Introduction of Pathophysiology1.PathophysiologyPathophysiology is a science to study on the mechanisms and laws of occurrence and development of diseases.Conspectus of Disease1.DiseaseDisease is referred as an aberrant manifestation of homeostatic disturbances caused by harmful agents.2.Causative factor / pathogenic causeCausative factor or pathogenic cause is referred as the factor that can cause a disease and determine its specificity.3.Alternation of the cause and effectAlternation of the cause and effect means that during the development of a disease, the original cause can result in certain changes of the body and these changes can in turn lead to another alternations under some conditions. That is to say, the original pathogenic factor of a disease leads to a result and the latter can be transformed into the cause of further alternations under certain conditions. In this way, the successive alternation and transformation of cause and effect promote the progression of the disease.4.Vicious cycleVicious cycle is a circular process of the alternate cause-effect, in which every alternation of cause and effect will bring about more serious injuries to the body and further spoil the health condition. The final result of this kind of alternative circulation is to cause the patient to die.5.Brain deathBrain death is a state of permanent irreversible cessation of whole brain activity. At that time, the function of the patient's body as a whole body has stopped forever.Water and Sodium Balance and Imbalance1.Hypovolemic hyponatremiaHypovolemic hyponatremia is hyponatremia with decreased extracellular fluid volume. In this situation, sodium loss is more than water loss, and serum sodium concentration falls below 130mmol/L and plasma osmotic pressure is less than 280mmol/L. It is also termed hypotonic dehydration or hypo-osmotic dehydration.2.Hypovolemic hypernatremiaHypovolemic hypernatremia is hypernatremia with decreased extracellular fluid volume. In this situation, water loss is more than sodium loss, serum sodium concentration is more than 150mmol/L, and plasma osmotic pressure is more than 310mmol/L. It is also termed hypertonic dehydration or hyperosmotic dehydration.3.Isotonic dehydrationIsotonic dehydration means that water loss is proportional to salt loss, so both the serum sodium concentration and plasma osmotic pressure are normal, but blood volume is decreased. It is also termed iso-osmotic dehydration. 4.EdemaEdema means that excessive fluid accumulates in interstitial compartment and some cavities in the body.5.HypokalemiaHypokalemia is defined as a decrease in serum K+ concentration less than 3.5 mmol/L.6.HyperkalemiaHyperkalemia is defined as an increase in serum K+ concentration more than 5.5 mmol/L.7.Hypervolemic hyponatremiaHypervolemic hyponatremia is hyponatremia with increased extracellular fluid volume resulting from excessivewater intake, meanwhile accompanied by decreased excretory function of kidney that leads to the accumulation of hypotonic fluid in exterior and interior of cells. In this situation, serum sodium concentration and plasma osmotic pressure are less than 130mmol/L and 280mmol/L, respectively, but the total amount of body sodium is normal or increased. It is also called water intoxication or hypo-osmotic overdehydration.8.PseudohyperkalemiaIn some conditions, the increase of serum K+concentration results from an artifact of laboratory measurement (due to release of potassium from blood cells during or after drawing of the blood specimen), but in fact the K+ level of plasma or serum within the body is not increased. This hyperkalemia is referred to as pseudohyperkalemia.9.Hyperpolarization blockingIn acute hypokalemia, the ICF/ECF ratio of K+ concentration increases, and the K+ efflux out of cells increases, so the voltage of the membrane potential becomes more negative than the normal resting membrane potential. At this time, the membrane becomes hyperpolarized; the difference between the resting membrane potential and the threshold potential increases with the hyperpolarization of the cell membrane; the cell membrane becomes less reactive to any stimulus that would initiate an action potential under normal circumstances. This state is referred to as hyperpolarization blocking.10.Depolarization blockingIn severe acute hyperkalemia, the resting membrane potential decreases and may fall close to the threshold potential. At this time, the cell membrane is too depolarized, which causes many voltage-gated Na+ channels to inactivate, and the action potential will not be initiated by any normal stimulus. That is, the irritability of the nerve and muscle cells is decreased. This phenomenon is termed depolarization blocking.Acid-base Balance and Imbalance1.Metabolic acidosisIt is a kind of simple acid-base disorder, which results from multiple causes and