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{{Reperfusion injury}}
__NOTOC__
'''Editors-In-Chief:''' {{AC}}; [[C. Michael Gibson]], M.S., M.D. [mailto:Mgibson@perfuse.org]; '''Associate Editors-In-Chief: '''[[User:Kashish Goel|Kashish Goel, M.D.]]
{{CMG}} {{AE}} {{Shivam Singla}} {{AC}} [[User:Kashish Goel|Kashish Goel, M.D.]]
 
==Overview==
==Overview==
[[Reperfusion injury]] may be responsible for about 50% of the total infarct size after an acute [[myocardial infarction]] as well as [[myocardial stunning]], [[congestive heart failure]] and [[reperfusion arrhythmias]] such as [[ventricular arrhythmias]].<ref name="pmid17855673">{{cite journal |author=Yellon DM, Hausenloy DJ |title=Myocardial reperfusion injury |journal=N. Engl. J. Med. |volume=357 |issue=11 |pages=1121–35 |year=2007 |month=September |pmid=17855673 |doi=10.1056/NEJMra071667 |url=}}</ref>.
[[Reperfusion injury]] mechanism is mostly studied by scientists in cats and dogs with the first experimental study done in 1955 by Sewell and later different studies were done to understand more about the [[reperfusion injury]] mechanisms. Most of the [[complications]] associated with [[reperfusion injury]] are mainly due to the formation of [[reactive oxygen species]] and [[neutrophil]] activation ultimately resulting in [[tissue]] damage-causing [[Ischemia]], [[Infarction]], [[Haemorrhage]], and [[edema]]. Prognosis, in general, is poor with Ischemia-reperfusion injury resulting in tissue injury and damage. The most important determinant of prognosis is the time taken to reperfuse the [[ischemic tissue]]. More the delay in time to [[reperfusion]], worse the prognosis is. 
 
==Natural History==
[[File: Reperfusion Injury History.jpg|thumb|336x336px|Reperfusion Injury Natural History along with the different terms given by various scientists along the course of time starting from 1950's- 1980. [https://www.slideshare.net/prabeshrajjk/09-ir-injury]]]
The [[Ischemia]]-[[reperfusion]] [[injury]] was first seen in 1955 by Sewell while performing ligation of Dog's [[coronary]] [[arteries]]
 
Then later Jennings gave the term [[Myocardial]] IRI in 1960. He is the first person to name the term Ischemia [[Reperfusion Injury]](IRI) on the basis of [[histological]] changes in canine [[myocardium]].
 
Later various terms were given by the scientist depending upon the various [[organ system]] involved:
 
* In 1968 Ames gave the term [[Brain]] [[IRI]]
 
* 1972 Flore gave the term [[Kidney]] [[IRI]]
 
* Then Modry gave the term [[Lung]] [[IRI]] in 1978
 
* Greenberg gave the term [[Intestinal]] [[IRI]] in 1981 by his experiment showing [[reperfusion]] induced damage in the [[intestinal]] [[mucosal cells]] of a cat after long hours of [[ischemia]].  
 
[[Ischemic]] [[preconditioning]] was first explained by Murry et al. In 1986 he performed a study in dog explaining the importance of [[ischemia]] [[reperfusion]] in dogs on [[infarct]] size reduction<ref name="pmid32804120">{{cite journal |vauthors=Varga G, Ghanem S, Szabo B, Nagy K, Pal N, Tanczos B, Somogyi V, Barath B, Deak A, Matolay O, Bidiga L, Peto K, Nemeth N |title=Which remote ischemic preconditioning protocol is favorable in renal ischemia-reperfusion injury in the rat? |journal=Clin. Hemorheol. Microcirc. |volume= |issue= |pages= |date=August 2020 |pmid=32804120 |doi=10.3233/CH-200916 |url=}}</ref>.
[[File: History of IRI.jpg|thumb|Natural History Of Reperfusion Injury. [https://www.onlinejacc.org/content/65/14/1454.abstract]]]
[[Ischemic]] post-conditioning was given by Zhao et al in 2003 and explained this with the help of an [[experiment]] showing a small episode of [[Ischemia]] or [[reperfusion]] performed immediately after the [[resumption]] of flow following a period of [[ischemia]]. They found that this helped in the reduction of [[infarct]] size in dogs by up to 40%<ref name="pmid28296005">{{cite journal |vauthors=Mentias A, Mahmoud AN, Elgendy IY, Elgendy AY, Barakat AF, Abuzaid AS, Saad M, Kapadia SR |title=Ischemic postconditioning during primary percutaneous coronary intervention |journal=Catheter Cardiovasc Interv |volume=90 |issue=7 |pages=1059–1067 |date=December 2017 |pmid=28296005 |doi=10.1002/ccd.26965 |url=}}</ref>.


==Complications==
==Complications==
* [[Myocardial stunning]]: Delayed recovery, usually 2-3 days, of the viable myocardium after reperfusion is termed as "myocardial stunning". It is mainly due to the release of reactive oxygen species and intracellular calcium overload.
 
