Biomedical subjects

T Hobara

Publications and source records attributed to T Hobara.

63 records · Page 4Linked to original sources

PubMed1981

[Diminution of 1, 1, 1- and 1, 1, 2- trichloroethane in the blood and their excretion by the lungs (author's transl)].

In order to investigate the diminution of 1, 1, 1-trichloroethane (1, 1, 1-TCE) and 1, 1, 2-trichloroethane (1, 1, 2-TCE) in the blood and the excretion of them by the lungs, 100 mg and 50 mg per kg body weight of 1, 1, 1-TCE were intravenously administered to 12 and 13 dogs, respectively, and the same amounts of 1, 1, 2-TCE to 5 and 8 dogs, respectively. The arterial blood gathered and the expired air collected by the time up to 60 minutes after the injection were analysed with a FID-gas-chromatography for the concentrations of the solvents. The results obtained are as follows. 1. Concentrations of 1, 1, 1-TCE in the blood were maintained significantly lower always from 2 to 60 minutes after the injection than those of 1, 1, 2-TCE. 2. While highest concentrations of the solvents in the expired air were found about 1 minute after the injection for both 1, 1, 1-and 1, 1, 2-TCE, values 1 minute after for the former were seven to ten times higher than those for the latter. However, no significant differences in the concentration were seen between both solvents after 15-40 minutes of administration in the expired air. 3. Ratios of the amounts expired by the lungs during 60 minutes after the injection to the total were 61-68% for 1, 1, 1-TCE, whereas only 21-32% for 1, 1, 2-TCE, respectively. 4. Highly significant linear regression was found between the concentrations of the solvent in the blood and those in the expired air for each of 1, 1, 1- and 1, 1, 2-TCE.

Animals↗

PubMed1981

[A role of the autonomic nervous system in alterations of blood pressure and heart rate induced by 1, 1, 1-trichloroethane (author's transl)].

An experiment was conducted to clarify effect of 1, 1, 1- trichloroethane (1, 1, 1-TCE) on blood pressure and heart rate, and to investigate the role of the autonomic nervous system in these responses. Adult mongrel dogs were anesthetized with sodium pentobarbital (25-30 mg/kg, i. v.) and the respiration was maintained artificially with positive pressure ventilation. Fifty mg/kg of 1, 1, 1-TCE was intravenously injected. The left kidney was exposed by flank incision, and discharges of efferent renal sympathetic nerve were recorded using bipolar platinum electrodes. 1, 1, 1-TCE induced 39.6 +/- 3.1% (mean +/- S. E.) diminution in systemic blood pressure compared to each pre-administration level, but the blood pressure gradually returned to the control level in the vagi intact group. A fall in blood pressure to 39.3 +/- 5.1% level was induced by 1, 1, 1-TCE in the group which had been bilaterally vagotomized or treated with atropine, but it was not significantly different from that in the vagi intact group. Immediately after the administration of 1, 1, 1-TCE, heart rate significantly decreased from 122, 3 +/- 9.1 to 86 +/- 5.6 beats/min in the vagi intact group, but remained unchanged in the vagotomy or atropine group. Discharges of efferent renal nerve were augmented and blood pressure fell, after injection of nitroglycerin. A decrease in the discharge of efferent renal sympathetic nerve and an increase in the blood pressure were observed after injection of norepinephrine. On the other hand, discharges obviously decreased dispite a fall in the blood pressure after administration of 1, 1, 1-TCE. This response showed that the decrease of efferent renal sympathetic nerve activity may be related to the fall in the blood pressure after 1, 1, 1-TCE. On the basis of the results obtained, it is suggested that the autonomic nervous system may play a major role in the effects of 1, 1, 1-TCE on the blood pressure and heart rate in anesthetized dogs.

Animals↗

PubMedDate not supplied

Biliary excretion of trichloroethylene and its metabolites in dogs.

