovery of substance P almost 80 years ago. Substance P was found to be accumulated in ischemic tissues and quickly disappeared after reperfusion
N. Vadivelu et al. (eds.), Essentials of Pain Management,
DOI 10.1007/978-0-387-87579-8_24, © Springer Science+Business Media, LLC 2011
(Cervero 1994). A better understanding of pathophysiology of ischemic pain brought by basic studies should promote the development of more effective treatment modalities of this type of pain (Bonica 1990a).
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