is characterized by primary reduction of [HCO3-] in plasma.2.Respiratory acidosisIt is a kind of simple acid-base disturbance，which results from the exhaust deficiency or abnormal inhale of CO2 and is characterized by primary increase of [H2CO3] in plasma or PaCO2.3.Paradoxical aciduriaIt refers to the situation that the patient with alkalemia exhibits abnormally acidic urine. Generally, the urine is basic when the patient has an alkalosis. But in the body of patient with hypokalemia, potassium ions would shift out of the cells because of low [K+] in extracellular fluid. Meanwhile, hydrogen ions outside the cells move into the cells, as a result, alkalosis in extracellular fluid ensues. At this time, because of the increase of H+and decrease of K+ in the cells, the epithelium of renal tubules secretes more H+ and less K+ into the urine to make it become abnormally more acidic.4.Paradoxical alkaluria (alkaline urine)It refers to the situation that the patient with acidemia exhibits abnormally alkaline urine. Generally, the urine is asidic when the patient has an acidosis. But in the body of patient with hyperkalemia, potassium ions would move into the cells because of high [K+] in extracellular fluid. Meanwhile, hydrogen ions in the cells move out, as a result, acidosis in extracellular fluid ensues. At this time, because of the increase of K+ and decrease of H+ in the cells, the epithelium of renal tubules secretes more K+ and less H+ into the urine to make it become abnormally more alkaline or exhibit neutral. This situation can be also found in those patients with renal tubular acidosis (RTA).5.PaCO2It refers to the partial pressure exerted by CO2 gas molecules dissolved in arterial plasma, which pressure range is normally 33～46mmHg (4.39～6.25kPa), and its average is normally 40mmHg (5.32kPa).6.Standard bicarbonate (SB)It refers to the concentration of bicarbonate in arterial plasma, which should be measured under the standard conditions. The standard conditions include a temperature of 38℃, the hemoglobin oxygen saturation of 100% and the balanced CO2 gas partial pressure of 40mmHg(5.32kPa). The normal range of this parameter is 22～27 mmol/L with an average of 24 mmol/L.7.Actual bicarbonate (AB)Under the conditions of actual hemoglobin oxygen saturation and PaCO2, the bicarbonate concentration of arterial plasma in airtight blood sample is measured. This measured parameter is termed as actual bicarbonate and reflects the actual status of an individual. Its normal value should be consistent with that of the standard bicarbonate.8.Buffer base (BB)It is the summation of all alkaline buffer substances with negative charges in blood, mainly including HCO3-, HPO42-, Pr-, Hb--, HbO2-, etc. The normal value range is 45～52mmol/L with an average of 48mmol/L9.Base excess (BE)It is a parameter measured under the standard conditions of the temperature of 38℃, the hemoglobin oxygen saturation of 100%, and PCO2 of 40mmHg. Under these conditions, the milligram molecular weight of acid or base consumed in titrating 1 litre blood or plasma sample to make its pH to 7.4. The value of base excess is positive if acid is needed, and negative if base is needed. The normal range of base excess is 0±3 mmol/L.10.Anion gap (AG)It is the deference between the concentrations of unmeasured anion (UA) and unmeasured cation (UC) in plasma (AG=UA-UC). The AG value can be obtained by calculating the difference between plasma concentration of major measured cation (Na+) and the sum of the plasma concentrations of major measured anions (Cl-and HCO3-), that is, AG = [Na+] - ([Cl-] + [HCO3-]). Its normal range is 12±2 mmol/L.11.Fixed acidsFixed acids, which are also called nonvolatile acids, are referred to as the substances which cannot be converted into gases to be removed from the body by the lungs but can be eliminated in urine by the kidneys. For example, the catabolism of some bodily substances such as certain amino acids，phospholipid and nuclear acids that contain nitrogen, sulphur and phosphorus can produce sulphuric acid, phosphoric acid and uric acid; The incomplete oxidation of carbohydrates and fats can yield some glyceric acid, pyruvic acid, lactic acid, ß-hydroxybutyric acid and acetoacetate, etc.12.Metabolic alkalosisIt is a kind of simple acid-base disorder，which is caused by multiple causes and characterized by primary increase of [HCO3-] in plasma.13.Respiratory alkalosisIt is a kind of simple acid-base disorder, which results from pulmonary hyperventilation and is characterized by primary decrease of [H2CO3] in plasma or PaCO214.Mixed acid-base disorderIt means the concurrence of two or more kinds of simple acid-base disorders in the same patient. But it is impossible that both respiratory acidosis and respiratory alkalosis occur simultaneously in the same body15.Concentrated alkalosisIt is a kind of