* [[Myocardial infarction]]: Irreversible myocyte cell death secondary to reduced oxygen delivery for more than 20-30 minutes, will lead to infarction. Reperfusion helps prevent complete loss of the involved area, however oxidative stress due to this may prevent complete resolution.
* [[Myocardial stunning]]: It is mainly defined as an abnormality in the contractile function of [[myocardium]] that sometimes persists even after the return of [[reperfusion]] and resolution of [[ischemia]]. It is mainly due to the release of
* Acute [[heart failure]]: Loss of myocardial contractility and systolic dysfunction associated with ischemia/reperfusion injury may lead to development of acute heart failure. Early reperfusion in the course of [[STEMI]] prevents myocardial necrosis and may lead to complete recovery of function.
** [[Reactive oxygen]] species
* [[Ventricular arrhythmia]]s: Reperfusion of the blocked coronary artery can also precipitate arrhythmias ranging from [[ventricular premature beat]]s to life-threatening [[ventricular fibrillation]].
** [[Intracellular]] [[calcium]] overload.
 
* [[Myocardial infarction]]: [[Irreversibility|Irreversible]] myocyte cell death secondary to reduced [[oxygen]] delivery for more than 20-30 minutes will eventually leads to [[infarction]]. [[Reperfusion]] helps prevent complete loss of the involved area, however [[oxidative stress]] due to this may prevent complete resolution<ref name="pmid23281415">{{cite journal |vauthors=Hausenloy DJ, Yellon DM |title=Myocardial ischemia-reperfusion injury: a neglected therapeutic target |journal=J. Clin. Invest. |volume=123 |issue=1 |pages=92–100 |date=January 2013 |pmid=23281415 |pmc=3533275 |doi=10.1172/JCI62874 |url=}}</ref>.
 
* Acute [[heart failure]]: Loss of [[myocardial]] [[contractility]] and [[systolic]] dysfunction associated with [[ischemia]]/reperfusion injury may lead to the development of [[acute heart failure]]. [[File:IRI Complications.jpg|thumb|383x383px|Complications of IRI. [http://cs149.stanford.edu/fall19/lecture/snoopcoherence]]]
 
* Early [[reperfusion]] in the course of [[STEMI]] prevents [[myocardial]] [[necrosis]] and may lead to complete recovery of function resulting in a better prognosis as compared to a situation where there is a delay in perfusion<ref name="pmid31268854">{{cite journal |vauthors=Niccoli G, Montone RA, Ibanez B, Thiele H, Crea F, Heusch G, Bulluck H, Hausenloy DJ, Berry C, Stiermaier T, Camici PG, Eitel I |title=Optimized Treatment of ST-Elevation Myocardial Infarction |journal=Circ. Res. |volume=125 |issue=2 |pages=245–258 |date=July 2019 |pmid=31268854 |doi=10.1161/CIRCRESAHA.119.315344 |url=}}</ref>.
 
* [[Ventricular arrhythmia]]s: [[Reperfusion]] of the blocked [[coronary artery]] can also precipitate [[arrhythmias]] ranging from [[ventricular premature beat]]s to life-threatening [[ventricular fibrillation]].
 
* [[Intestinal]] [[ischemia]] [[reperfusion]] is associated with the development of [[necrotizing enterocolitis]], [[hypotension]], and [[thrombosis]].
** It is mainly seen as a consequence of [[acute mesenteric ischemia]] that mainly results due to impaired [[blood]] flow to the [[intestines]] through the [[mesenteric]] [[vessels]]<ref name="pmid25414098">{{cite journal |vauthors=Gonzalez LM, Moeser AJ, Blikslager AT |title=Animal models of ischemia-reperfusion-induced intestinal injury: progress and promise for translational research |journal=Am. J. Physiol. Gastrointest. Liver Physiol. |volume=308 |issue=2 |pages=G63–75 |date=January 2015 |pmid=25414098 |pmc=4297854 |doi=10.1152/ajpgi.00112.2013 |url=}}</ref>.
 
== Prognosis ==
Prognosis in [[CNS]] patients
 
* Those [[patients]] who are identified and treated early, the [[prognosis]] is better along with the decreased [[incidence]] of [[Intracranial hemorrhage|intracranial]] [[hemorrhage]]. Outcomes usually depend on the timely recognition and [[prevention]] of precipitating factors. [[Hypertension]] management is most important before it can inflict damage in the form of [[edema]] or [[hemorrhage]]<ref name="pmid31610199">{{cite journal |vauthors=Yang JL, Yang YR, Chen SD |title=The potential of drug repurposing combined with reperfusion therapy in cerebral ischemic stroke: A supplementary strategy to endovascular thrombectomy |journal=Life Sci. |volume=236 |issue= |pages=116889 |date=November 2019 |pmid=31610199 |doi=10.1016/j.lfs.2019.116889 |url=}}</ref>
**The prognosis following [[hemorrhagic]] transformation is poor. [[Mortality]] in such cases is 63%, and 80% of survivors have significant [[morbidity]].
*In the case of [[Central nervous system]] the [[brain]] is a very sensitive organ to [[ischemia]] and results in death within 5 minutes of the onset of [[ischemia]]. [[Reperfusion]] is usually beneficial if it is conducted within a very short period of time after the onset of [[ischemia]] but in most cases, [[reperfusion]] leads to the development of [[cerebral ischemia]] and [[hemorrhage]] resulting in a bad [[prognosis]].
*[[Ischemia]] [[reperfusion]] injury in [[kidneys]] is mainly associated with the development of [[high morbidity]] and [[mortality]], worse prognosis with the involvement of [[corticomedullary junction]].
*In [[CVS]] patients [[reperfusion]] [[injury]] is mainly associated with [[Arrhythmias]], [[myocardial stunning]], and [[myocyte death]], which mainly results in the occurrence of [[Myocardial Infarction]] with a worse [[prognosis]].


