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Biomedical subjects

Chieko Mitaka

Publications and source records attributed to Chieko Mitaka.

12 recordsLinked to original sources
PubMed2007

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 < 0.01). The expression of TNF-alpha, which was detected as immunofluorescence signals on CD34-positive endothelial cells, was observed in ischemic LLs; the highest expression being that in the TACEI(+) group. Wet/dry ratio and protein content in bronchoalveolar lavage fluid were higher in LLs than in RLs, and among the RLs, these 2 parameters were significantly increased in the TACEI(-) group (P < 0.01) in which the RLs were exposed to the TNF-alpha-rich perfusate. On the other hand, protein content in bronchoalveolar lavage fluid of the TACEI(+) group in which RLs were exposed to recirculating perfusate containing little TNF-alpha was decreased to a level close to but still higher than that in the non-R group (P < 0.05). The unilateral I/R lung affected the permeability of the nonischemic lung by liberating mainly TNF-alpha and induced TNF-alpha, interleukin (IL)-1beta, IL-6, and IL-10 messenger RNA expression in the nonischemic lung. These findings support the idea of organ-organ interaction in which an injured organ affects a remote organ by liberating humoral mediators.

ADAM Proteins↗
PubMed2006

Prevention of ischemia reperfusion injury by positive pulmonary venous pressure in isolated rat lung.

Pulmonary ischemia-reperfusion (I/R) without tissue hypoxia induces inflammatory cytokine mRNA expression in the lung under the condition of 0 mm Hg pulmonary venous pressure (0PVP), which might be a cause of I/R injury. Our aim is to determine whether the pulmonary vascular endothelium expresses cytokine mRNAs and their corresponding proteins or develops I/R injury when positive PVP is maintained during ischemia to provide a positive stretch to the endothelium throughout the ischemic period. In isolated, perfused, and ventilated rat lungs, the right and left pulmonary arteries were isolated, and the left lung was selectively occluded for 60 min and then reperfused for 30 min. During ischemia, the left atrial pressure was maintained at 5 mm Hg (5PVP) or 0PVP. TNF-alpha, IL-1beta, IL-6, and IL-10 mRNA expression in the lungs was evaluated by RT-PCR and in situ hybridization, and the production and localization of corresponding proteins were determined by staining with fluorescence-labeled antibodies against the cytokines and an antibody against CD34. Pulmonary vascular/epithelial permeability was evaluated by measuring albumin content in bronchoalveolar lavage (BAL) fluid and wet/dry ratio. At 5PVP, there were no increases in the left lung perfusion pressure, albumin content in BAL fluid, wet/dry ratio, or expression of cytokine mRNAs and their corresponding proteins on the vascular endothelium by I/R. In contrast, at 0PVP, the increased expression of cytokine mRNAs and their corresponding proteins on the vascular endothelium by I/R was verified. The finding that the application of 5PVP during ischemia abolished the expression of cytokine mRNAs and their corresponding proteins as well as the I/R injury gives us new insights in the study of lung preservation for transplantation.

Animals↗
PubMed2005

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). INTERVENTIONS: Dogs were mechanically ventilated and monitored with a pulmonary arterial catheter and a gastric tonometer. A central venous catheter was inserted into the femoral vein, and lactated Ringer's solution (10 ml/kg per hour) was administered throughout the study period. Three groups of animals were studied: (a) the lipopolysaccharide (LPS) group (n=8), which received LPS (250 ng/kg per minute for 2 h); (b) the LPS plus N2733 group (n=8), which received N2733 (30 mg/kg intravenously and 10 mg/kg hour for 6 h) after the start of LPS; and (c) the N2733 group (n=7), which received N2733 (30 mg/kg intravenously and 10 mg/kg per hour for 6 h). MEASUREMENTS AND RESULTS: Changes in hemodynamics, blood gas, gastric intramural pH, and renal and hepatic function were measured for 6 h. Coadministration of N2733 increased oxygen delivery index and prevented the LPS-induced hypotension, metabolic acidosis, and gastric mucosal acidosis but did not affect renal or hepatic function. CONCLUSIONS: Administration of N2733 increased oxygen delivery index and prevented the LPS-induced hypotension and metabolic and gastric mucosal acidosis in an anesthetized canine endotoxic shock model, suggesting its beneficial effect on local blood flow against tissue hypoxia. These findings suggest that blockade of NF-kappaB activation prevents hypodynamic shock and gastric hypoperfusin in endotoxic shock.

Animals↗
PubMed2005

Clinical laboratory differentiation of infectious versus non-infectious systemic inflammatory response syndrome.

