Lung-lung interaction in isolated perfused unilateral hyperventilated rat lungs.

The technique of conducting high tidal volume (TV) ventilation-induced lung inflammation including remote organs is still open to discussion, and our aim is to investigate this issue in isolated ventilated rat lungs perfused with salt solution. Selective right lung (RL) hyperventilation (TV of 15 mL/kg with air containing 5% CO(2) on zero or 2.5 cm H(2)0 end expiratory pressure [ZEEP or PEEP] in addition to left lung (LL) on 2.

A longer duration of polymyxin B-immobilized fiber column hemoperfusion improves pulmonary oxygenation in patients with septic shock.

Endotoxin plays an important role in the pathogenesis of septic shock. Exposure of endothelial cells to endotoxin activates endothelial cells and increases the surface expression of adhesion molecules, markers of endothelial damage in organ dysfunction. Endotoxin adsorption therapy by polymyxin B-immobilized fiber column (PMX) hemoperfusion has been used for the treatment of septic shock patients.

Salvage of nonischemic control lung from injury by unilateral ischemic lung with apocynin, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, in isolated perfused rat lung.

Ischemia reperfusion (I/R) injury of the lung affects the function of the nonischemic lung. Our objective is to determine how apocynin, which is a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, protects the nonischemic control right lung (RL) from injury by the unilateral ischemic left lung (LL). In isolated ventilated (by air containing 5% CO(2)) rat lungs, in which differential perfusion of the RL or LL was feasible, the LL was selectively made ischemic (60 min) and reperfused (30 min) in a nonrecirculating or recirculating manner with buffer (Krebs-Henseleit) solution, or in a recirculating manner with buffer that contained apocynin (10 mmol/L) or apocynin + TACEI (tumor necrosis factor)-alpha converting enzyme inhibitor; 10 microg/mL) (each group: n = 12) or with buffer that contained SOD (superoxide dismutase, 3000 U before ischemia and at reperfusion) or SOD + TACEI (each group: n = 5).

Apaf-1-deficient fog mouse cell apoptosis involves hypo-polarization of the mitochondrial inner membrane, ATP depletion and citrate accumulation.

To explore how the intrinsic apoptosis pathway is controlled in the spontaneous fog (forebrain overgrowth) mutant mice with an Apaf1 splicing deficiency, we examined spleen and bone marrow cells from Apaf1(+/+) (+/+) and Apaf1(fog/fog) (fog/fog) mice for initiator caspase-9 activation by cellular stresses. When the mitochondrial inner membrane potential (Deltapsim) was disrupted by staurosporine, +/+ cells but not fog/fog cells activated caspase-9 to cause apoptosis, indicating the lack of apoptosome (apoptosis protease activating factor 1 (Apaf-1)/cytochrome c/(d)ATP/procaspase-9) function in fog/fog cells. However, when a marginal ( approximately 20%) decrease in Deltapsim was caused by hydrogen peroxide (0.

Effects of human atrial natriuretic peptide on renal function in patients undergoing abdominal aortic aneurysm repair.

Objective: Ischemia-reperfusion injury is an important cause of renal dysfunction after abdominal aortic aneurysm repair. Human atrial natriuretic peptide (hANP) is a potent endogenous natriuretic, diuretic, and vasorelaxant peptide. The objective of the present study was to evaluate the effects of hANP on renal function in patients undergoing abdominal aortic aneurysm repair.

Pioglitazone reduces systematic inflammation and improves mortality in apolipoprotein E knockout mice with sepsis.

Objective: To determine whether peroxisome proliferator-activated receptor (PPAR) gamma ligands improve survival of patients with septic shock we treated a mouse model of sepsis [apolipoprotein (Apo) E) knockout mice] with pioglitazone, a PPAR-gamma ligand. ApoE knockout mice have a high mortality rate due to sepsis because the endotoxin is not cleared.

Design And Setting: Prospective study in a university laboratory.

Nonischemic lung injury by mediators from unilateral ischemic reperfused lung: ameliorating effect of tumor necrosis factor-alpha-converting enzyme inhibitor.