==References==
==References==
{{reflist|2}}
[[Category:Physiology]]
[[Category:Physiology]]
[[Category:Cardiology]]
[[Category:Cardiology]]
[[Category:Up-To-Date cardiology]]
[[Category:Up-To-Date cardiology]]

Latest revision as of 19:40, 21 August 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[5] Anjan K. Chakrabarti, M.D. [6] Kashish Goel, M.D.

Overview

Reperfusion injury mechanism is mostly studied by scientists in cats and dogs with the first experimental study done in 1955 by Sewell and later different studies were done to understand more about the reperfusion injury mechanisms. Most of the complications associated with reperfusion injury are mainly due to the formation of reactive oxygen species and neutrophil activation ultimately resulting in tissue damage-causing Ischemia, Infarction, Haemorrhage, and edema. Prognosis, in general, is poor with Ischemia-reperfusion injury resulting in tissue injury and damage. The most important determinant of prognosis is the time taken to reperfuse the ischemic tissue. More the delay in time to reperfusion, worse the prognosis is.

Natural History

Reperfusion Injury Natural History along with the different terms given by various scientists along the course of time starting from 1950's- 1980. [1]

The Ischemia-reperfusion injury was first seen in 1955 by Sewell while performing ligation of Dog's coronary arteries

Then later Jennings gave the term Myocardial IRI in 1960. He is the first person to name the term Ischemia Reperfusion Injury(IRI) on the basis of histological changes in canine myocardium.

Later various terms were given by the scientist depending upon the various organ system involved:

  • Then Modry gave the term Lung IRI in 1978

Ischemic preconditioning was first explained by Murry et al. In 1986 he performed a study in dog explaining the importance of ischemia reperfusion in dogs on infarct size reduction[1].

Natural History Of Reperfusion Injury. [2]

Ischemic post-conditioning was given by Zhao et al in 2003 and explained this with the help of an experiment showing a small episode of Ischemia or reperfusion performed immediately after the resumption of flow following a period of ischemia. They found that this helped in the reduction of infarct size in dogs by up to 40%[2].

Complications

  • Early reperfusion in the course of STEMI prevents myocardial necrosis and may lead to complete recovery of function resulting in a better prognosis as compared to a situation where there is a delay in perfusion[4].

Prognosis

Prognosis in CNS patients

References

  1. Varga G, Ghanem S, Szabo B, Nagy K, Pal N, Tanczos B, Somogyi V, Barath B, Deak A, Matolay O, Bidiga L, Peto K, Nemeth N (August 2020). "Which remote ischemic preconditioning protocol is favorable in renal ischemia-reperfusion injury in the rat?". Clin. Hemorheol. Microcirc. doi:10.3233/CH-200916. PMID 32804120 Check |pmid= value (help).
  2. Mentias A, Mahmoud AN, Elgendy IY, Elgendy AY, Barakat AF, Abuzaid AS, Saad M, Kapadia SR (December 2017). "Ischemic postconditioning during primary percutaneous coronary intervention". Catheter Cardiovasc Interv. 90 (7): 1059–1067. doi:10.1002/ccd.26965. PMID 28296005.
  3. Hausenloy DJ, Yellon DM (January 2013). "Myocardial ischemia-reperfusion injury: a neglected therapeutic target". J. Clin. Invest. 123 (1): 92–100. doi:10.1172/JCI62874. PMC 3533275. PMID 23281415.
  4. Niccoli G, Montone RA, Ibanez B, Thiele H, Crea F, Heusch G, Bulluck H, Hausenloy DJ, Berry C, Stiermaier T, Camici PG, Eitel I (July 2019). "Optimized Treatment of ST-Elevation Myocardial Infarction". Circ. Res. 125 (2): 245–258. doi:10.1161/CIRCRESAHA.119.315344. PMID 31268854.
  5. Gonzalez LM, Moeser AJ, Blikslager AT (January 2015). "Animal models of ischemia-reperfusion-induced intestinal injury: progress and promise for translational research". Am. J. Physiol. Gastrointest. Liver Physiol. 308 (2): G63–75. doi:10.1152/ajpgi.00112.2013. PMC 4297854. PMID 25414098.
  6. Yang JL, Yang YR, Chen SD (November 2019). "The potential of drug repurposing combined with reperfusion therapy in cerebral ischemic stroke: A supplementary strategy to endovascular thrombectomy". Life Sci. 236: 116889. doi:10.1016/j.lfs.2019.116889. PMID 31610199.