alkalosis in which the total amount of HCO3- in the extracellular comparment does not change but its concentration rises with the decrease (or contraction) of extracellular fluid volume because of the loss of NaCl solution (e.g. administration of diuretics except the carbonic anhydrase inhibitors).16.CO2 narcosisIt refers to the situation that when PaCO2rises over 80mmHg (10.7KPa) because of the retention of CO2, the excessive high PaCO2 exerts a narcotic effect on the central nervous system.The patient with CO2 narcosis would produce those symptoms and signs including headache, fainting, dysphoria, alalia, asterixis, delirium, somnolence, twitch, even coma and respiratory inhibition, etc.17.Acid-base disturbanceAcid-base disturbance is a common basic pathological process in which, because of the actions of certain causative factors, the quantitative abnormal changes of acidic or alkaline substance within the body (overload or obvious shortage) are beyond the regulative abilities of the body, or the regulative mechanisms themselves are disrupted, or the coexistence of these two situations occurs, the normal acid-base homeostasis is damaged.ctic acidosisWhen oxygen's deficiency occurs due to various causes, glucose can be converted into lactic acid by the way of anaerobic glycolysis. If the increase of lactic acid exceeds the utilization ability of the liver, or if the lactic acid cannot be utilized sufficiently by the severely damaged liver, the concentration of lactic acid in blood will rise remarkably and a metabolic acidosis follows. At this time, the sodium bicarbonate in blood is consumed in the process of neutralizing increased hydrogen ions dissociated from lactic acid. Meanwhile, the latter's remainder, the radical of lactic acid, joins the AG. Therefore lactic acidosis is a kind of metabolic acidosis with a high AG. 19.Keto-acidosisUnder the conditions of diabetes, hunger or alcohol intoxication, etc., because of the shortage or metabolic obstruction of glucose, the catabolism of fats is accelerated so as to produce large amount of fatty acid. The latter is brought by the blood flow to the liver where it is split into ketone body. The ketone body possesses strong acidity. When the amount of ketone body exceeds the oxidative ability of peripheral tissue as well as the removal ability of the kidneys, it would be accumulated in the blood and this situation is then called keto-acidosis, which belongs to the kind of metabolic acidosis with a high AG.20.Renal tubular acidosis (RTA)It is a kind of disorder that mainly results from a defect in renal tubular excretion of hydrogen ion or in reabsorption of bicarbonate, or both. The main causes of this disorder include chronic renal failure, insufficient aldosterone secretion (Addison's disease), and some hereditary or acquired disorders leading to decreased renal tubular function, such as Fanconi's syndrome etc. Nevertheless the glomerular function maintains normal. Under this situation, serious acidemia can occur while the urine is paradoxically alkaline or neutral.Hypoxia1.HypoxiaHypoxia can be defined as a deficiency in either oxygen delivery or its utilization at the tissue level or the deficiency of both, which can lead to changes in function, metabolism and even structure of the body.2.CyanosisCyanosis refers to the violaceous color of skin and mucous membranes which occurs as the deoxyhemoglobin concentration of the blood in capillaries becomes greater than 5g/dl.3.Hemic hypoxiaHemic hypoxia refers to hypoxia resulting from a low carrying capacity of oxygen in the blood caused by an altered affinity of Hb for oxygen or a decrease in the amount of Hb in the blood.4.Enterogenous cyanosisWhen pickled vegetables containing nitrate are consumed in large amounts, the reabsorbed nitrate reacts with HbFe2+to form HbFe3+OH. The color of skin becomes coffee color. This phenomenon is called enterogenous cyanosis.5.Partial pressure of oxygen (PO2)PO2 is the tension produced by oxygen molecules physically dissolved in plasma.6.Oxygen binding capacity of hemoglobin (CO2max)CO2max is the maximal amount of O2 that can be potentially combined to hemoglobin in 100ml blood.7.Oxygen content in blood (CO2)CO2is the actual oxygen content in 100ml blood, including oxygen combined to Hb and oxygen physically dissolved in plasma (only 0.3ml/dl).8.Oxygen saturation of hemoglobin (SO2)SO2 is the percentage of haemoglobin present as oxyhaemoglobin, normally 97～99% in arterial blood and about 75% in venous blood.9.Ischemic hypoxiaThe deficiency of blood perfusion to tissues caused by decreased arterial pressure or obstruction of arteries is called ischemic hypoxia.Fever1.FeverFever is a complicated pathological process characterized by a regulated elevation of core body temperature, in which the hypothalamic set point is temporarily reset at an elevated