MindMap Gallery ischemia-reperfusion injury
A mind map of ischemia-reperfusion injury. The basics of prevention and treatment include restoring blood flow as early as possible and controlling reperfusion conditions, scavenging and reducing free radicals, alleviating calcium overload, and applying cytoprotective agents and neutrophil inhibitors.
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This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
ischemia-reperfusion injury
Common conditions
ischemia time
collateral circulation
aerobic level
Conditions for reperfusion
Reperfusion fluid pressure, temperature, pH, and electrolyte concentration
The mechanism
Increased free radicals
mechanism
mitochondrial damage
During hypoxia, there is a third-stage obstacle to oxygen oxidation. During reperfusion, oxygen undergoes single-electron reduction to generate an increase in reactive oxygen species.
Neutrophil recruitment and activation
Chemokines can be produced during hypoxia to attract and activate neutrophils. During reperfusion, activated neutrophils consume more oxygen and produce a large amount of oxygen free radicals.
Increased formation of xanthine oxidase
Ca-dependent proteolytic enzyme converts XD to XO
A large amount of hypoxanthine accumulates in ischemic tissue. During reperfusion, oxygen oxidizes hypoxanthine under the action of xanthine oxidase to generate uric acid and H₂O₂, resulting in a large increase in reactive oxygen species.
Increased autooxidation of catecholamines
The stress reaction produces a large amount of catecholamines and a large amount of oxygen free radicals through self-oxidation.
Mechanisms that cause body damage
membrane lipid peroxidation
Destruction of cell and organelle membrane structures
Increased production of biologically active substances
Reduced ATP production
protein function inhibition
Nucleic acid damage and DNA fragmentation
calcium overload
mechanism
Abnormal Na-Ca2 exchange
Na-Ca2 exchanger antiporter
direct activation
Reduced ATP production, resulting in reduced sodium pump activity and increased intracellular sodium content
indirect activation
Hypoxia and anaerobic metabolism are enhanced, leading to acidosis. During reperfusion, the H concentration in the interstitial fluid decreases, but the intracellular concentration remains high, activating H-Na exchange proteins and causing an increase in intracellular Na.
Increased catecholamine release
Acts on α₁-R to promote the decomposition of PIP₂ to form IP₃ and DG
IP₃ promotes the release of Ca from the endoplasmic reticulum and increases the intracellular Ca concentration.
DG activates PKC to promote H-Na exchange, which in turn promotes Na-Ca2 exchange. Ca2 influx increases and the concentration increases.
Acts on β-R, activates CA, increases the opening of calcium channels, and promotes the influx of calcium ions
biofilm damage
cell membrane damage
mechanism
Increased membrane permeability to Ca2
Reperfusion generates free radicals that damage membrane structure
Intracellular Ca2 activates phospholipase, destroys membrane structure, and increases permeability
mitochondrial membrane damage
mechanism
Cell membrane damage, increased Ca2 influx, resulting in calcium salt deposition in mitochondria, mitochondrial dysfunction, reduced ATP production, and inhibition of energy-consuming ion pump function
Ischemia-reperfusion generates free radicals and reactive oxygen species
Free radical damage and degradation of membrane phospholipids damage the mitochondrial membrane and reduce ATP production.
endoplasmic reticulum membrane damage
mechanism
Endoplasmic reticulum calcium uptake consumes energy, while ATP production is reduced during ischemia, and the generated free radicals and degradation of membrane phospholipids can damage the endoplasmic reticulum membrane.
Mechanisms that cause body damage
energy metabolism disorder
Mitochondria absorb Ca2, which consumes energy. After entering the mitochondria, calcium phosphate is formed, causing mitochondrial dysfunction and reduced ATP production.
Decomposition of cell membrane and structural proteins
Activate phospholipases to promote membrane phospholipid degradation
Activates calcineurin to promote the breakdown of cell membrane and structural proteins
Activates endonucleases, causing chromosomal damage
Opens the mitochondrial permeability transduction pore, inhibits respiratory function and promotes the release of cytochrome C, promoting cell apoptosis.
aggravate acidosis
Enhanced anaerobic glycolysis and increased lactic acid
High intracellular calcium activates certain ATPases, hydrolyzes high-energy phosphates, and releases H
Overactivation of inflammatory response
mechanism
Increased production of cell adhesion molecules
Increased production of chemokines and cytokines
Mechanisms that cause body damage
Microvascular damage
Microvascular hemorrheological changes
Increased microvascular permeability
cell damage
Functional metabolic changes
myocardium
reperfusion arrhythmia
The mechanism
Heterogeneity of action potential duration between reperfused myocardium
Cardiomyocyte calcium overload
Increased free radicals and reactive oxygen species
Increased endogenous catecholamines
myocardial systolic dysfunction
reperfusion myocardial stunning
myocardial stunning
After the blood perfusion of the ischemic myocardium is restored, the myocardial diastolic and systolic functions will take a long time to recover, which is a reversible myocardial dysfunction.
Microvascular obstruction
Structural changes in myocardium
brain
damage mechanism
Excitatory amino acid toxic effects
Increased free radicals, reactive oxygen species and inflammatory mediators
calcium overload
other organs
lung
liver
kidney
intestinal
The basis of disease prevention and treatment
Early restoration of blood flow and control of reperfusion conditions
Scavenge and reduce free radicals, reduce calcium overload
Use of cytoprotective agents and neutrophil inhibitors
Activate endogenous protective mechanisms
ischemic preconditioning
Multiple cycles of brief ischemia and reperfusion before prolonged ischemia can reduce damage
Hardly used clinically
ischemic postconditioning
After prolonged ischemia, multiple cycles of brief ischemia and reperfusion can reduce damage.
Heart and brain unavailable
remote ischemic preconditioning
Repeated ischemia or hypoxia in non-vital organs other than the heart and brain, thereby improving vascular functional status and improving the ability of distant vital organs to tolerate severe ischemia or hypoxia
Wide range of clinical applications