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H Tojima

Publications and source records attributed to H Tojima.

At least 73 records · Page 4Linked to original sources
PubMed1988

Arterial to end-tidal PCO2 difference varies with different ventilatory conditions during steady state hypercapnia in the rat.

To estimate the influence of ventilatory conditions on the CO2 equilibration between the alveolar gas and arterial blood during steady state hypercapnia, we measured arterial and end-tidal PCO2 (PaCO2, PETCO2) of the anesthetized rat under the following three conditions: spontaneously breathing with CO2 inhalation, artificial respiration with gas mixture containing CO2, and artificial respiration with reduced ventilatory volume (hypoventilation). In each ventilatory condition, PaCO2 correlated linearly with PETCO2. However, in spontaneously breathing animals, the PaCO2-PETCO2 difference which was positive in a control condition (without CO2 inhalation) became negative during CO2 inhalation. The mean (+/- S.D.) difference was -3.6 +/- 1.5 mmHg (n = 9, p less than 0.001) at the PETCO2 range from 72 to 77 mmHg. During artificial respiration with constant ventilatory volume, initial positive PaCO2-PETCO2 difference approached zero when CO2 was administered into inspiratory gas. In both ventilatory conditions the slope of the PETCO2-PaCO2 relation line was less than 1.0, whereas the PaCO2-PETCO2 difference remained positive when PCO2 level was increased with reducing the ventilatory volume (accumulation of endogenous CO2). These observations suggest that for a given increase in PCO2 by administration of exogenous CO2, the extent to which PaCO2 increases is smaller than that of PETCO2. This peculiar relationship together with changes in breathing pattern during CO2 inhalation likely results in "negative" PaCO2-PETCO2 difference in the spontaneously breathing animal. We conclude that the PaCO2-PETCO2 difference, either as positive or negative values, depends upon both the level of PCO2 and the ventilatory condition to increase PCO2.

Animals↗
PubMed1988

Delayed ventilatory response to CO2 after carbonic anhydrase inhibition with acetazolamide administration in the anesthetized rat.

In order to estimate to what extent the stimulatory action of CO2 on ventilation is mediated by the formation of H+, we studied effects on the temporal profile of ventilatory response to CO2 of carbonic anhydrase (CA) inhibition with acetazolamide in the halothane anesthetized spontaneously breathing rat. Since hydration reaction of CO2 yielding H+ is delayed by CA inhibition, the time courses of changes in tidal volume (VT), respiratory frequency (f), and minute ventilation (VE) in response to a stepwise increase in end-tidal PCO2 (delta PETCO2 15 mmHg) were compared before (control state) and after i.v. injection of acetazolamide (50 mg/kg) in the hyperoxic condition. In the control state, an increase in VT was significantly slower than that in f, and the mean response half-times (T1/2) for the increase in VT, f, and VE were 50.6, 18.1, and 31.0 s, respectively. After acetazolamide administration, responses to CO2, especially f-response and consequently VE-response became much slower, and the T1/2 for VT, f, and VE were 67.9, 55.0, and 63.0 s, respectively. The delay in VT-response was not statistically significant. The magnitude of increase in VE in the steady state hypercapnic stimulation was almost the same before and after acetazolamide administration. The results suggest that a rapid increase in f during CO2 inhalation occurs predominantly through an increase in H+ produced by hydration of CO2 with CA, whereas VT-response may occur without involvement of this process. The different time courses of VT- and f-responses and possible effects of molecular CO2 and/or H+ on the regulatory mechanisms for ventilatory pattern were discussed.

Acetazolamide↗
PubMed1988

Viral infection in acute peripheral facial palsy. Investigation in Yamagata Prefecture.