To examine the biliary excretion of trichloroethylene (TRI) and its metabolites, we carried out various experiments with TRI and its metabolites, i.e., chloral hydrate (CH), free-trichloroethanol (F-TCE) and trichloroacetic acid (TCA), using anesthetized dogs. The amount of biliary excretion was significantly increased with the administration of CH and F-TCE, whereas it remained at control levels with the administration of TRI and TCA. The substances excreted into bile were conducted in the form of conjugated-TCE (Conj-TCE) in over 90% of the CH, F-TCE and TRI administration groups. About 95% of these Conj-TCE were conjugated with glucuronic acid. The cumulative excretion ratios of substances and metabolites to dose were 20% for CH and F-TCE, and about 1% for TCA and TRI 2 h after administration.

Animals↗

PubMedDate not supplied

Neural control of blood pressure following 1,1,1-trichloroethane inhalation: a role of sympathetic nervous system.

The effects of 1,1,1-trichloroethane (1,1,1-TCE) inhalation on arterial blood pressure and renal sympathetic nerve activity were investigated in anesthetized dogs. In acute inhalation experiments, the threshold concentration of 1,1,1-TCE required to produce a decrease in blood pressure was 0.4 to 0.5% in inspired air; moreover, a dose-response relationship between the decrease in blood pressure and 1,1,1-TCE concentration which exceeded the threshold level was observed. In addition, renal nerve activity increased and was associated with a slight decrease in blood pressure following inhalation of relatively low concentrations of 1,1,1-TCE. Following inhalation of relatively high concentrations of 1,1,1-TCE, however, renal nerve activity decreased and was accompanied by a marked decrease in blood pressure. Opposite reactions of renal nerve activity were observed when blood pressure decreased to 70-80 mm Hg following inhalation. It is suggested that systemic hypotension resulting from 1,1,1-TCE inhalation may be controlled by two different reactions of sympathetic nerve activity.

Animals↗

PubMedDate not supplied

Peripheral vasodilatation following 1,1,1-trichloroethane inhalation: peripheral vessels as a site of action.

The effects of 1,1,1-trichloroethane (1,1,1-TCE) inhalation on total peripheral vascular resistance and the possibility of the peripheral vessels being a site of action for 1,1,1-TCE were investigated in anesthetized dogs. In acute inhalation experiments, a decrease in total peripheral vascular resistance was observed following inhalation of 1,1,1-TCE concentrations sufficient to induce systemic hypotension. The threshold concentration of 1,1,1-TCE required to produce a decrease in perfusion pressure of the isolated hindlimb was approximately 0.4-0.5% in inspired air. A dose-response relationship between the decrease in perfusion pressure and 1,1,1-TCE concentration, which exceeded the threshold level, was observed. It is suggested that the decrease in total peripheral vascular resistance is related to systemic hypotension following 1,1,1-TCE inhalation; further, this vasodilator effect may be induced in the peripheral vessels, which is one of the sites where 1,1,1-TCE acts.

Animals↗

PubMedDate not supplied

Respiratory disorders following 1,1,1-trichloroethane inhalation: a role of reflex mechanism arising from lungs.

The effects of 1,1,1-trichloroethane (1,1,1-TCE) inhalation on respiration and afferent activity of the lung stretch receptor were investigated in anesthetized dogs. In acute inhalation experiments, rapid and shallow breathing was observed following inhalation of high 1,1,1-TCE concentrations. The threshold concentration of 1,1,1-TCE to produce an increase in respiratory rate was approximately 0.9% in inspired air. Moreover, a dose-response relationship was observed between the increase in respiratory rate and concentrations which exceeded the threshold level. An inspiratory action of respiration markedly decreased for high 1,1,1-TCE concentrations. Both the increase in respiratory rate and the decrease in the inspiratory action for high 1,1,1-TCE concentrations were significantly inhibited, however, these reactions were not completely blocked by bilateral vagotomy. Afferent impulses of the lung stretch receptor in the vagus nerve obviously increased following 1,1,1-TCE whose concentrations were more than 0.9% in inspired air. It is suggested that rapid and shallow breathing following higher 1,1,1-TCE concentrations may be related to the increase in the activity of the lung stretch receptor. It is further suggested that a part of rapid and shallow breathing is not based on anesthetic effects but enhancement of Hering Breuer reflex following 1,1,1-TCE inhalation.

