Biomedical subjects

Y Kumeta

Publications and source records attributed to Y Kumeta.

9 recordsLinked to original sources

PubMed1995

[A survey of perioperative bronchospasm in 105 patients with reactive airway disease].

We investigated the relationship between the intra- and postoperative incidence of bronchospasm and the predisposing preoperative factors in 105 patients with reactive airway disease. (1) The incidence of bronchospasm in intra- and postoperative period was not associated with age, sex, duration of bronchial asthma, severity of disease, duration of the anesthesia and operation, or with FEV1.0%. (2) The incidence of intraoperative bronchospasm was high with general anesthesia using endotracheal intubation (8.9%), but low with general anesthesia using mask and regional anesthesia (0% and 2.2%, respectively). (3) The incidence of postoperative bronchospasm was about 20% with both general and regional anesthesia. However, the incidence of postoperative bronchospasm was higher in thoracic and abdominal surgeries than in other surgeries (39.5%:10.4%). (4) The incidences of intra- and postoperative bronchospasm increased in proportion to the proximity of the latest asthmatic attack to the operative date. (5) Prophylactic preoperative inhalation of bronchodilators was effective in the prevention of intraoperative bronchospasm, but some patients developed postoperative wheezing within a few days after the cessation of postoperative inhalation.

Adolescent↗

PubMed1995

[Effects of oral alpha 2 adrenergic agonists, clonidine and tizanidine, on tetracaine spinal anesthesia].

This study was conducted to evaluate the effects of oral clonidine and tizanidine, alpha 2 adrenergic agonists, as premedication for tetracaine spinal anesthesia in 63 gynecological patients. The patients were randomly allocated to one of six groups. Group 1 (n = 7), group 2 (n = 8) and group 3 (n = 7) received 13 mg of tetracaine intrathecally in 10 % glucose solution 2.6 ml. Group 4 (n = 13), group 5 (n = 14) and group 6 (n = 13) received 13 mg of tetracaine intrathecally in a volume of 2.6 ml of 10 % glucose solution which contained 0.65 mg of phenylephrine. As premedication, group 1 and 4 received 0.25 mg of oral triazolam; group 2 and 5 received 3 mg of oral tizanidine; group 3 and 6 received 0.15 mg of oral clonidine. Group 2 and 3, or group 5 and 6 (clonidine or tizanidine group, respectively) needed significant longer time for regression of Th10 sensory blockade than group 1 or 4 (triazolam). The time for appearance of postoperative pain and the time to require postoperative analgesics were longer in the groups which had received either clonidine or tizanidine than in the groups which had received triazolam. Heart rate and systolic blood pressure in group 6 (clonidine-tetracaine-phenylephrine group) showed significant decreases (P < 0.05) after the spinal anesthesia. We concluded that oral premedication of clonidine and tizanidine prolonged tetracaine spinal anesthesia. From the view point of the prolongation of spinal anesthesia and the hemodynamic stability, oral premedication with tizanidine seems to be useful.

Administration, Oral↗

PubMed1989

Intrathecal clonidine suppresses noxiously evoked activity of spinal wide dynamic range neurons in cats.

The analgesic effectiveness of perispinal clonidine administration prompted us to evaluate clonidine effects on spinal dorsal horn wide dynamic range neurons. Intrathecal clonidine produced a dose-dependent (10 and 30 micrograms), yohimbine-reversible suppression of noxiously evoked activity in decerebrate, spinal cord-transected cats. In addition, combining ineffective intrathecal doses of morphine (25 micrograms) and clonidine (5 micrograms) produced statistically significant, reversible suppression of noxiously evoked activity. The time course of suppression was similar to that observed behaviorally. These results support the role of spinal alpha 2-adrenergic receptors in clonidine analgesia.

Analgesics↗

PubMed1988

Fentanyl suppression of nociceptive neurons in the superficial dorsal horn of the cat.

This study was designed to examine the influence of spinally administered fentanyl on the spontaneous and noxiously evoked activity of high threshold (HT) and wide dynamic range (WDR) neurons in the superficial layers (lamina I and II) of the dorsal horn of cats made decerebrate and in which the spinal cord had been transected. Single unit activity was recorded using extracellular microelectrode recording techniques. Neuronal activity was evoked by the presentation of noxious radiant heat (51 degrees C) to the cells' receptive fields on the hind paws. Evoked activity of WDR neurons was monitored, both before and after the spinal administration of either 10 micrograms (n = 9) or 25 micrograms (n = 10) of fentanyl. HT neurons were examined before and after either 25 micrograms (n = 7) or 50 micrograms (n = 7) of spinally administered fentanyl. In all cases 31 min after fentanyl administration naloxone (0.1 mg) was administered intravenously (iv), and its antagonistic effect on the fentanyl suppression was determined. All doses of fentanyl tested suppressed both spontaneous and evoked activity of both types of neurons. Within 30 minutes 10 and 25 micrograms of fentanyl reduced the mean evoked activity of WDR neurons to 61% and 19% of control values, respectively, and 25 and 50 micrograms of fentanyl reduced the mean evoked activity of HT neurons to 70% and 47% of control values, respectively. Naloxone reversed the suppression seen in all cells studied. The results of the present study demonstrate that HT neurons are significantly less suppressed by the spinal administration of fentanyl than WDR neurons located in the same superficial layers of the dorsal horn.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988