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I Yoshiya

Publications and source records attributed to I Yoshiya.

At least 19 recordsLinked to original sources
PubMed1992

Volatile anesthetics-induced activation phenomena of alpha-chymotrypsin-catalyzed hydrolysis.

The rates of hydrolysis of p-nitrophenyl acetate (pNPA), p-nitrophenyl propionate (pNPP), p-nitrophenyl butanate (pNPB), and p-nitrophenyl valerate (pNPV) catalyzed by alpha-chymotrypsin (alpha-CHT) were measured with and without volatile anesthetics at 25.0 degrees C. Halothane activated the hydrolysis of pNPA and pNPP, meanwhile inhibited that of pNPB and pNPV. The activation phenomena were explained by the existence of a 1:1 enzyme-anesthetics complex and the opening of an activated pathway. The rate constant of pNPA hydrolysis catalyzed by alpha-CHT of the activated pathway kA by halothane was 0.269 s-1, whereas that of the normal pathway was k0 0.093 s-1. The free energy of activation was stabilized at 0.64 kcal/mol by halothane. The mechanisms of the activation and inhibition are discussed in terms of the molecular size of the substrate and anesthetics.

Anesthetics↗
PubMed1992

Carbon dioxide reactivity and local cerebral blood flow during prostaglandin E1- or nitroglycerin-induced hypotension.

The aims of this randomized study were to determine the effect of prostaglandin-(PGE1) or nitroglycerin-(TNG) induced hypotension on local cerebral blood flow (LCBF) and carbon dioxide reactivity during isoflurane anaesthesia in 20 patients after subarachnoid haemorrhage (SAH) scheduled for aneurysm clip ligation. Mean arterial blood pressure decreased immediately, after giving either PGE1 or TNG. The LCBF, measured using a thermal gradient blood flowmeter, was unchanged after PGE1, while the LCBF increased after TNG infusion (control; 47.6 + 10.0, 60 min after infusion; 55.1 +/- 6.5 (P < 0.05), before clipping; 55.5 +/- 7.8 (P < 0.05)) but returned to control values after its discontinuation. Carbon dioxide reactivity, calculated from % delta LCBF/delta PaCO2 was unchanged during PGE1- or TNG-induced hypotension (PGE1; 2.13 +/- 0.9, 2.48 +/- 0.68 and 2.31 +/- 0.79%/mmHg for before, during and after hypotension respectively) (TNG; 2.08 +/- 0.68, 2.17 +/- 0.64 and 2.02 +/- 0.69%/mmHg for before, during and after hypotension respectively). Carbon dioxide reactivity correlated with presurgical neurological status (rs = -0.7, -0.648 and -0.458 for before, during and after hypotension respectively) and the initial LCBF (rs = -0.605). These results suggest that both PGE1 and TNG are useful drugs for induced hypotension for cerebral aneurysm surgery, because neither decreased LCBF.

Adult↗
PubMed1992

Selective beta 1 and beta 2 adrenoceptor blockade on epinephrine-induced arrhythmias in halothane anaesthetized dogs.

Beta 2 as well as beta 1 adrenoceptors have been recognized in the heart of vertebrates. They mediate a positive chronotropic action of catecholamines. We compared the effect of selective beta 1 and beta 2 adrenoceptor antagonists on the genesis of halothane-epinephrine arrhythmias in dogs. The arrhythmogenic dose (AD) of epinephrine was increased in the presence of l-metoprolol, a selective beta 1 antagonist (8.40 +/- 1.13 micrograms.kg-1 x min-1; mean +/- SEM), compared with control value (2.62 +/- 0.56) (P < 0.05). In contrast, ICI-118,551, a selective beta 2 antagonist, did not change the AD (2.36 +/- 0.43). Adding ICI-118,551 to l-metoprolol did not affect the AD of epinephrine in the presence of l-metoprolol alone (6.34 +/- 0.74 vs 8.40 +/- 1.13). These results suggest that selective beta 1 blockade is effective in preventing halothane-epinephrine arrhythmias, but selective beta 2 blockade is not.