temperature in response to pyretic substances.2.Pyrogenic activatorsFever can be caused by a number of microorganisms and non-microbial pyretic substances, which are collectively called pyrogenic activators.3.Endogenous pyrogensEndogenous pyrogens are described as cytokines inducing fever, which are produced and released by EP cells, such as interleukin-1, tumor necrosis factor, etc.4.HyperthermiaHyperthermia is described as the elevation of body temperature that occurs without changes of the set point in the hypothalamic thermoregulatory center. It occurs when the thermoregulatory mechanisms are overwhelmed.5.Exogenous pyrogensMicroorganisms and their products are also called exogenous pyrogens.Stress1.StressIt is defined as a systemic nonspecific response of the body to environmental demands or pressures made upon it.2.General adaptation syndromeIt refers to a series of physiological, psychological and behavioral adaptive responses of the body after its homeostasis is threatened and disturbed. When the stressor continues its effect on the body, general adaptation syndrome manifest a dynamic, continuous process, and can finally lead to collapse of adaptive mechanism, occurrence of diseases and even death. General adaptation syndrome is a collective term for various damages and injuries of the body caused by stress response.3.Heat shock proteinsHeat shock proteins are a family of stress proteins which synthesis is elicited or up-regulated in response to a variety of stimuli such as “heat stress”. They are considered intracellular, and non-secreted proteins which functions include helping the proper folding of newly synthesized proteins and guiding their movement, helpingthe repair, removal, and proteolysis of damaged proteins.4.StressorThe stimulus that provokes a stress response is referred to as stressor.5.Acute phase proteinIn response to stressors, such as infection, inflammation, or tissue injuries, the body is elicited to evoke rapid-mobilized defensive and non-specific responses, such as rise of body temperature, raised level of blood glucose, increase of white blood cell amounts, nuclear left shift, and increase of some plasma protein concentrations. The responses listed above are called “acute phase responses”. And the plasma proteins which level in plasma increase quickly is called 'acute phase proteins' and are secreted proteins.6.Molecular chaperoneIt is also termed as “heat shock protein”. It can participate in the proper folding, movements and maintenance of newly synthesized proteins. It also can recognize and bind to the exposed hydrophobic domain of denatured proteins to prevent them from aggregating. Then it will help the protease system produce proteolystic effects on those proteins or refold them into nature conformation.Shock1.ShockShock is a pathological process caused by various drastic etiological factors, which is characterized by microcirculation failure resulting from decreased effective circulatory blood volume and inadequate tissue perfusion with the results of cellular metabolism impediment and dysfunction of multiple vital organ.2.Auto blood transfusionAt the early stage of shock, vessel constriction because of release of a large amount of vasoconstrictors may mobilize the stored blood to participate in the circulation, which is considered as compensation of venous return.3.Auto fluid transfusionAt the early stage of shock, significant decrease of hydrostatic pressure in capillary may drive fluid to shift from interstitial space to the vascular compartment, and as a result, the plasma volume can be partly restored as a compensatory responseCoagulation-Anticoagulation Balance and Imbalance1.3P test3P test is a test for detecting fragment X of FDP. Normal serum contains no detectable level of FDP. In patient with DIC, the activated fibrinolysis can result in an increase in fragment X of FDP which usually combines with fibrinmonomer to form soluble fibrinmonomer complex. Fragment X may dissociate from the soluble complex and then fibrinmonomers are polymerized to form gelatinous fibrin precipitate in the presence of protamine. The positive result of 3P test indicates the activation of fibrinolysis and the presence of DIC.2.Disseminated intravascular coagulation (DIC)DIC is a pathological process caused by disturbance of the kinetic balance between coagulation and anticoagulation systems (including fibrinolytic system). Etiologic factors activate extensive intravascular coagulation and secondary fibrinolysis. The clinical features of DIC are bleeding, shock, organ dysfunction and microangiopathic hemolytic anemia.3.Fibrin degradation products (FDP)Fibrinolysis is initiated by fibrin clot and plasminogen activator in DIC. Plasmin can degrade fibrin to form a series of protein fragments, called fibrin degradation products (FDP). FDP may act as antithrombin to inhibit