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Biomedical subjects

K Tajimi

Publications and source records attributed to K Tajimi.

31 records · Page 2Linked to original sources
PubMed1986

Impaired effect of dopamine on cardiac output during octopamine infusion.

The hemodynamic effects of octopamine (OCT) were studied before and during dopamine (DA) infusion in six normal dogs. Before OCT infusion, DA significantly increased cardiac index (CI) from 3.24 +/- 0.20 to 4.90 +/- 0.30 L/min X m2 and significantly decreased systemic vascular resistance index (SVRI) from 3700.2 +/- 212.5 to 2618.3 +/- 156.6 dyne X sec/cm5 X m2, without changing heart rate. During OCT infusion, DA failed to increase CI or decrease SVRI; however, it significantly increased heart rate from 153.3 +/- 12.9 to 183.0 +/- 17.0 beat/min. This suppression of a DA-related increase in cardiac output may explain why DA is ineffective in those septic patients with elevated plasma OCT levels.

Analysis of Variance↗
PubMed1985

Effect of reduced glutathione on hemodynamic responses and plasma catecholamine levels during metabolic acidosis.

The effects of reduced glutathione (GSH) on plasma catecholamine (CA) levels and hemodynamics were studied in seven severely acidotic dogs, before and after dopamine (DA) infusion. Seven other dogs, also acidotic, received lactated Ringer's solution instead of GSH. Although metabolic acidosis decreased cardiac index (CI) in both groups, the decrease was significantly less in the GSH group. The significantly increased systemic vascular resistance index (SVRI) in the control group was suppressed by GSH infusion, although similarly high plasma CA levels were maintained in both groups. This suggests that GSH has certain vasodilating effects not related to adrenosympathetic activity. CI did not improve and DA infusion significantly increased SVRI in the control group, whereas CI increased with a mild decrease of SVRI in the GSH group. The rise of plasma norepinephrine after DA infusion was low in the GSH group compared to the increase in the control group. This study suggests that during acidosis GSH improves hemodynamics and restores the effects of DA on cardiac output.

Acidosis↗
PubMed1985

Effects of dopamine and dobutamine on hemodynamics and plasma catecholamine levels during severe lactic acid acidosis.

This study was designed to evaluate the effects of dopamine and dobutamine on hemodynamics and plasma catecholamine levels during experimental lactic acid acidosis in dogs. During the normal acid-base state (pH 7.4, PCO2 40 mm Hg), cardiac output and stroke volume were significantly increased and systemic vascular resistance was decreased by the infusion of dopamine or dobutamine 20 mcg/kg/min. Dobutamine produced identical changes in cardiac output, stroke volume, and systemic vascular resistance even during severe lactic acid acidosis (pH 7.0, PCO2 40 mm Hg). Dopamine, however, failed to increase cardiac output and stroke volume and to decrease systemic vascular resistance during lactic acidosis. The plasma norepinephrine level was elevated from 0.49 to 3.01 ng/ml during normal acid-based state and from 1.76 to 9.53 ng/ml during severe lactic acid acidosis by the infusion of dopamine. Dobutamine infusion did not affect the plasma norepinephrine level during normal acid-base state but reduced the level during lactic acid acidosis. The marked increase in plasma norepinephrine following dopamine infusion may explain both the decrease in cardiac output and the increase in systemic vascular resistance in response to dopamine infusion during severe lactic acid acidosis. These results indicate that dobutamine may be more useful than dopamine in improving cardiac output during severe acidosis.

Acid-Base Equilibrium↗
PubMed1983

Plasma catecholamine levels and hemodynamic responses of severely acidotic dogs to dopamine infusion.

Changes in plasma catecholamine (CA) levels and hemodynamic responses after a dopamine (DA) infusion of 20 micrograms/kg body weight per min were studied in dogs with a normal acid-base state (pH 7.4, PaCO2 40 torr) and in the same animals after induction of severe metabolic acidosis (pH 7.0, PaCO2 40 torr). DA increased plasma norepinephrine (NE) levels from .487 +/- .109 ng/ml to 3.077 +/- 0.357 ng/ml in the normal acid-base state, and from 1.762 +/- .521 ng/ml to 9.533 +/- 1.403 ng/ml in acidosis. Plasma epinephrine (E) levels in normal and acidotic states were also increased by DA infusion. In the normal acid-base state DA increased myocardial contractility and cardiac index (CI). DA also increased myocardial contractility during acidosis, but the response of CI to DA was abolished. DA significantly decreased systemic vascular resistance index (SVRI) in the normal acid-base state and significantly increased SVRI in acidosis. Acidosis appears to enhance the rate of conversion of DA to NE and E. The failure of DA to increase CI in acidosis may be a result of the increased afterload on the left ventricle.

Acidosis↗
PubMedDate not supplied

Involvement of IL-18 and soluble fas in patients with postoperative hepatic failure.

We measured the levels of tumor necrosis factor alpha (TNF-alpha), interleukins (IL)-6 and -18, and soluble Fas (sFas) in 11 patients with postoperative hepatic failure and assessed whether IL-18-mediated apoptosis is involved in the onset of liver dysfunction. The serum TNF-alpha, IL-18, and sFas levels were significantly higher in patients with sepsis as a complication than in those without sepsis. The TNF-alpha and IL-18 levels were significantly higher in nonsurvivors than in survivors. Significant correlations were observed between TNF-alpha and IL-6, between TNF-alpha and IL-18, and between TNF-alpha and sFas levels. These results showed that Fas-mediated hepatocyte apoptosis functions as an important mechanism responsible for the onset of postoperative hepatic failure in humans. They especially suggested that IL-18 and TNF-alpha function both as apoptosis-promoting factors and as apoptosis-inhibiting factors, depending on the conditions to which hepatocytes are subjected.

Aged↗