We studied viral involvement in Bell's palsy and Ramsay Hunt syndrome. In the CF test, viral infection was confirmed in 2 of 84 patients. Of the 12 patients with Ramsay Hunt syndrome, 5 showed a significantly high titre for varicella zoster and one for rubella. The ELISA test, performed in 60 patients with Bell's palsy, revealed significantly high titres for varicella zoster in 5 patients and for herpes simplex in 4 patients. All 5 patients with Ramsay Hunt syndrome showed significantly high titres for varicella zoster. The ELISA test showed a higher sensitivity than the CF test. The incidence of viral infection in the present study was lower than that in similar investigations. Possible reasons for this are epidemicity or regional differences year from year.

Acute Disease↗
PubMed1988

Nationwide investigation on diagnostic methods for facial palsy.

We investigated the present status concerning the performance of examinations of facial nerve function for facial palsy, based on statistics obtained from the project supported by a Grant-in-Aid for Co-operative Research (A) from the Ministry of Education. The project is called An Epidemiological and Clinical Study on the Idiopathic Facial Palsy. In an analysis of the questionnaire "individual investigation card for idiopathic facial palsy" obtained from 28 medical facilities throughout Japan between 1984 and 1986, the outline of the examinations performed for peripheral facial palsy was examined.

Electrodiagnosis↗
PubMed1988

Measurement of facial nerve conduction velocity and its application to patients with Bell's palsy.

Motor nerve conduction velocity (MCV) of the facial nerve was measured by electrical stimulation of the marginal mandibular branch and by evoked electromyography of the mentalis muscle. Normal MCV was 48.8 +/- 3.68 (mean +/- SD) m/s. In 132 patients with Bell's palsy, the minimum MCV was investigated within 2 weeks after onset. Sixty patients with normal MCV completely recovered in 1 month, but in the other patients with lower MCV, recovery was delayed. All of the 19 patients with markedly decreased MCV (0 to 10 m/s) exhibited partial recovery at 6 months after onset. MCV in Bell's palsy provides a good reflection of the prognosis, and of the degree of nerve damage.

Adult↗
PubMed1988

Effects of Aciclovir in Ramsay Hunt syndrome.

Nine patients with Ramsay Hunt syndrome were treated with Aciclovir and the effects of this treatment were observed for 6 months. The results were excellent in 5 cases, fair in 3, and poor in one case. Otalgia and auricular herpes was improved rapidly after the administration of Aciclovir. No severe side effect was observed in this study.

Acyclovir↗
PubMed1987

Effect of chlormadinone acetate, a synthetic progesterone, on hypoxic ventilatory response in men.

Ten healthy young males were studied with a double-blind, cross-over trial to determine whether or not chlormadinone acetate (CMA), a potent synthetic progesterone, augments hypoxic chemosensitivity. Seven days after CMA administration, inspiratory minute volume (VI) and tidal volume (VT) significantly increased. PaCO2 decreased by 3.0 +/- 2.6 (S.D.) Torr (p less than 0.05) and plasma bicarbonate decreased by 2.9 +/- 1.1 mM (p less than 0.01). During CMA administration, the atmospheric hypoxic ventilatory response (HVR), assessed by minute ventilatory (delta VI/delta SaO2), and occlusion pressure responses (delta P .2/delta SaO2), significantly increased about 1.9 (p less than 0.05) and 1.6 times (p less than 0.01) compared to the placebo response, respectively. The calculated normocapnic HVR (delta VI/delta SaO2) increased about 2.3 times the placebo run. Hypoxic response evaluated by the withdrawal test, which represents the peripheral chemosensitivity without involving the influence due to secondary hypoxic depression, was about 1.7 times the placebo response (p less than 0.05). We conclude that CMA augments hypoxic respiratory chemosensitivity.

Adult↗
PubMed1986

Control of ventilation in extreme-altitude climbers.