Adrenergic beta-Antagonists↗
PubMed1992

Prostaglandin E1 and carbon dioxide reactivity during cerebral aneurysm surgery.

The purpose of this study was to evaluate the effect of prostaglandin E1 (PGE1) on CO2 reactivity during cerebral aneurysm surgery in 37 patients under neuroleptoanaesthesia (NLA). The patients were divided into two groups based on the timing of surgery (A: late surgery B: early surgery). In the early surgery group, aneurysm surgery was performed within three days of subarachnoid haemorrhage (SAH) and in the late surgery group surgery was performed more than four days after SAH. Presurgical neurological status was worse in the early surgery group than in the late surgery group (P less than 0.01). Local cerebral blood flow (LCBF) measurements were made using a thermal gradient blood flow meter. Hypotension was induced by PGE1 administration at an initial dose of 0.1 micrograms.kg-1.min-1 and adjusted to maintain the mean arterial pressure (MAP) at about 70 mmHg. The CO2 reactivity was calculated by the % change in LCBF divided by the change in PaCO2 (% delta LCBF/delta PaCO2 (%.mmHg-1)). LCBF, heart rate and mean arterial blood pressure were measured during and after PGE1 infusion. Carbon dioxide reactivity was measured before, during and after PGE1 administration. The LCBF did not change throughout the study but CO2 reactivity was greater in Group A (before hypotension: 2.74 +/- 0.85 %.mmHg-1, during hypotension: 2.54 +/- 0.73 % .mmHg-1, after hypotension: 2.59 +/- 1.17 %.mmHg-1) than in group B (before hypotension: 1.54 +/- 0.57%.mmHg-1, during hypotension: 1.56 +/- 0.59 %.mmHg-1, after hypotension: 1.49 +/- 0.42%.mmHg-1) (P less than 0.01). Outcome which was graded by Glasgow Outcome Scale at discharge, was better in Group A (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Carbon dioxide reactivity during prostaglandin E1 induced hypotension for cerebral aneurysm surgery.

The cerebral vasomotor reactivity to carbon dioxide was studied, using a thermal gradient blood flow meter in 43 patients with intracranial cerebral aneurysm under deliberate hypotension induced by prostaglandin E1 (PGE1) infusion. The patients were divided into three groups according to the neurological status. Patients in Groups A and B had subarachnoid haemorrhage due to ruptured cerebral aneurysms. Group A consisted of 23 patients with a neurological grade of I-II and Group B consisted of 11 patients with a grade of III-V. Nine patients with non-ruptured cerebral aneurysm served as controls (Group C). After the dura was opened, local cerebral blood flow (LCBF) was measured. The PGE1 was started with an initial dose of 0.1 microgram.-kg-1.min-1 and the dose was adjusted to maintain MAP at about 70 mmHg. The LCBF and carbon dioxide (CO2) reactivity were estimated during and after PGE1 administration. The LCBF did not change among groups throughout the study period. Carbon dioxide reactivity was estimated as follows: absolute; delta LCBF/delta PaCO2, and relative; % delta LCBF/delta PaCO2 after changing PaCO2 by increasing minute ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

The solubility of volatile anaesthetics in water at 25.0 degrees C using 19F NMR spectroscopy.

Anaesthetic concentration is very important for the quantitative treatment of anaesthesia theory. Traditionally concentration values have been derived from the water/gas partition coefficient. However, the values from many investigators show discrepancies. This study reports the accurate solubility of methoxyflurane (9.1 mM), halothane (18.0 mM), enflurane (11.9 mM) and isoflurane (13.5 mM) in water at 25.0 degrees C using 19F NMR spectroscopy. The method has advantages in that the dissolved molecule in solution can be separately quantified from undissolved anaesthetic. Saturated solutions of the anaesthetic agents were prepared in situ in a NMR tube to avoid pressure and temperature changes in the solution.

