Humans ; Myocardial Infarction ; complications ; therapy ; Myocardial Reperfusion Injury ; etiology ; therapy

A series of studies demonstrated that myocardial damage and cardiac dysfunction occur immediately after severe burn even before the intervention of significant reduction in blood volume as a result of increased capillary permeability. Because the heart is the power organ of the circulation, such myocardial damage and cardiac dysfunction lead not only to cardiac deficiency, it is also a precipitating factor of burn shock and ischemic/hypoxic injury. Therefore, we nominate this phenomenon as "shock heart". New measures including "volume replacement" plus "dynamic support" proposed according to this new recognition is of important clinical significance for burn shock resuscitation and prevention and treatment of ischemic/hypoxic injury, as well as reducing organ complications resulting from insufficient or excessive fluid resuscitation during early postburn stage.
Burns ; complications ; Humans ; Hypoxia ; etiology ; Myocardial Reperfusion Injury ; etiology ; Shock ; etiology

Animals ; Cardiovascular Diseases ; etiology ; Coronary Disease ; etiology ; Humans ; Hydrogen Sulfide ; metabolism ; Hypertension ; etiology ; Hypertension, Pulmonary ; etiology ; Myocardial Reperfusion Injury ; etiology

Ischemia/hypoxia is one of the key clinical issues following severe burns, and ischemic/hypoxic damage of tissues and organs is still hard to be prevented or minimized by various fluid resuscitation regimens. To those who suffered severe burns, even though fluid replacement therapy is delivered promptly, ischemic/hypoxic damage of organs is still inevitable. Previously, blood flow in vital organs such as heart was considered not to be reduced because of blood redistribution under the circumstance of stress. The postburn cardiac dysfunction has been mainly attributed to the reduced blood flow returned to the heart due to decreased blood volume caused by increased capillary permeability. Therefore, postburn cardiac dysfunction has been considered to be the result of burn shock. During the past two decades, we have performed serial studies on severe burns, and found that ischemic/hypoxic myocardial damage and functional impairment of myocardium due to activation of renin angiotensin system existing in the heart itself occur immediately after severe burns even before significant reduction in blood volume secondary to an increase of capillary permeability. Such prompt myocardial damage leads to cardiac deficiency, and it is also a precipitating factor for burn shock and ischemic/hypoxic injury of systemic tissues and organs. Therefore, we called it "shock heart" in our reports. The cellular and molecular mechanisms leading to myocardial damage were systematically investigated. Strategies for prevention of early postburn myocardial damage and dysfunction, and a new effective burn shock resuscitation regimen "volume replacement" plus "dynamic support" (cardiac support and myocardial protection) have been proposed based on our previous studies.
Burns ; complications ; metabolism ; Humans ; Hypoxia ; etiology ; prevention & control ; Myocardial Reperfusion Injury ; etiology ; prevention & control ; Myocardium ; metabolism

Animals ; Humans ; Ischemic Preconditioning, Myocardial ; methods ; Myocardial Ischemia ; complications ; therapy ; Myocardial Reperfusion ; methods ; Myocardial Reperfusion Injury ; etiology ; prevention & control

OBJECTIVETo investigate the clinical implications of reperfusion arrhythmias during primary percutaneous coronary intervention (PCI) for patients with acute myocardial infarction (AMI).

METHODSData from 228 AMI patients in whom the infarct-related artery (IRA) were successfully recanalized by primary PCI were retrospectively analyzed. The 228 patients were divided into 2 groups: myocardial ischemia-reperfusion injury (MIRI) group (n=119) in whom MIRI events occurred within minutes after successful recanalization of IRA, and non-MIRI group (n=109). The 119 patients in MIRI group were further divided into 3 subgroups: severe bradycardia with hypotension (brady-arrhythmia subgroup), lethal ventricular arrhythmias requiring electrical cardioversion (tachy-arrhythmia subgroup), and IRA antegrade flow less than or equal to TIMI 2 grade without angiographic evidence of abrupt closure (no-reflow subgroup).

RESULTS(1) Clinical and angiographic data: Compared with non-MIRI group, MIRI group was characterized by more inferior infarct location, shorter ischemic duration, more frequently right coronary artery as IRA, more diseased vessels, more often TIMI 0 grade of initial antegrade flow in IRA, less pre-infarction angina, more renal insufficiency, and higher in-hospital mortality (13.4% vs. 4.6%, P=0.021). (2) The peak CK level was remarkably lower in brady-arrhythmia subgroup than that in non-MIRI group (2010 IU/L vs. 2521 IU/L, P=0.039). The peak CK or CK-MB level was notably higher in no-reflow subgroup than in non-MIRI group (4573 IU/L, 338 IU/L, respectively, P=0.000). (3) Left ventricular ejection fraction in no-reflow subgroup was significantly lower than in non-MIRI group (38.7% +/- 8.3% vs. 51.2% +/- 8.1%, P=0.000), left ventricular end-diastolic volume in no-reflow subgroup was greater than that in tachy-arrhythmia subgroup [(135 +/- 32) ml vs. (105 +/- 19) ml, P=0.029].

