Paper Information

Title: 

HYPEROXIA AND TISSUE PRECONDITIONING

Type: PAPER
Author(s): KHOUSHBATEN A.*
 
 *DEPT. OF PHYSIOLOGY, SCHOOL OF MEDICINE, BAGHIATALLAH UNIVERSITY OF MEDICAL SCIENCES
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Cellular hypoxia, due to tissue ischemia is a dangerous event which if extended, could inevitably lead to cellular damages and necrosis. Paradoxically re-oxygenation, due to reperfusion causes tissue injury. One of the most important factors in pathophysiology of ischemia reperfusion (IR) injury is Reactive Oxygen Species (ROS), which especially increases in reperfusion phase. The endogenous antioxidants which are responsible for defense against ROS during reperfusion have an important role in decreasing IR injury. Superoxide dismutase (SOD) and catalase (CAT) are the most important antioxidant enzymes of tissues. Glutathione (GSH), a free radical scavenger, also plays a key role in maintenance of the cellular redox environment. Ischemia-reperfusion injuries can be divided in two different parts, 1) Ischemia injury which is defined as depletion of the cellular energy stores (ATP and CrP), depression of Ca2+-ATPase of SR and Na/K-pump, increase in cytosolic Na+ and Ca2+ with a concomitant loss of intracellular K+, acidosis, increased osmotic load, production of ROS, and activation of Ca2+-sensitive enzymes (proteases and lipases), and finally rupture of the cell membrane and cell death. 2) Reperfusion injury which is characterized by: Return of oxygen and nutrients with reperfusion allows the tissues to resume energy production, further increase of cytosolic Ca2+ during the early reperfusion phase, Ca2+ overload lead to a particularly cytotoxic burst of ROS production. ROS can initiate: lipid peroxidation, oxidize proteins, and DNA strand breaks. Ischemic preconditioning (IPC) has been defined as increased tolerance to ischemia produced by short (non-injurious) ischemic insult. The phenomenon of IPC has been observed in various tissues. This IPC could be as an acute or delayed IPC form. Immediate development of ischemic tolerance has been also reported, especially in in-vitro studies, and it has been suggested that the mechanisms of immediate and delayed tolerance are different. In vivo, immediate tolerance seems to provide a short-term protection, and probably only delays the time course of cellular death. Different methods of preconditioning have been reported to be used in different tissues such as: Ischemic Preconditioning (IPC), Pharmacological preconditioning (PPC), Hypoxia induced preconditioning, Hyperthermia induced preconditioning, and Hyperoxia induced preconditioning. Free radical damage might be worsened by hyperoxia. But experimental, as well as clinical, data suggest that hyperoxic PaO2 (500–700 mmHg) leads to myocardial reperfusion damage; maintaining a more physiologic PaO2 during reperfusion following ischemia may attenuate injury. Hyperoxic reperfusion exacerbated renal dysfunction after 30 min of complete normothermic ischemia in mongrel rabbits. In contrast, eubaric Hyperoxemia improved neurological and neuropathological outcome after transient cerebral ischemia in rats. Continuous oxygen therapy offered the greatest benefit, while increased oxygen tension beyond 200 mmHg was of no further advantage. The mechanism of benefit of hyperoxemia might involve the vascular component, with impaired autoregulation in the area of ischemia. Vasoconstriction caused by a high PaO2 allows shunting of blood into the infarct from adjacent normal in regards to immune defense, surgical site infection and brain.

 
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