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Biomedical subjects

K Kinouchi

Publications and source records attributed to K Kinouchi.

52 records · Page 3Linked to original sources
PubMed1994

[FIO2 and SpO2 during cardiac surgery in neonates and infants].

Fractional inspired oxygen (FIO2) applied before and after a repair or palliative procedure for cardiac defects along with SpO2 measured by pulse oximeter were reviewed from anesthetic records of 62 neonates and infants. Fentanyl was used for anesthesia, except in cases without i.v. route in which sevoflurane with nitrous oxide in oxygen was used for induction of anesthesia. FIO2 was adjusted using air and oxygen. The lower FIO2 was applied to the patients for a closure of ventricular septal defect, a reconstruction of coarctation or interrupted aortic arch, and pulmonary artery banding, while the higher FIO2 was used for systemic-to-pulmonary artery shunts and the repair of tetralogy of Fallot. In the congenital heart disease with the intracardiac shunt, the magnitude of the shunt flow and hemodynamics can be altered by changing systemic and pulmonary vascular resistance which could be induced by various ways. Since alveolar oxygen tension is a known determinant of pulmonary vascular resistance, an appropriate FIO2 should be applied to each patient with different pathophysiology. A low FIO2 should be set for the cases with nonrestrictive left-to-right shunting, since a high FIO2 may cause a torrential pulmonary blood flow. A high FIO2 is preferable for the cases with right-to-left shunting and a concomitant decreased pulmonary blood flow.

Anesthesia↗
PubMed1993

[Anesthetic management for cesarean section in two parturients with quintuplet gestation].

Two parturients with quintuplet pregnancy underwent urgent or elective cesarean section under general anesthesia at 30 and 29 week gestational ages respectively. Since multiple gestation pregnancy requires enough medical staffs and instruments for preterm newborn resuscitation, emergency cesarean delivery was avoided. For cesarean delivery, the operation was started immediately after crash induction and intubation, and less than 1% isoflurane balanced with 60% nitrous oxide was used before birth in attempt to maintain uterine relaxation and sufficient utero-placental perfusion. After the delivery, aggressive maneuvers with PGE1 infusion, intravenous ergometrine and oxytocin, and interruption of volatile anesthetic inhalation (replaced by buprenorphine) were employed for decreasing the blood loss. The anesthesia and postoperative course of two patients and their babies were uneventful. Thus, anesthetic considerations may include; 1) high risk pregnancy related with huge pregnant uterus, 2) preterm labor, 3) preparation of sufficient man-power and instruments, 4) to avoid uterine contraction before delivery for fetal oxygenation, and 5) the puerperal promotion of uterine contraction to decrease blood loss.

Adult↗
PubMed1993

[The anesthetic management of cesarean section for multiple pregnant patients].

Anesthetic management of cesarean section for twenty multiple pregnant patients, who were pregnant with triplet or quadruplet, was compared with that for 325 single pregnant patients and 21 twin pregnant patients. For anesthetic methods, spinal anesthesia was chosen most frequently in the multiple pregnant patients, as in single and twin (more than 75 percent). In multiple pregnant patients, the incidence of emergency operation was less. In multiple pregnant patients who received spinal anesthesia, gestational age was lower; birth weight was lighter; length of fundus uteri was longer; and blood loss including amniotic fluid was larger. In triplets, the third infants' UID-time was prolonged and their Apgar score was lower.

Anesthesia, Epidural↗
PubMed1992

Duration of apnea in anesthetized infants and children required for desaturation of hemoglobin to 95%. The influence of upper respiratory infection.

Sixty-one patients ASA physical status 1-2 aged 1 month to 12 years undergoing elective surgery were included in the study. Anesthesia was induced via a mask with sevoflurane up to 5% and 66% nitrous oxide in oxygen. After paralysis with vecuronium (0.12 mg/kg iv), the trachea was intubated and the lungs were ventilated manually with 3% sevoflurane in oxygen until the end-tidal nitrous oxide decreased to less than 5%. Apnea was started by disconnecting the breathing circuit from the endotracheal tube. The time from the start of apnea to Spo2 of 95% was measured. Manual ventilation was reinstituted when Spo2 decreased to 95% and another set of vital signs was recorded. Twenty of 61 patients had symptoms of upper respiratory infection. The time to Spo2 of 95% correlated well with height, age, and body weight both by linear and non-linear regression analyses. The patients with symptomatic upper respiratory infection required less time for Spo2 to decrease to 95% compared to the asymptomatic children. We conclude that younger children require less time for Spo2 to decrease to 95%. The presence of upper respiratory infection is an additional factor increasing the susceptibility of small children to hypoxemia.