coagulation process.Heart failure1.Heart failureHeart failure is a pathological process in which the systolic or/ and diastolic function of the heart is impaired, and as a result, cardiac output decreases and is unable to meet the metabolic demands of the body.2.High-output failureHigh-output failure indicates that the cardiac output may be supra- normal but inadequate owing to excessive metabolic needs. The causes of high-output heart failure include severe anemia, fever, hyperthyroidism and pregnancy, etc.3.Myogenic dilationThe heart is overfilled to such an extent that the contractility produced by the slide of actin and myosin filaments decreases, with the result, the further increase of ventricular filling may produce a decrease in cardiac output. This kind of cardiac dilation is called myogenic dilation.4.Concentric hypertrophyIt is a type of myocardial hypertrophy. It, as a myocardial response to pressure overload, is associated with increased numbers of sarcomeres arranged in parallel (parallel hyperplasia of myocardial fibers) which lead to an increase in cardiac wall thickness without the increase of internal chamber size.5.Eccentric hypertrophyIt is a type of myocardial hypertrophy and it, as a myocardial response to volume overload, results from increased numbers of sarcomeres arranged in series (series lengthening of myocardial fibers) which produce an decrease in cardiac wall thickness with increase of internal chamber size.6.OrthopneaOrthopnea refers to shortness of breath that occurs when the patient with heart failure and pulmonary circular congestion is lying down in a horizontal position. Because of that, the patient has to sit up in a forward-leaning posture or by supporting the back of his/her body with several pillows so as to lessen dyspnea. The horizontal position redistributes body fluid, increases blood return from the extremities, leads to abdominal contents to exert pressure on the diaphragm, or reduces the efficiency of the respiratory muscles.7.Paroxysmal nocturnal dyspneaParoxysmal nocturnal dyspnea is a sudden attack of dyspnea that occurs during sleep in a recumbent posture. The patients with left heart failure wake up at night gasping for air and have to sit up or stand to relieve the dyspnea. It is precipitated by the development of interstitial pulmonary edema because of the redistribution of body fluid.8.Myocardial remodelingMyocardial remodeling is a process based on the alteration of gene expression involving myocardial cells, non-myocardial cells and extracellular matrix (ECM). It includes myocardial hypertrophy and phenotype alteration, non-myocardial cellular proliferation and ECM rebuilding.Respiratory Failure1.Dead space like ventilationIt indicates that the blood flow in the ventilated alveoli is reduced because of diseases. So the air in these alveoli cannot be exploited sufficiently. This situation is just like dead space ventilation.2.Functional shuntBecause of obstructive or restrictive ventilation dysfunction, the involved alveoli have hypoventilation but their blood flow does not reduce, thus the ratio of V A/Q is lowered, leading to the venous blood passing through the alveolar capillaries to flow into pulmonary vein without enough oxygenation. This condition is called venousadmixture, just like artery-vein shunt.3.Pulmonary encephalopathyIt means the central nervous system dysfunction resulting from chronic respiratory failure. The reason why it occurs is that hypoxia, hypercapnia and acidosis produce the damage effects on the cerebral vessels and cerebral cells, resulting in cerebral vasodilation, the increases in cerebral blood flow and cerebral vascular permeability, the edema and electric activity dysfunction of brain cells and intracellular lysosomal enzyme release.4.Acute respiratory distress syndrome (ARDS)It is a pathological process caused by severe shock, infection and intoxication, et al. Its basic pathological change is the acute injuries of alveolar- capillary membrane. ARDS induces acute respiratory failure, characterized by progressive dyspnea and refractory hypoxemia.5.Respiratory failureRespiratory failure is a syndrome, in which the severe external respiratory dysfunction leads to a PaO2 below 60 mmHg (8.0kPa) with or without a PaCO2 above 50 mmHg (6.67kPa) in a resting subject breathing air at sea level.6.Restrictive hypoventilationIt means hypoventilation caused by the restriction of alveolar dilation or inflation during inspiration.7.Obstructive hypoventilationIt means hypoventilation that caused by the stenosis or obstruction of airway and the increased airway resistance.Hepatic Failure1.Hepatic insufficiencyHepatic insufficiency is referred to a syndrome, in which severe liver damage results in severe dysfunctions, including jaundice, bleeding, infection, renal dysfunction or encephalopathy.2.Hepatic