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Biomedical subjects

T Niimi

Publications and source records attributed to T Niimi.

121 records · Page 7Linked to original sources
PubMed1986

[Clinical studies on te concentration of cefaclor in sera and lung tissues of patients with respiratory diseases].

A 500 mg dose of cefaclor (CCL) was administered orally before surgery to each of patients with respiratory diseases and in fasting. Average concentrations of CCL in sera were 4.04 micrograms/ml at 1.5 hours, 3.03 micrograms/ml at 2 hours, 1.68 microgram/ml at 3 hours and 0.45 microgram/ml at 5 hours after administration. Average concentrations in lung tissues during operation were 0.120 microgram/g at 3 hours, 0.272 microgram/g at 4 hours and 0.297 microgram/g at 5 hours after administration. Ratios of concentrations of CCL in lung tissues to that in sera were from 7.1 to 66.0 percent. The CCL was considered to be a useful antibiotic for the treatment of patients with respiratory diseases.

Administration, Oral↗
PubMed1978

Chemical control of cerebral circulation. Modification by a new vasodilator (YC-93).

This study was undertaken to investigate influences of a new vasodilator, YC-93, a derivative of 1,4-dihydropyridine, on cerebral circulation and cerebrovascular CO2 reactivity. Cerebrocortical PO2, cerebrocortical PCO2, cerebrocortical blood flow and arterial blood pressure were continuously recorded by means of a PO2 electrode, a PCO2 electrode and a plate-type crossed thermocouple flowmeter placed on an exposed pial surface of the cat brain. The changes in each parameter induced by YC-93 were compared with those induced by papaverine hydrochloride. The effects of 5% CO2 inhalation were compared before and after the intravenous injection of YC-93. YC-93 (0.01 mg/kg) showed a more marked and longer-lasting hypotensive effect that papaverine (1 mg/kg) and yet produced a significant increase in cerebrocortical PO2. After the administration of YC-93, the degree of the increase in cerebrocortical PO2 during 5% CO2 inhalation was reduced significantly in comparison with that before the administration. The above data indicates that YC-93 has a vasodilating effect on cerebral blood vessels and that the drug causes a decrease in cerebrovascular CO2 reactivity.

Animals↗
PubMedDate not supplied

Modification of cerebrovascular CO2 reactivity by inhibition of dopamine beta-hydroxylase.

The influence of sympathetic nervous activity on cerebral circulation and cerebrovascular CO2 reactivity was investigated through inhibition of dopamine beta-hydroxylase (DBH). A PO2 electrode, a PCO2 electrode and a plate-type thermocouple-flowmeter were placed on the pial surface of the cat brain. Cerebrocortical PO2, PCO2, cerebrocortical blood flow and arterial blood pressure were continuously recorded before, during and after intracarotid infusion of 10 mg/kg of fusaric acid, a potent DBH inhibitor. The effects of 5% CO2 inhalation and hyperventilation were measured before and after the inhibition of DBH. Following the intracarotid infusion of fusaric acid, cerebrocortical PO2 and cerebrocortical blood flow increased significantly. After the inhibition of DBH, the degree of the increase in cerebrocortical PO2 during 5% CO2 inhalation was enhanced while the degree of the decrease in cerebrocortical PO2 during hyperventilation did not show any significant change. The cerebral vasodilatation caused by fusaric acid suggests that the sympathetic nervous system takes part in the resting tone of cerebral blood vessels. The increase in the cerebrovascular CO2 reactivity produced by the inhibition of DBH suggests that the sympathetic nervous system modifies cerebrovascular CO2 reactivity.

Animals↗