Ten climbers who participated in the Nepal-Japan Kangchenjunga Expedition (altitude, 8,478-8,586 m) in 1984 were examined for their hypercapnic and isocapnic hypoxic ventilatory responses (HCVR and HVR) at sea level before and after the expedition. Five climbers who reached an altitude higher than 8,000 m, [designated high-performance climbers (HPC)] exhibited significantly higher HVR than five climbers who did not [low-performance climbers (LPC)]. On the other hand, no significant difference in HCVR was seen between HPC and LPC. Our results were in agreement with the findings reported by Schoene et al. (J. Appl. Physiol. 56: 1478-1483, 1984) obtained in the American Medical Research Expedition to Everest in 1981. Significant depression in HVR in five climbers was found even 35-40 days after the expedition, which was accompanied by decreased arterial partial pressure of CO2 and increased pH at rest. Hence, the effect of altitude acclimatization in the climbers exposed to extreme altitude may have still persisted at the time of the postexpedition study. Our results confirmed that HRV evaluated at sea level may be used as an indicator of a climber's capability at great high altitude.

Adult↗
PubMed1986

Effect of chlormadinone acetate on ventilatory control in patients with chronic obstructive pulmonary disease.

Twelve patients with chronic obstructive pulmonary disease (COPD) were studied to determine the effect of ventilatory stimulation with chlormadinone acetate (CMA), a potent synthetic progesterone, on chemical and neuromechanical respiratory controls and pulmonary gas exchange. Using a randomized, double-blind, cross-over trial, 1 wk of CMA therapy caused a significant reduction in arterial CO2 tension (Paco2) by 4.6 +/- 0.6 (SE) mmHg. This Paco2 fall was associated with increased minute ventilation (Vl), tidal volume (VT), and mean inspiratory flow (VT/Tl). During CMA administration, occlusion pressure response to CO2 with and without inspiratory flow-resistive loading increased significantly (p less than 0.01) over that during placebo administration, whereas ventilatory response to CO2 did not. In addition, normocapnic ventilatory and occlusion pressure response to hypoxia were significantly elevated (p less than 0.01) during CMA therapy. Furthermore, the degree of load compensation, which was assessed by the ratio of the loaded to unloaded slope in the occlusion pressure response to CO2, increased in all subjects after CMA administration. These results indicate that CMA augments not only the respiratory neuromuscular response to hypercapnia and hypoxia, but also flow-resistive load compensation in patients with COPD, and it may provide support for the use of CMA in patients who are able to decrease their Paco2 with this agent.

Biomechanical Phenomena↗
PubMed1986

Difference in the effects of acetazolamide and ammonium chloride acidosis on ventilatory responses to CO2 and hypoxia in humans.

The effects of acetazolamide, a potent carbonic anhydrase inhibitor, and ammonium chloride (NH4Cl) on arterial blood gas tension, resting ventilation, and ventilatory responses to CO2 (HCVR) and hypoxia (HVR) were studied in healthy male subjects. Both drugs induced chronic metabolic acidosis with the reduction in plasma bicarbonate by a mean of 7.0 +/- 2.0 (S.D.) mM after acetazolamide and by 5.6 +/- 1.8 mM after NH4Cl. The ratio in the decrement of PaCO2 to that of plasma bicarbonate (delta PaCO2/delta [HCO3-]) was 1.51 in the former and 0.98 in the latter. Both drugs increased inspiratory minute ventilation (VI) predominantly due to increased tidal volume (VT) with acetazolamide and to increased respiratory frequency (f) with NH4Cl. In HCVR, the increments in CO2- ventilation slope and in ventilation at PETCO2 60 mmHg after drug administration were 0.77 +/- 0.51 l X min-1 X mmHg-1 and 20.0 +/- 11.2 l/min with acetazolamide and 0.59 +/- 0.40 l X min-1 X mmHg-1 and 8.0 +/- 2.8 l/min with NH4Cl, respectively. On the other hand, HVR both in terms of delta VI/delta SaO2 slope and of ventilation at SaO2 75% significantly increased after NH4Cl but not after acetazolamide administration. Thus, augmented VT and HCVR in the acetazolamide group and increased f and HVR in the NH4Cl group suggested that the central chemosensitive mechanism in the former and the peripheral chemosensitive mechanism in the latter may predominantly be responsible for the elevated ventilatory activities.

Acetazolamide↗