failureHepatic failure is a terminal stage of hepatic insufficiency. Hepatic encephalopathy and hepatorenal syndrome are the primary clinical manifestations.3.Hepatic encephalopathyHepatic encephalopathy is a complex, potentially reversible disturbance in central nervous system that occurs as a consequence of severe liver diseases. It is characterized by neuropsychical manifestations ranging from a slightly altered mental status to coma.4.Gamma-aminobutyric acid (GABA) hypothesisGamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the central nervous system. Increased GABA is observed in patients with cirrhosis, perhaps because of decreased hepatic metabolism of GABA When GABA crosses the blood-brain barrier of patients with cirrhosis, it interacts with supersensitive postsynaptic GABA receptors. Activation of the GABA receptor increases neuronal membrane permeability to Cl-by opening the Cl- ionophore. When the Cl- resting potential of the neurons is more negative than the neuronal resting membrane potential, Cl- will enter the neurons causing membrane hyperpolarization, thus leading to the dysfunction of CNS.5.Ammonia intoxication hypothesisAmmonia intoxication hypothesis holds that the patient with hepatic cirrhosis has hyperammonemia and the occurrence of hepatic encephalopathy is due to entering of ammonia into the brain. All of the neuropsychiatric symptoms are due to the poisonous action of ammonia to central nervous system.6.False neurotransmitter hypothesisIn the patient with hepatic failure, false neurotransmitters are accumulated in the synapse of the reticular structure in the brain stem. The false neurotransmitters can compete with true neurotransmitters because their chemical structure is similar to the true neurotransmitters. When false neurotransmitters replaces true neurotransmitter inthe reticular structure, the disorders of CNS occur.Renal Failure1.Renal osteodystrophyRenal osteodystrophy is a serious complication of CRF (especially, of uremia), which includes renal rickets (for children), adult osteomalacia, osteitis fibrosa, osteoporosis, osteosclerosis, and etc.2.Trade-off hypothesisTrade-off hypothesis indicates that as the nephrons are progressively destroyed, increased blood concentration of some solutes stimulate over-secretion of some related regulatory factors (such as hormones) in order to increase the excretion function. At the same time, however, high blood levels of the regulatory factors will result in some other metabolic disorders.3.UremiaIt comes from the Greek 'urine in the blood'. Uremia is a clinical and biochemical syndrome that occurs either abruptly or gradually as renal function declines acutely or chronically. Uremia is the end-stage of renal failure, with which the patients have to receive treatment in the form of dialysis or renal transplantation.4.Acute renal failure (ARF)Acute renal failure is a pathological progress, which is characterized by a deterioration of renal function over a period of hours to days, resulting in failure of kidney to excrete nitrogenous waste products and to maintain fluid, electrolyte homeostasis and acid-base balance. The patients often present azotemia, water intoxication, hyperkalemia and metabolic acidosis.5.Chronic renal failure (CRF)Chronic renal failure is a syndrome of impaired homeostasis owing to structural damage (reduced functional nephrons) of the kidneys. The disturbances are characterized by metabolic acidosis, hypocalcemia, hyperphosphatemia, alteration in vitamin D metabolism and the presence of certain toxic materials in body fluid.Ischemia- reperfusion injury1.Ischemia- reperfusion injuryThe restoration of blood flow after transient ischemia may be associated with further reversible or irreversible cell damage, which is called ischemia-reperfusion injury or reperfusion injury.2.Calcium overloadCalcium overload refers to that intracellular content of calcium is increased abnormally during ischemia and reperfusion, which results in the disorder of cellular structure and function.3.No-reflow phenomenonNo-reflow phenomenon refers to a paradoxical phenomenon that the relief of blood vessel occlusion (or other causes responsible for ischemia) cannot make the ischemic area obtain sufficient blood perfusion. The significant impairment of flow may occur at microvascular level. The main determinant of no-reflow is the activation of neutrophils in microvesseles.4.Respiratory burstNeutrophils (NADPH oxidase etc) activated by ischemia may obviously increase the production of oxygen free radicals (e.g., O2－·, H2O2) during reperfusion regaining O2 supplement, the phenomenon is called respiratory burst.5.Oxygen paradoxOxygen paradox refers to that the restoration of the oxygen partial pressure in perfusion solution after transient hypoxia may be associated with increase in membrane permeability and cell death.。