Anesthetics↗
PubMed1992

Effect of prostaglandin E1-induced hypotension on carbon dioxide reactivity and local cerebral blood flow after subarachnoid haemorrhage.

The effect of prostaglandin E1 (PGE1) on local cerebral blood flow (LCBF) and carbon dioxide reactivity (CO2R) was studied during cerebral aneurysm surgery for subarachnoid haemorrhage in 24 patients under neuroleptanaesthesia. Eleven patients had good neurological status (Hunt and Kosnik grade I: group A) and 13 patients poor status (grades II-IV: group B). Arterial hypotension was induced with PGE1 0.1 micrograms kg-1 min-1 initially and adjusted to maintain mean arterial pressure at about 70 mm Hg. PGE1 was discontinued at the completion of aneurysm clipping. LCBF and CO2R were measured during and after administration of PGE1. LCBF was unchanged and CO2R preserved in both groups. The carbon dioxide response was better in group A than in group B (P less than 0.01). PGE1 may be a suitable agent for hypotensive anaesthesia in these patients.

Adult↗
PubMed1992

Prolongation of canine epidural anesthesia by liposome encapsulation of lidocaine.

The purpose of our study was to produce a long-acting lidocaine by using a liposome that would entrap the drug. Egg yolk phosphatidylcholine and cholesterol were used as liposome materials. After epidural administration, the pharmacodynamics and pharmacokinetics of liposomal and free lidocaine were studied in 20 dogs. Two percent liposomal or free lidocaine (3.0 mL) was injected into the lumbar epidural space. Nerve blocking effects were estimated by measuring somatosensory evoked potentials. Recovery time from the epidural block in the liposomal lidocaine group (170 +/- 49.5 min) was approximately three times longer than that in the free lidocaine group (61 +/- 18.1 min). The areas under the drug concentration-time curves (AUC0-infinity) and time to maximal concentration (Tmax) in the liposomal lidocaine group were significantly larger than those in the free lidocaine group. These results suggest that the prolongation of epidural blockade by liposomal lidocaine is caused by a slow release of the drug from liposomes. The present study suggests that liposomal lidocaine can be used as a long-acting local anesthetic.

Amines↗
PubMed1992

Segmental analgesic effect and reduction of halothane MAC from epidural fentanyl in humans.

To clarify the site of action of epidural fentanyl, we compared the effects of epidural and intravenous fentanyl on the change in pressure pain threshold (PPT) and the minimum alveolar concentration (MAC) of halothane. Seventy patients who underwent gastrectomy in the PPT study group and 84 female patients who underwent hysterectomy in the MAC study group were assigned randomly to seven groups in each study. The seven groups each received a bolus injection of 1, 2, or 4 micrograms/kg of fentanyl, either intravenously or epidurally, and of saline solution epidurally. Compared with intravenous fentanyl, epidural fentanyl significantly increased (P less than 0.01) PPT around surgical incisions by approximately 50%, 100%, and 150% of preadministration levels 1 h after administration of 1, 2, and 4 micrograms/kg, respectively, and significantly reduced (P less than 0.05) halothane MAC at the same doses. These data suggest that the more potent analgesic and anesthetic effects of epidural fentanyl, compared with intravenous fentanyl, are due mainly to the segmental analgesia produced by its spinal analgesic action.

Adult↗
PubMed1992

Capnometry during high-frequency oscillatory ventilation.

We used capnometry during high-frequency oscillatory ventilation (HFOV), and compared CO2 measurements at the distal and proximal ends of an endotracheal tube with arterial CO2 values. Ten white rabbits (mean weight, 2.00 +/- 0.2 [SD] kg) underwent tracheostomy under anesthesia with pentobarbital. The trachea was intubated with an endotracheal tube with a second lumen for sampling respiratory gas at the distal tip. Capnometry was performed through the lumen (CO2d) and the proximal end of the endotracheal tube (CO2p). The internal carotid artery was cannulated to sample blood for measuring arterial blood gases. The differences between CO2d, CO2p, and PaCO2 were measured. Only the relation between CO2d and PaCO2 was good (r = 0.915). We concluded that capnometry can be used during HFOV to estimate PaCO2 provided that respiratory gas is sampled from the distal tip of the endotracheal tube.