We hypothesized that the ischemic reperfused (I/R) lung expresses and liberates tumor necrosis factor-alpha (TNF-alpha) to injure the nonischemic lung, and that a TNF-alpha-converting enzyme inhibitor (TACEI) prevents injury of the nonischemic lung by blocking TNF-alpha liberation from the I/R lung. In isolated ventilated rat lungs in which differential perfusion to the right (RL) or left (LL) lung was feasible, LLs were selectively made ischemic (60 min) while maintaining perfusion to RLs, then reperfused (30 min) in a nonrecirculating manner with buffer solution (non-R; n = 18) or in a recirculating manner with buffer containing TACEI (TACEI[+]; n = 18) or without TACEI (TACEI[-]; n = 18). Ischemia reperfusion induced TNF-alpha messenger RNA expression in the ischemic LLs; the expression was highest in TACEI(+) group (P < 0.

Blockade of nuclear factor-kappaB activation prevents hypodynamic shock and gastric hypoperfusion induced by endotoxin in anesthetized dogs.

Objective: To investigate whether pyrrolidinone derivative (N2733), an inhibitor of nuclear factor (NF)-kappaB activation, improves altered metabolic and hemodynamic changes and organ dysfunctions caused by endotoxic shock.

Design And Setting: Prospective, randomized, animal study in a laboratory at a university hospital.

Subjects: Twenty-three anesthetized male beagle dogs (10-14 kg).

Atrial natriuretic peptide infusion improves ischemic renal failure after suprarenal abdominal aortic cross-clamping in dogs.

Objective: The suprarenal abdominal aortic cross-clamping during aortic aneurysm repair causes renal dysfunction after surgery. Atrial natriuretic peptide (ANP), a hormone synthesized by the cardiac atria, induces diuresis-natriuresis and increases glomerular filtration rate. Therefore, we tested the hypothesis that prophylactic ANP infusion could limit the development of acute renal failure after aortic cross-clamping.

Relationships of circulating nitrite/nitrate levels to severity and multiple organ dysfunction syndrome in systemic inflammatory response syndrome.

Excessive nitric oxide (NO) production has been implicated to be responsible for the development of septic shock. To determine whether plasma nitrite/nitrate (NOx) levels are related to the severity of systemic inflammatory response syndrome (SIRS) and the degree of multiple organ dysfunction, we studied plasma NOx levels in 70 patients with SIRS consisting of noninfectious SIRS (n = 32), sepsis (n = 23), and septic shock (n = 15). Infection is a microbial phenomenon characterized by an inflammatory response to the presence of microorganism.

An increase in urinary nitrite/nitrate excretion is associated with the hyperdynamic state after cardiovascular surgery.

Objectives: To test the hypotheses (1) that nitric oxide (NO) production is stimulated after cardiovascular surgery and is related to the hyperdynamic state and (2) that NO production is more prominent in patients with cardiopulmonary bypass.

Design: Prospective, clinical study.

Setting: Intensive care unit in a university hospital.

Atrial natriuretic peptide improves pulmonary gas exchange by reducing extravascular lung water in canine model with oleic acid-induced pulmonary edema.

Objective: The purpose of this study was to examine and compare the effects of atrial natriuretic peptide and furosemide on pulmonary gas exchange, hemodynamics, extravascular lung water, and renal function in a dog model of oleic acid-induced pulmonary edema.

Design: Prospective, comparable, experimental study.

Setting: Laboratory at a university hospital.

Continuous monitoring of gastric intraluminal carbon dioxide pressure, cardiac output, and end-tidal carbon dioxide pressure in the perioperative period in patients receiving cardiovascular surgery using cardiopulmonary bypass.

Objective: To verify the hypothesis that the gastric intraluminal PCO2 (PgCO2) changes independently of the change in cardiac output (CO) during and after cardiovascular surgery using cardiopulmonary bypass (CPB), and that the elevation of PgCO2 affects the patients' morbidity.

Design: Prospective, noninterventional study.

Setting: Medical/surgical intensive care unit and operating theater of a university hospital.