[Statistical observation on 1,000 cases of facial nerve paralysis--with special refernce to the etiology of Bell's palsy].
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Cold Temperature↗
Biomedical subjects
T Totoki
Publications and source records attributed to T Totoki.
Prevention by ulinastatin of decreased carbonic anhydrase activity induced by PMN elastase in vitro.
Disturbed carbon dioxide (CO2) elimination in adult respiratory distress syndrome (ARDS) has been considered to result from the dead space created by microthrombosis and vasoconstriction. However, another disturbance factor in CO2 elimination has been reported; the chemical dead space resulting from the inhibition of carbonic anhydrase (CA). This experiment was conducted to quantify the inhibition of CA activity by polymorphonucleocyte (PMN) elastase, which increases in ARDS. Different flasks containing solutions of CA, buffer, elastase, ulinastatin (an elastase antagonist), CA with PMN elastase, and CA with both PMN elastase and ulinastatin were prepared. Each flask was injected with sodium bicarbonate labeled with radioactive carbon (14C) and was shaken for 20 minutes; CA activity in each flask was measured by calculating the decrease in the coefficient (K) of 14C. It was observed that CA activity was inhibited dose-dependently by PMN elastase and that the inhibited activity was recovered by ulinastatin, which can inhibit PMN elastase. These findings indicate that CA activity in vitro could be inhibited by PMN elastase, which increases in ARDS, and suggests that disturbance of CO2 elimination could be reduced by using ulinastatin. It was concluded that ulinastatin could prevent the CA activity induced by PMN elastase in vitro.
Carbonic Anhydrase Inhibitors↗
Retention of carbon dioxide in tissue following carbonic anhydrase inhibition in dogs.
To evaluate the retention of carbon dioxide in tissue during the reduction of carbonic anhydrase activity following the administration of 5, 10, 20, or 30 mg/kg of acetazolamide in dogs, we measured carbon dioxide pressure (PCO2) in arterial blood, mixed venous blood, alveoli, and tissue. Respiration was maintained at a constant level. In the control (noninjected) group, PCO2 in tissue did not change for 3 hours under controlled respiration. Following the injection of 5 to 30 mg/kg of acetazolamide, PCO2 increased in arterial blood, mixed venous blood, and tissue in a dose-related manner, and decreased in the alveoli. The (a-et)PCO2 widened to 21.9 +/- 1.0 mmHg from 0.6 +/- 1.0 mmHg, and the (t-v)PCO2 to 16.1 +/- 2.0 mmHg from 5.1 +/- 0.6 mmHg, in response to acetazolamide. It is suggested that carbon dioxide is retained in tissue when carbonic anhydrase activity is inhibited by acetazolamide.
Acetazolamide↗
MR imaging of idiopathic trigeminal neuralgia: correlation with non-surgical therapy.
Magnetic resonance (MR) findings in patients with idiopathic trigeminal neuralgia were evaluated and correlated with the effectiveness of non-surgical treatments. Thirty-four patients with idiopathic trigeminal neuralgia (ITN) were examined using T1- and T2-weighted spin-echo (SE) pulse sequence techniques to evaluate their trigeminal root-entry zones and the vessels contacted prior to non-surgical treatment (retrogasserian glycerol injection, peripheral nerve block, or only oral analgesics). Vascular contact at the proximal portion of the preganglionic segment (PGS) of the trigeminal nerve and deformity of the PGS on the affected side were observed in 97% and 47% of the patients, respectively. Non-surgical treatments were curative in 12 (67%) but failed in two (11%) of the 18 patients without deformed PGS. However, among 16 patients with deformed PGS, they were curative in only six (37.5%) and failed in four (25%). Results of this study suggest that MR imaging could be useful in the clinical assessment of trigeminal neuralgia prior to instituting non-surgical treatment.
Administration, Oral↗