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Biomedical subjects

I Yoshiya

Publications and source records attributed to I Yoshiya.

At least 109 records · Page 6Linked to original sources
PubMed1993

Effect of local anaesthetics on the stimulus-secretion coupling in bovine adrenal chromaffin cells.

This study was carried out to determine the relative potencies of local anesthetics to inhibit the cholinergic synaptic transmission using cultured bovine adrenal chromaffin cells, and to clarify if the inhibitory action would correlate with biophysical and pharmacological properties. Local anaesthetics (bupivacaine, etidocaine, tetracaine, lignocaine and procaine; 0.02-2 mM) inhibited carbachol-induced catecholamine release from the cells in a concentration-dependent manner. This inhibition was completely reversible. IC50 (concentration of 50% inhibition) of each anaesthetic showed no correlation with the lipid solubility. The local anaesthetics showed greater inhibitory potency at a higher extracellular pH. The results suggest that clinically relevant concentrations of local anaesthetics inhibit the stimulus-secretion coupling in the chromaffin cells. The un-ionized based form plays a major role, and the inhibitory potency does not depend on the lipid solubility of the anaesthetics.

Adrenal Medulla↗
PubMed1993

Adrenoceptor mechanism involved in thiopental-epinephrine-induced arrhythmias in dogs.

The authors investigated the role of alpha 1- and beta-adrenoceptors on induction of ventricular arrhythmias during thiopental anesthesia in dogs and compared with that during halothane anesthesia. Throughout this study, arrhythmogenic threshold of epinephrine during thiopental anesthesia was designed to be comparable with that during halothane anesthesia. Phenylephrine, an alpha 1-agonist, and isoproterenol, a beta-agonist, consistently failed to provoke arrhythmias during thiopental or halothane anesthesia. The interaction between phenylephrine and isoproterenol in inducing arrhythmias was synergistic and additive during halothane and thiopental anesthesia, respectively, indicating that adrenoceptor mechanism in thiopental-epinephrine arrhythmias is different from that in halothane-epinephrine arrhythmias. During thiopental anesthesia, incidence of arrhythmias with blood pressure elevation by epinephrine, phenylephrine, or angiotensin II was not different, and increasing heart rate by electrical pacing did not replace isoproterenol in the arrhythmogenic interaction between isoproterenol and phenylephrine. The results indicate that blood pressure elevation due to the combined inotropic action of alpha 1- and beta-adrenoceptor agonists is a critical factor in the genesis of thiopental-epinephrine arrhythmias.

Adrenergic alpha-Agonists↗
PubMed1993

Anesthetic interaction between midazolam and halothane in humans.

The present study was undertaken in humans to determine the anesthetic efficacy of midazolam in terms of its ability to reduce halothane minimum alveolar anesthetic concentration (MAC). Fifty women scheduled for simple or radical hysterectomy were allocated randomly to one of four groups; group A was given no midazolam as a control; groups B, C, and D were given midazolam intravenously by a bolus of 0.1, 0.2, and 0.4 mg/kg followed by infusion of 1, 2, and 4 micrograms.kg-1 x min-1, respectively. Halothane MAC was 0.78%, 0.47%, 0.38%, and 0.23% at mean serum midazolam concentrations of 0, 134, 250, and 539 ng/mL in groups A, B, C, and D, respectively. The interaction between halothane and midazolam in the anesthetic efficacy conformed to an exponential fit. The results indicate that midazolam produces marked reduction of halothane MAC in humans at serum concentrations lower than that required to cause sleep. Lastly, midazolam's potentiation of halothane has a saturated nature.

Adult↗
PubMed1993

The effect of nicardipine on carotid blood flow velocity, local cerebral blood flow, and carbon dioxide reactivity during cerebral aneurysm surgery.

We studied the effects of nicardipine (initial infusion rate 0.5 micrograms.kg-1 x min-1) on blood flow velocity in the internal carotid artery, local cerebral blood flow (LCBF), and carbon dioxide reactivity in 20 patients undergoing craniotomy for cerebral aneurysm clipping under isoflurane anesthesia. The blood flow velocity in the internal carotid artery was measured at T0 and T3 by a 20-MHz pulsed ultrasound Doppler flowmeter. LCBF was measured by the thermal gradient blood flow meter. Group A consisted of 10 patients with a good neurologic status (Hunt and Kosnik Grade I); Group B consisted of 10 patients with a poor status (Grades II-IV). Nicardipine was infused until the mean arterial blood pressure decreased to about 75% of the initial value and was maintained at this level until the completion of aneurysm clipping. The measurements of hemodynamics and LCBF were performed after the exposure of the internal carotid artery (T0), and 10 and 30 min after the start of nicardipine (T1 and T2, respectively), before aneurysm clipping (T3), and 30 min after its discontinuation (T4). Carbon dioxide reactivity [% ALCBF/APaCO2 (%/mm Hg)] was evaluated at T0, T3, and T4. Mean arterial blood pressure decreased after nicardipine infusion in both groups. LCBF did not change during nicardipine infusion in either group. Blood flow velocity increased significantly in Group A after nicardipine infusion from 45.1 +/- 6.9 to 51.5 +/- 6.4 cm/s (P < 0.05), but in Group B flow velocity did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Time-related differential effects of epidural morphine on the neuraxis.

To clarify the site and potency of the analgesic and anesthetic action of epidurally administered morphine, we investigated the effects of epidurally and intravenously administered morphine (100 micrograms/kg) on change in the pressure pain threshold (PPT) and the minimum alveolar concentration (MAC) of halothane. Epidural morphine (EM) increased PPT significantly (P < 0.01) at the points around the surgical incision by 40% and 60% from baseline compared with intravenous morphine (IM) with which PPT remained at baseline 1 and 2 h after administration, respectively. Duration of analgesia was much longer in EM than in IM (18 h vs 1.7 h). EM increased PPT from preoperative value at the forehead and the points around the surgical incision by 9.9% and -24.9% at 1 h, by 10.9% and 3.8% at 4 h, and by -19.5% and -50.4% at 12 h after administration at mean values, respectively. Halothane MAC in EM and IM were 0.54% and 0.57%, respectively, 40 min after administration. Halothane MAC in EM at 4 h and 12 h after administration were 0.45% and 0.70%, respectively. The results suggest that EM provides long-lasting analgesia by its time-related differential effects on the neuraxis.

Adult↗
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↗