Action Potentials↗

PubMedDate not supplied

Effect of 1,1,1-trichloroethane inhalation on heart rate and its mechanism: a role of autonomic nervous system.

The response of heart rate to acute 1,1,1-trichloroethane (1,1,1-TCE) inhalation and its mechanism via the autonomic nervous system were studied in anesthetized dogs in acute inhalation experiments. Concentrations of 1,1,1-TCE in inspired air of 1.32 +/- 0.14% (mean +/- S.E.) increased heart rate, but 2.79 +/- 0.24% decreased heart rate. Opposite reactions of heart rate were observed when blood pressure decreased to 70-80 mm Hg following inhalation. Moreover, both tachycardia from relatively low concentrations and bradycardia from higher concentrations were blocked by pre-administration of adrenergic beta blocker, but were only slightly affected by vagotomy. It is suggested that both tachycardia and bradycardia following 1,1,1-TCE inhalation may be controlled by the sympathetic nervous system.

Administration, Inhalation↗

PubMedDate not supplied

Influence of heart rate on left ventricular dp/dt following 1,1,1-trichloroethane inhalation.

The effect of acute 1,1,1-trichloroethane (1,1,1-TCE) inhalation on left ventricular contractility and influence on heart rate were investigated in anesthetized dogs. In the acute inhalation experiment, a decrease in the maximum left ventricular dp/dt (peak dp/dt) was observed following inhalation of higher 1,1,1-TCE contentrations. The threshold concentration of 1,1,1-TCE that decreased peak dp/dt was approximately 0.2% in inspired air. A dose-response relationship was observed between the decrease in peak dp/dt and 1,1,1-TCE concentration. Heart rate recorded simultaneously increased with relatively low concentrations and decreased with higher concentrations. Increase or decrease in peak dp/dt was observed to be dependent on changes in heart rate induced by right atrial pacing. Thus, the degree of the decrease in peak dp/dt during pacing experiments was compared with those of nonpacing experiments. At low concentrations, peak dp/dt during pacing decreased more than in nonpacing experiments. With higher concentrations, the decreases in peak dp/dt during pacing was slightly less than in the nonpacing experiments. Heart rate may be important in regulating peak dp/dt for relatively low 1,1,1-TCE concentrations. However, the effect of heart rate on peak dp/dt is slight at higher concentrations.

Administration, Inhalation↗

PubMedDate not supplied

Effects of diethyldithiocarbamate on activating mechanisms of neutrophils.

The effects of diethyldithiocarbamate on superoxide release by rat neutrophils were investigated in a chemiluminescence study. Diethyldithiocarbamate augmented lucigenin-dependent chemiluminescence in a concentration-dependent manner and inhibited luminol-dependent chemiluminescence at concentrations of 0.1-1 microM. In contrast, after the addition of 0.1 mM diethyldithiocarbamate, the chemiluminescence was markedly enhanced. Diethyldithiocarbamate inhibited both the myeloperoxidase activity of neutrophils and the chemiluminescence generated in a cell-free horseradish peroxidase/H2O2 and H2O2/HOCl system. The increase in lucigenin-dependent chemiluminescence brought about by diethyldithiocarbamate was inhibited by H-7, ML-7, W-7, EGTA and pertussis toxin. These results suggest that diethyldithiocarbamate may stimulate O2- production by a guanosine 5'-triphosphate protein-mediated and Ca(2+)-dependent process and that the increase in O2- release by neutrophils may be dependent not only on the direct stimulation of the signal transduction pathway but also on the increase in O2- by reducing the effect of the hydroperoxide (H2O2)-myeloperoxidase system.

Acridines↗