OBJECTIVE: To evaluate the accuracy of C-reactive protein (CRP), procalcitonin (PCT), neopterin, and endotoxin in the differential diagnosis of sepsis and non-infectious systemic inflammatory response syndrome (SIRS). METHODS: A Medline database and references from identified articles were used to perform a literature search relating to the differential diagnosis of sepsis versus non-infectious SIRS. RESULTS: CRP, PCT, and neopterin are released both in sepsis and in non-infectious inflammatory disease. CRP and PCT are equally effective, although not perfect, in differentiating between sepsis and non-infectious SIRS. However, CRP and PCT have different kinetics and profiles. The kinetics of CRP is slower than that of PCT, and CRP levels may not further increase during more severe stages of sepsis. On the contrary, PCT rises in proportion to the severity of sepsis and reaches its highest levels in septic shock. PCT tends to be higher in nonsurvivor than in survivor. Therefore, PCT demonstrated a closer correlation with the severity of sepsis and outcome than CRP. Unlike CRP and PCT, neopterin is increased in viral infection as well as bacterial infection, and neopterin is also a useful indicator of sepsis. Endotoxemia was detected in no more than half of patients with Gram-negative bacteremia, and Gram-negative bacteremia was detected in half of patients with endotoxemia. CONCLUSIONS: The diagnostic capacity of PCT is superior to that of CRP due to the close correlation between PCT levels and the severity of sepsis and outcome. Neopterin is very useful in the diagnosis of viral infection. The endotoxin assay in combination with CRP, PCT, or neopterin may help as a diagnostic marker for Gram-negative bacterial infection.

Animals↗
PubMed2004

Cytokine mRNA expression in unilateral ischemic-reperfused rat lung with salt solution supplemented with low-endotoxin or standard bovine serum albumin.

Our aim was to determine whether cytokine mRNA expression is induced by experimental manipulation including artificial perfusate or ischemia-reperfusion (I/R) in an isolated, perfused rat lung model. Constant pulmonary flow [Krebs-Henseleit solution supplemented with low-endotoxin (LE) or standard (ST) bovine serum albumin 4%, 0.04 ml/g body wt] and ventilation were maintained throughout. Right and left pulmonary arteries were isolated, and the left pulmonary artery was occluded for 60 min and then reperfused for 30 min. Analysis of tumor necrosis factor-alpha, IL-1 beta, IL-6, IL-10, and IFN-gamma mRNA expression by RT-PCR and evaluation of vascular permeability by bronchoalveolar lavage (BAL) fluid albumin content were conducted separately in right and left lung. Both LE and ST groups (each 12 rats) showed increases in vascular permeability by I/R (BAL fluid albumin content: 5.53 +/- 1.55 vs. 15.63 +/- 8.87 and 4.76 +/- 2.71 vs. 16.72 +/- 4.85 mg.ml BAL fluid-1.g lung dry wt-1, mean +/- SD; right vs. left lung in LE and ST groups, P < 0.05 between right and left). Cytokine mRNA expression was significantly higher in the I/R lung than in the control lung in the LE group, whereas it was higher in the control lung in the ST group (P < 0.05). mRNAs of not only proinflammatory but also anti-inflammatory cytokines were expressed in I/R lung, which are expected to aggravate I/R injury. The reversed pattern of cytokine mRNA expression in the ST group was possibly due to the longer perfusion of control lung with perfusate containing endotoxin, which caused no lung damage without I/R.

Animals↗
PubMed2003

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. Positive culture for microorganism is regarded as infectious SIRS (sepsis and septic shock) and negative culture is regarded as noninfectious SIRS. Plasma samples collected from each patient within 24 h from admission to the intensive care unit were subjected for measurement of NOx levels, the stable end products of NO, by the high performance liquid chromatography-Greiss system. Mean plasma NOx levels in patients with SIRS were 52.8 +/- 44 microM/L, ranging from 8.1 to 186.2 microM/L. Plasma NOx levels were positively correlated with Acute Physiology, Age, and Chronic Health Evaluation (APACHE) III score (r = 0.414, P < 0.01) and sequential organ failure assessment (SOFA) score (r = 0.433, P < 0.01). Plasma NOx levels in patients with sepsis (51.0 +/- 38.5 microM/L) and septic shock (94.5 +/- 53.7 microM/L) were significantly (P < 0.01) higher than those in patients with noninfectious SIRS (25.8 +/- 16.9 microM/L) and healthy subjects (29.6 +/- 8.9 microM/L). Our study shows that plasma NOx levels are increased in patients with infectious, but not noninfectious SIRS, which increase as the severity of SIRS and the development of multiple organ dysfunction syndrome, suggesting its possible pathogenic role in SIRS.

APACHE↗
PubMed2003

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. DESIGN: Prospective, comparative, experimental study. SETTING: Laboratory at a university hospital. SUBJECTS: Twelve male beagle dogs (10-13 kg) with mechanical ventilation under pentobarbital anesthesia. INTERVENTIONS: A catheter was inserted into the femoral vein, and lactated Ringer solution (10 mL/kg/hr) was administered throughout the study period. Two groups of animals were studied: the control group (n = 6), which received saline vehicle before and after suprarenal abdominal aortic cross-clamping for 1.5 hrs; and the ANP group (n = 6), which received ANP (1 microg/kg/min) for 5 hrs, starting from 10 mins before suprarenal abdominal aortic cross-clamping until the end of procedure. MEASUREMENTS AND MAIN RESULTS: Changes in systemic and renal hemodynamics, blood gases, and renal function were measured at baseline and 1, 2, 3, 4, and 5 hrs after aortic cross-clamping. After aortic cross-clamping, urine volume, renal blood flow, and creatinine clearance significantly (p <.01) decreased, and serum creatinine concentrations significantly (p <.01) increased, but these effects were limited by continuous ANP infusion. CONCLUSIONS: The present study shows that ANP infusion preserved renal function after suprarenal abdominal aortic cross-clamping in dogs. These results justify a trial of ANP infusion in humans during aortic aneurysm repair.