CONCLUSIONReperfusion arrhythmias may imply the existence of much survived myocardium and do not enhance myocardial damage, while no-reflow increases myocardial injury and induces permanent impairment of cardiac function.

Arrhythmias, Cardiac ; complications ; Cell Survival ; Humans ; Myocardial Infarction ; therapy ; Myocardial Reperfusion ; Myocardial Reperfusion Injury ; etiology ; Myocardium ; enzymology ; Retrospective Studies

OBJECTIVESulfur dioxide was considered to be toxic and detrimental to human health. However, this review highlights recent advances that suggest sulfur dioxide might be a novel endogenous gaseous signaling molecule involved in the regulation of cardiovascular functions.

DATA SOURCESThe data used in this review were mainly from the studies reported in Medline and PubMed published from 1986 to 2010.

STUDY SELECTIONOriginal articles and critical reviews selected were relevant to exogenous and endogenous sulfur dioxide.

RESULTSThe sulfur dioxide/aspartate amino transferase pathway is endogenously generated in the cardiovascular system, and sulfur dioxide shows broad bioactive effects, such as antihypertension, vasodilation, and amelioration of vascular remodeling. A disturbed sulfur dioxide/aspartate amino transferase pathway is known to be involved in the pathogenesis of many cardiovascular diseases, such as ischemia-reperfusion injury, monocrotaline-induced pulmonary hypertension, athrosclerosis, spontaneous hypertension and hypoxic pulmonary hypertension. Furthermore, in experimental studies the prognosis of these cardiovascular diseases can be improved by targeting endogenous sulfur dioxide.

CONCLUSIONThe findings suggest that sulfur dioxide is a novel endogenous gaseous signaling molecule involved in the regulation of cardiovascular functions.

Animals ; Cardiovascular Diseases ; etiology ; Humans ; Hypertension, Pulmonary ; etiology ; Myocardial Reperfusion Injury ; etiology ; Rats ; Rats, Inbred SHR ; Signal Transduction ; physiology ; Sulfur Dioxide ; metabolism

Interests on the effects of cytochrome P450 (CYP450) monooxygenases and epoxyeicosatrienoic acids (EETs) on myocardial ischemic-reperfusion injury has been increased in recent years. The CYP450/EET system may influence the degree of myocardial ischemic-reperfusion injury through "poly-targets", such us oxygen free radical, calcium overload, leukocytes adherence, nitric oxide, ATP-sensitive K+ channels, and mitogen activated protein kinase. The exaggeration or recovery of injury depends on the physical status. Study of factors that affects CYP450/EET, particularly identification of their involvement in cardioprotective signaling and specific roles, will elucidate the mechanisms of myocardial ischemic-reperfusion injury, and find a new way of prevention and treatment. This article will review the relationship between the changes of CYP450/EETs system and myocardial ischemic-reper-
Animals ; Cytochrome P-450 Enzyme System ; metabolism ; Eicosapentaenoic Acid ; metabolism ; Humans ; Mixed Function Oxygenases ; metabolism ; Myocardial Reperfusion Injury ; etiology ; metabolism

AIMTo investigate the expression and role of inducible NOS (iNOS) and endothelial NOS (eNOS) in acute lung injury following limb ischemia/reperfusion (4h/4h).

METHODSWistar rats were randomized into four groups: control group, ischemia/reperfusion (I/R) group, L-Arginine (L-Arg) pretreatment group, Aminoguanidine (AG) pretreatment group. The lung tissue of each group was subjected to assay of content of MDA, MPO, W/D and NO2-/NO3-. The expression of iNOS and eNOS was examined with immunohistological staining. The pulmonary morphologic changes were observed under microscope respectively.

RESULTSThe acute lung injury existed after limb ischemia/reperfusion. The eNOS downregulation and iNOS upregulation among I/R, L-Arg and AG groups were observed contrasted to the control group. There was no expressional and statistical difference of iNOS between I/R group and L-Arg group. The expression of eNOS was similar between IR and AG but iNOS expression was downregulated in AG. The parameters of MDA, MPO, W/D and NO2-/NO3- in pulmonary tissue were significantly increased in I/R groups compared with those of the control group. The parameters of L-Arg and AG pretreatment groups in comparison with those of the I/R group showed significantly difference. Based on the results of pulmonary pathology, the congestion and infiltration of inflammatory cells existed obviously in IR group. L-Arg played definite role in militating lung injury and AG might make lung injury aggravated.

CONCLUSIONThe NO definite production from iNOS is possible to play a competitivly protective role in acute lung injury following limb ischemia/reperfusion and antagonist of iNOS may aggravate the lung injury.

Acute Lung Injury ; etiology ; metabolism ; Animals ; Extremities ; blood supply ; Male ; Nitric Oxide Synthase Type II ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism

Animals ; Blood Gas Analysis ; Brain Ischemia ; complications ; metabolism ; physiopathology ; Lung Injury ; etiology ; metabolism ; physiopathology ; Male ; Pyrazines ; pharmacology ; Rats ; Rats, Wistar ; Reperfusion Injury ; complications ; metabolism ; physiopathology