Anesthesia, Inhalation↗
PubMed1991

Identification and characterization of receptors for tumor necrosis factor-alpha in the brain.

Specific receptors for murine TNF have been identified in homogenates of rodent brain. These receptors are saturable and bind TNF with sufficient affinity to ensure occupancy by cytokine elaborated during infection. 125I-mTNF was detected in four specific complexes of Mr 130,000, 90,000, 66,000 and 60,000 after affinity labeling. Solubilization of brain membranes into detergent increased binding capacity 4-fold which indicates the presence of latent receptors for mTNF in the brain. Specific binding was greatest in the brainstem, least in the cerebellum and was also detected in the cortex, thalamus and basal ganglia.

Animals↗
PubMed1991

Evidence for kappa 1 opioid receptor multiplicity in the guinea pig cerebellum.

Both [3H]U69,593 alone and [3H]ethylketocyclazocine (EKC) in the presence of mu and delta blockers ([D-Ala2,MePhe4,Glyol5]enkephalin (DAMGO) and [D-Pen2,D-Pen5]enkephalin (DPDPE)) label kappa receptors in the guinea pig cerebellum. Dynorphin A(1-17) and nor-binaltorphimine (nor-BNI) potently competed the binding of both radioligands with Hill coefficients of approximately unity, strongly supporting a kappa classification of binding. However, saturation studies revealed that the Bmax for [3H]EKC binding was 45% greater than that for [3H]U69593, suggesting that [3H]EKC might be labeling more than one site. Although nonlinear regression analysis of dynorphin A(1-17) and nor-BNI competition of [3H]EKC binding best fit the curves with a one site model, competitions by dynorphin B, dynorphin A(1-9) and alpha-neoendorphin revealed Hill coefficients less than unity and were best fit to a two site model. Kinetic analysis also supported [3H]EKC binding heterogeneity. Together, these studies imply that under these conditions [3H]EKC labels more than one site in the guinea pig cerebellum. The sensitivity of all specific [3H]EKC binding to the selective kappa ligands dynorphin A(1-17) and nor-BNI indicates that both component are kappa while the differing sensitivities of dynorphin B, alpha-neoendorphin and dynorphin A(1-9) for these components support our previous hypothesis of kappa 1a and kappa 1b binding subtypes.

Animals↗
PubMed1991

Pentazocine-induced catecholamine efflux from the dog perfused adrenals.

This study has been undertaken to determine whether pentazocine induces catecholamine efflux from the adrenal medulla as a mechanism for its sympathomimetic effect. Dog isolated adrenals were perfused retrogradely with modified Locke's solution. The efflux of catecholamines from dog perfused adrenals was increased from the resting output of 0.18 +/- 0.04 micrograms min-1 (mean +/- s.e.), to 0.47 +/- 0.13 micrograms min-1 by the administration of pentazocine (50 microM). The pentazocine-induced catecholamine efflux was dose-dependent in the 50-400 microM dose range. This effect of pentazocine was not inhibited by either a combination of atropine and (+)-tubocurarine, or verapamil, in contrast to acetylcholine-induced catecholamine release. There was no significant difference in potency among stereoisomers, i.e. (+)-, (-)- and (+/-)-pentazocine, in inducing catecholamine efflux. Naloxone did not influence the effects of either (+)- or (-)-pentazocine. The interaction of pentazocine with acetylcholine-induced catecholamine release was also examined. Both (+)- and (-)-pentazocine inhibited acetylcholine-induced catecholamine release dose-dependently, and these inhibitory effects were not reversed by naloxone. Acetylcholine-induced catecholamine release was accompanied by increased dopamine-beta-hydroxylase release, whereas pentazocine-induced catecholamine efflux was not. These results suggest that pentazocine directly acts on the adrenal medulla to induce catecholamine efflux via a non-exocytotic mechanism, and that opioid receptors do not play a role in this action.

Acetylcholine↗
PubMed1991

Affinity labeling of mu and kappa receptors with naloxone benzoylhydrazone.