Acute Kidney Injury↗
PubMed2002

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. PATIENTS: One hundred patients after cardiovascular surgery: coronary artery bypass graft with (n=53) and without (n=17) cardiopulmonary bypass, valve surgery with cardiopulmonary bypass (n=23) and thoracic aortic replacement with cardiopulmonary bypass (n=7). INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Urinary nitrite/nitrate (NOx) excretion was measured by the high-performance liquid chromatography-Griess system as an index of endogenous NO production during the first 2 postoperative days. Hemodynamic variables, hematologic variables and serum C-reactive protein concentrations were measured after the operation. Urinary NOx concentrations were 146+/-70 and 190+/-93 micro mol/l, and the amounts of NOx excreted in the urine were 23+/-10 and 18+/-8 micro mol/h on the 1st and 2nd days, respectively. Urinary NOx excretions were positively correlated with the cardiac index (P<0.01), but inversely correlated with the systemic vascular resistance index (P<0.01). Urinary NOx concentrations were positively correlated with serum C-reactive protein concentrations (P<0.01), but inversely correlated with the cardiopulmonary bypass time (P<0.01). The urinary NOx concentration was highest in patients undergoing coronary artery bypass graft without cardiopulmonary bypass. CONCLUSION: These findings suggest, firstly, that NO production is stimulated by a surgical inflammatory response and, secondly, that the endogenous NO contributes to the increase in cardiac output that accompanies the reduced systemic vascular resistance after cardiovascular surgery.

Aged↗
PubMed2002

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. PATIENTS: Sixteen adults patients receiving elective cardiovascular surgery using CPB. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: After induction of anesthesia, the patients were fitted with a gastric tube equipped at the tip with a CO2 sensor (ion-selective field effect transistor) that can continuously measure real-time PgCO2, and a pulmonary artery catheter capable of monitoring continuous CO (CCO) and end-tidal CO2. Data from the devices was uploaded to a personal computer every 2 mins until the catheter was pulled off based on clinical judgment (PgCO2 values were blinded to everyone except the investigator). One patient expired as a result of multiple organ failure subsequent to sepsis, and postoperative morbidity assessed by the peak SOFA (sequential organ failure assessment) score (mean +/- SD 6.9 +/- 3.5; range, 2-13) was correlated with the peak PgCO2 during intensive care unit stay (mean +/- SD 74.1 +/- 30.7 mm Hg; range, 45-169 mm Hg) (p < .01, by regression analysis). The peak PgCO2 during surgery (mean +/- SD 71.1 +/- 18.1 mm Hg; range, 44-115 mm Hg) had no correlation with the postoperative morbidity. From analysis of CCO before, during, and after returning from the above 60 mm Hg of PgCO2, PgCO2 changed independently of CCO. CONCLUSIONS: PgCO2 changed independently of CCO, and its postoperative elevation was related to morbidity, even in the group of patients with a good outcome. Continuous monitoring of PgCO2 is useful for the detection of morbidity and can be expected to help elucidate the pathophysiology of change of PgCO2.

Aged↗
PubMed2002

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. SUBJECTS: Eighteen male beagle dogs were studied under mechanical ventilation with pentobarbital anesthesia. INTERVENTIONS: Oleic acid (0.08 mL/kg) was injected and allowed for 1 hr to achieve pulmonary edema with hypoxemia at Fio2 of 0.3. After lung injury, dogs were divided into three groups; control group (n = 6) receiving saline (2.5 mL/hr for 5 hrs), atrial natriuretic peptide group (n = 6) receiving atrial natriuretic peptide (1 microg x kg(-1) x min(-1) for 5 hrs), and furosemide group (n = 6) receiving furosemide (1 mg x kg(-1) x hr(-1) for 5 hrs). MEASUREMENTS AND MAIN RESULTS: Hemodynamics, arterial blood gases, extravascular lung water, and renal function were measured hourly for 7 hrs after injury. Oleic acid increased extravascular lung water and induced hypoxemia. In the atrial natriuretic peptide group, extravascular lung water was significantly (p <.05) lower and Pao2 was significantly (p <.05) higher than in the control and furosemide groups, respectively. Pulmonary hypertension induced by oleic acid was attenuated by atrial natriuretic peptide infusion but not by saline or furosemide. Increased natriuresis/diuresis did not significantly differ between the atrial natriuretic peptide and the furosemide group, whereas creatinine clearance in the atrial natriuretic peptide group was significantly higher than that in the furosemide group. CONCLUSIONS: These findings suggest that atrial natriuretic peptide improves pulmonary gas exchange by reducing extravascular lung water and pulmonary arterial pressure, possibly independently from natriuresis/diuresis in oleic acid-induced pulmonary edema.

Animals↗