Animals↗
PubMed1992

Local cerebral blood flow and CO2 reactivity during prostaglandin E1-induced hypotension in patients undergoing cerebral aneurysm surgery.

The effects of prostaglandin E1 (PGE1) on local cerebral blood flow and CO2 reactivity were studied in 30 patients undergoing cerebral aneurysm surgery in eight of whom the aneurysm had not ruptured and was an incidental finding. The aneurysms were clipped at various intervals depending upon clinical conditions. Blood flow on the open brain surface was measured with a thermal gradient blood flow-meter. Hypotension was initially induced with 0.1 microgram kg-1 min-1 of PGE1 and subsequently adjusted to maintain the mean arterial blood pressure at about 70 mmHg. Local cerebral blood flow and CO2 reactivity were studied during and after PGE1 administration. Both were preserved, but CO2 reactivity values were lower in patients in whom the aneurysm had ruptured than in those in whom it had not ruptured. PGE1 may be an appropriate drug with which to induce hypotension during cerebral aneurysm surgery because cerebral blood flow and CO2 reactivity is preserved.

Adult↗
PubMed1992

[A hypertensive crisis during surgery in a patient with neuroblastoma].

Neuroblastoma is the most common solid tumour in infancy and childhood. The tumour usually produces large amounts of catecholamines. Few patients with neuroblastoma, however, were reported to have become hypertensive because of catecholamine metabolism within the tumour itself. This is one of the most important differences compared with pheochromocytomas. We experienced a hypertensive crisis accompanied by tachycardia and an increase in the plasma catecholamine concentration during surgery in a patient with neuroblastoma. The plasma catecholamine level was comparable to that of pheochromocytoma. Phentolamine and propranolol were effective to control the hypertension and tachycardia.

Catecholamines↗
PubMed1991

Local cerebral blood flow with prostaglandin E1 or trimethaphan during cerebral aneurysm clip ligation.

This study was performed to examine changes in local cerebral blood flow during hypotensive anaesthesia with either prostaglandin E1 (PGE1) or trimethaphan (TMP). Local cerebral blood flow (LCBF), mean blood pressure (MBP), heart rate (HR), and hourly urine output (UO) were studied in 51 patients undergoing cerebral aneurysm surgery with neuroleptanalgesia (NLA). The incidence of vasospasm after aneurysm surgery, and outcome (Glasgow Outcome Scale) at discharge were evaluated. Measurements of LCBF were made using a thermal gradient blood flow meter. The dose of PGE1 or TMP was adjusted to maintain MBP at about 70 mmHg, and LCBF was studied during and after PGE1 or TMP administration. Hypotensive drugs were discontinued at the completion of aneurysm clipping. After starting PGE1 or TMP, MBP decreased immediately, but HR did not change in either group. The LCBF decreased 30 min after the start of TMP administration and increased immediately after its discontinuation, whereas PGE1 did not affect LCBF. Urine output increased during PGE1 administration but was unchanged during TMP. Neither drug affected surgical outcome or the incidence of vasospasm. These results suggest that PGE1 may be preferable to trimethaphan for hypotensive anaesthesia in cerebral aneurysm surgery because LCBF is maintained.

Adult↗
PubMed1991

Myocardial epinephrine sensitization with subanesthetic concentrations of halothane in dogs.