Naloxone benzoylhydrazone (NalBzoH) labels both mu and kappa receptors in standard homogenate binding assays. We now report that [3H]NalBzoH can effectively photoaffinity label opioid receptors. By modifying [3H]NalBzoH binding conditions, we can selectively label either mu or kappa 3 receptors in calf striatal membranes or classical U50,488-sensitive kappa 1 receptors in guinea pig cerebellar membranes. After removal of unbound radioligand, the [3H]NalBzoH-labeled membranes were irradiated with UV light to couple the bound radioligand to its binding site. No specific mu, kappa 1, or kappa 3 binding remained after a 20-hr dissociation at 25 degrees without UV irradiation. In contrast, approximately 45% of mu and 40% of kappa 1 and kappa 3 binding remained after 2 min of UV exposure. In time course studies, increasing the UV exposure from 30 sec to 3 min produced a progressive increase in radioligand incorporation, which did not increase further with UV exposure times up to 5 min. A portion of the binding in irradiated membranes appeared to be covalently coupled to proteins. Following solubilization of irradiated membranes with sodium dodecyl sulfate, approximately 30-40% of the specifically bound radioactivity precipitated with trichloroacetic acid (TCA). These levels of TCA-precipitable binding corresponded to the amount of dissociation-resistant binding described above. No specific binding could be TCA precipitated in samples that were not exposed to UV. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of [3H]NalBzoH-labeled membranes revealed a number of labeled peaks with levels of radioactivity that did not correspond to the intensity of the protein bands, suggesting that this technique was not randomly labeling proteins. This approach may be a useful method to affinity label, characterize, and purify mu and kappa opiate receptor subtypes.

Affinity Labels↗
PubMed1989

Effects of pentazocine and other opioids on the potassium-evoked release of [3H]noradrenaline from guinea pig cortical slices.

Noradrenaline release and its modulation via presynaptic opioid receptors were examined in guinea pig cortical slices. Slices preloaded with [3H]noradrenaline were superfused in the presence of desipramine (1 microM) and were stimulated by 16 mM K+. 1-Pentazocine inhibited the K+-evoked release of [3H]noradrenaline in a dose-dependent manner (3 x 10(-7)-10(-5) M), while d-pentazocine did not inhibit. This inhibitory effect of 1-pentazocine was antagonized by Mr 2266 (10(-6) M) but not by naloxone (10(-6) M). Among other opioids, dynorphin A-(1-13) and ethylketocyclazocine (kappa agonists) decreased the K+-evoked release of [3H]noradrenaline. Tyr-D-Ala-Gly-NMe-Phe-Gly-ol (DAGO, mu agonist) also inhibited [3H]noradrenaline release but was less potent than the kappa agonists. [D-Pen2,D-Pen5]enkephalin (DPDPE, delta agonist) and phencyclidine (sigma agonist) had no effects on the stimulated release of [3H]noradrenaline. Thus, it was shown that kappa receptors are the major subtype of opioid receptor involved in modulation of noradrenaline release in guinea pig cortex, and that 1-pentazocine inhibits the K+-evoked release of noradrenaline through activation of these receptors.

Animals↗
PubMed1989

Effects of d- and l-pentazocine on the release and uptake of norepinephrine in rat brain cortex.

Effects of d- and l-pentazocine on the release and uptake of norepinephrine and other neurotransmitters were examined in rat cerebral cortex. D- and l-pentazocine (10(-6)-10(-4) M) evoked the release of tritium from rat cortex slices preloaded with [3H]norepinephrine. Both isomers of pentazocine (3 x 10(-5) M) also evoked the release of tritium from slices preloaded with [3H]dopamine and [3H]5-hydroxytryptamine ([3H]5-HT) but did not from those preloaded with [3H] gamma-aminobutyric acid ([3H]GABA) and [3H]choline. The releasing effect of pentazocine was neither dependent on the extracellular calcium nor antagonized by naloxone. Both isomers inhibited the uptake of [3H]norepinephrine, [3H]dopamine and [3H]5-HT but not that of [3H]GABA and [3H]choline into synaptosomes prepared from the cortex. These results suggest that the effects of d- and l-pentazocine on release and uptake are relatively specific to monoamines and might explain some aspects of pharmacological actions of pentazocine.

Animals↗
PubMed1986

Stereospecific effects of d- and l-pentazocine on contractions of the mouse vas deferens.

The effects of the d- and l-isomers of pentazocine were compared to that of racemic pentazocine on contractions of the mouse isolated vas deferens. L-pentazocine inhibited electrically evoked contractions of the mouse vas deferens (MVD) in a dose-dependent manner (ID50 0.37 +/- 0.04 microM). In contrast, d-pentazocine augmented field stimulated contractions dose-dependently; per cent increases in contractions at 10 and 30 microM were 57.8 +/- 18.0 and 98.0 +/- 15.1%, respectively. Racemic pentazocine produced an intermediate effect between the two isomers. The effect of 1-pentazocine was antagonized by naloxone, whereas that of d-pentazocine was not. L-pentazocine did not effect the response of the MVD to exogenous norepinephrine at any concentration tested, while d-pentazocine depressed the response of the MVD to exogenous norepinephrine at one dose (0.3 microM). These findings demonstrate that d- and l-pentazocine produce opposite effects on the MVD. The effects of l-pentazocine are opioid mediated, while those of d-pentazocine are not. In the racemic mixture the opposing effects of the two isomers modulate each other, resulting in a diminished effect.

Animals↗