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S Oohashi

Publications and source records attributed to S Oohashi.

7 recordsLinked to original sources
PubMed2001

Continuous intra-jugular venous blood-gas monitoring with the Paratrend 7 during hypothermic cardiopulmonary bypass.

We measured the accuracy of the continuous intra-vascular blood-gas monitoring system (Paratrend 7, PT7) placed in the jugular venous bulb in 18 adult patients having cardiac or aortic surgery with hypothermic cardiopulmonary bypass (CPB). After induction of anaesthesia, a PT7 sensor was inserted through a 20-gauge venous catheter into the right jugular venous bulb. Blood samples were drawn from the venous catheter and measured with a blood gas analyser (BGA). Five to eight paired measurements using the PT7 and blood samples were made per patient, and bias and precision were calculated for each patient using the Bland-Altman method. The ranges for the blood sample measurements were: pH 7.12 to 7.59, PCO(2) 3.7 to 9.6 kPa, PO(2) 3.5 to 16.0 kPa, oxygen saturation 40 to 99%, bicarbonate 18.6 to 34.4 mmol l(-1), and base excess -7.8 to 12.5 mmol l(-1). Bias and precision values were 0.014/0.071 for pH, 0/0.90 kPa for PCO(2), and -0.16/1.18 kPa for PO(2). These values were comparable with those previously made on arterial blood. However, precision for oxygen saturation in each patient varied 2.3 to 23.6% (95% CI: 6.3 to 12.9%), which was unsatisfactory for clinical measurements. Deep hypothermia ( approximately 19.6 degrees C) and marked haemodilution ( approximately 13.5%) during CPB did not influence the reliability of the PT7 sensor. Thus, we concluded that continuous intra-jugular venous blood-gas monitoring is clinically feasible using the PT7 and may provide valuable information during CPB.

Adult↗
PubMed1991

Intranasal administration of His-D-Trp-Ala-Trp-D-Phe-LysNH2 (growth hormone releasing peptide) increased plasma growth hormone and insulin-like growth factor-I levels in normal men.

The effects of intranasal and iv administration of His-D-Trp-Ala-Trp-D-Phe-LysNH2 (GHRP) on plasma GH, PRL, LH, FSH, TSH, cortisol, insulin, IGF-I as well as GHRH-like immunoreactivity (LI) levels were examined in 6 healthy male subjects. An iv bolus injection of GHRP(1 micrograms/kg BW) caused a remarkable increase in plasma GH levels with a mean (+/- SE) peak of 54.9 +/- 4.2-micrograms/L. In addition an intranasal administration of GHRP resulted in a significant, dose-related increase in plasma GH with peaks of 39.6 +/- 15.3 micrograms/L at a dose of 30 micrograms/kg BW, 14.1 +/- 5.0 micrograms/L at 15 micrograms/kg BW and 7.5 +/- 5.7 micrograms/L at 5 microgram/kg BW. Plasma PRL and cortisol levels were slightly but significantly increased after iv administration of GHRP, whereas GHRP totally failed to affect plasma TSH, LH, FSH, insulin, blood sugar and GHRH-LI levels. Seven consecutive, intranasal administrations of 15 micrograms/kg BW GHRP every 8h were well tolerated in all subjects examined. During this treatment, GH responsiveness to GHRP was not attenuated by desensitization and plasma IGF-I was increased from 94.5 +/- 5.8 micrograms/L before GHRP to 125.8 +/- 6.0 micrograms/L after repeated GHRP administration. These findings indicate that intranasal administration of GHRP stimulates GH secretion and consequently enhances IGF-I production in normal subjects. If GHRP is demonstrated to be beneficial in the treatment of some patients with GH deficiency, the intranasal route of administration may be more useful than the painful injection because a prolonged period is required for the treatment.

Administration, Intranasal↗
PubMed1987

Immunoperoxidase evaluation of pneumonic lesions induced by Pasteurella haemolytica in calves.

Calves inoculated with Pasteurella haemolytica serovar 1 developed lesions of coagulation necrosis in the lungs that were sharply demarcated by leukocytes. The P haemolytica antigen was detected in the area of coagulation necrosis in histologic sections, using an immunoperoxidase technique. In the central area of the necrotic tissue, the bacterial antigen was diffusely presented in the necrotic alveolar wall, fibrin, serous exudate, and degenerated leukocyte. The bacterial antigen also was found in some groups of degenerating leukocytes around the necrotic tissue. The bacterial colonies among these leukocytes had strong specific reactions against P haemolytica. The bacterial antigen was observed in the cytoplasm of macrophages in alveoli around the necrotic lesion. These findings confirmed that coagulation necrosis is an important lesion in calves with pneumonia caused by P haemolytica.

Animals↗