The authors investigated myocardial epinephrine sensitization by subanesthetic concentrations of halothane. The dose-response relationship for the action of halothane was examined with etomidate plus varying subanesthetic concentrations of halothane in dogs. The arrhythmogenic threshold of epinephrine was decreased in a dose-dependent manner at end-tidal concentrations of halothane between 0.1 and 0.3%. At end-tidal halothane is greater than 0.3%, and no further reduction of arrhythmogenic threshold of epinephrine occurred. The plasma concentrations of epinephrine producing four or more premature ventricular contractions in 15 s were 201.3 +/- 34.3, 98.1 +/- 13.9, 60.3 +/- 8.63, 57.9 +/- 12.8, 54.5 +/- 8.61, and 53.9 +/- 4.86 ng/ml (mean +/- SEM), at 0, 0.1, 0.3, 0.5, 1.0, and 1.5% of halothane at end-tidal concentrations, respectively. The results suggest that in the presence of etomidate, halothane produces myocardial sensitization to epinephrine at subanesthetic concentrations as low as 0.1%. Increasing halothane to 0.3% produces a further reduction in the arrhythmogenic dose of epinephrine.

Anesthesia↗
PubMed1991

Dexmedetomidine prevents epinephrine-induced arrhythmias through stimulation of central alpha 2 adrenoceptors in halothane-anesthetized dogs.

Since alpha 2-adrenergic agonists have important effects on the adrenergic system that have recently been applied to the anesthetic setting, we investigated the effect of stimulation of alpha 2 adrenoceptors on epinephrine-induced arrhythmias in halothane-anesthetized dogs. The arrhythmogenic threshold for epinephrine was determined during halothane anesthesia in the presence of dexmedetomidine, a selective alpha 2 agonist, and L-medetomidine, a stereoisomer of medetomidine that lacks alpha 2-agonist activity. Dexmedetomidine increased the arrhythmogenic threshold for epinephrine in a dose-dependent manner during halothane anesthesia. At the highest dose of dexmedetomidine, 0.5 microgram.kg-1.min-1, there was a three-fold increase in both the arrhythmogenic dose of epinephrine and the plasma epinephrine concentration that was reached at this dose. On the other hand, L-medetomidine over the same dose range did not effect the arrhythmogenic dose of epinephrine. Atipamezole, a central alpha 2 antagonist that crossed the blood-brain barrier, blocked the antiarrhythmic action of dexmedetomidine. L-659,066 a peripheral alpha 2 antagonist that does not penetrate the blood-brain barrier, did not affect the antiarrhythmic action of dexmedetomidine. Thus, dexmedetomidine's antiarrhythmic effect on epinephrine-induced arrhythmias during halothane anesthesia appears to be mediated at least in part by stimulation of central alpha 2 adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1991

Enhancement by propofol of epinephrine-induced arrhythmias in dogs.

Although propofol is a widely used intravenous anesthetic, its effect on epinephrine-induced arrhythmias remains unknown. This study examined the possible interaction between propofol and epinephrine that might affect the induction of ventricular arrhythmias in dogs. The arrhythmogenic threshold of epinephrine was determined during anesthesia with halothane alone, propofol alone, etomidate alone, or etomidate plus varying doses of propofol. The arrhythmogenic dose and the corresponding plasma concentration of epinephrine during propofol anesthesia (blood propofol concentration 18.0 +/- 0.98 micrograms/ml) were 2.52 +/- 0.43 micrograms.kg-1.min-1 and 23.6 +/- 8.5 ng/ml, respectively. During halothane anesthesia (end-tidal 1.3 MAC), they were 2.66 +/- 0.21 micrograms.kg-1.min-1 and 35.7 +/- 1.9 ng/ml, respectively. During etomidate anesthesia, they were 9.67 +/- 1.06 micrograms.kg-1.min-1 and 205 +/- 27.5 ng/ml, respectively. The dose-effect relationship for propofol was examined during etomidate plus propofol anesthesia. Propofol reduced the arrhythmogenic plasma concentration of epinephrine in a concentration-dependent manner: at blood propofol concentrations of 2.33 +/- 0.46, 5.46 +/- 0.71, and 11.2 +/- 0.81 micrograms/ml, the corresponding plasma epinephrine concentrations were 182.6 +/- 52.5, 89.0 +/- 28.8, and 26.6 +/- 6.9 ng/ml, respectively. These results suggest that propofol enhances epinephrine-induced arrhythmias in a dose-dependent manner in dogs.

Anesthesia↗