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Biomedical subjects

I Yoshiya

Publications and source records attributed to I Yoshiya.

At least 127 records · Page 7Linked to original sources
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↗
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

Roles of beta 1- and beta 2-adrenoceptors in the mechanism of halothane myocardial sensitization in dogs.

The authors investigated the comparative roles of beta 1- and beta 2-adrenoceptors in myocardial sensitization by halothane in dogs. The arrhythmogenic dose (AD) of isoproterenol was determined in the presence of various doses of phenylephrine during halothane anesthesia in dogs, and the influences of 1-metoprolol (beta 1-antagonist) and ICI-118,551 (beta 2-antagonist) on the AD were examined. In the presence of 1-metoprolol, the AD of isoproterenol was significantly greater than the control, but in the presence of ICI-118,551, the AD of isoproterenol was lower. Blood pressure during the arrhythmias was higher in the presence of ICI-118,551 than that in controls. In addition, the AD of ritodrine (beta 2-agonist) was also determined at various doses of phenylephrine. The interaction between phenylephrine and ritodrine in inducing arrhythmias showed hyperbolic isoboles. However, 1-metoprolol completely inhibited the occurrence of arrhythmias induced by ritodrine and phenylephrine. The results suggest that myocardial beta 1-adrenoceptors play an essential role in the genesis of arrhythmias during halothane anesthesia in dogs, whereas beta 2-adrenoceptors do not.

Adrenergic beta-Agonists↗
PubMed1991

Contribution of the lungs to the clearance of exogenous dopamine in humans.

The contribution of the lungs to the clearance of exogenous dopamine was analyzed in humans by measuring plasma pulmonary concentrations of dopamine and the pulmonary plasma flow before and after infusion of dopamine. Contribution of the lungs was defined as the ratio between clearance by the lungs and the total plasma clearance of dopamine. Significant transpulmonary gradient of plasma dopamine was observed with infusions at rates of 1.0 and 2.0 micrograms.kg-1.min-1, but not at 0.5 micrograms.kg-1.min-1. The calculated contribution values were 4.90%, 19.23%, and 20.60% at the doses of 0.5, 1.0, and 2.0 micrograms.kg-1.min-1, respectively. The results suggest that the clearance mechanism of the lungs is effective when the plasma dopamine level becomes sufficiently high, and that the lungs clear 19%-21% of clinical doses of dopamine.

Adult↗
PubMed1991

[The effect of intravenous injection of isosorbide dinitrate on the hypertension during general anesthesia: a multi-center controlled study].

The antihypertensive effect of intravenous injection of isosorbide dinitrate (ISDN) was evaluated in 137 patients undergoing elective surgery during general anesthesia [neuroleptanesthesia (NLA) or enflurane-nitrous oxide-oxygen-anesthesia (GOE)]. ISDN in dose of 20 micrograms.kg-1 or 40 micrograms.kg-1 was given as a bolus injection in 30 sec. ISDN produced a significant decrease in arterial pressure and central venous pressure; the maximum decrease was observed in 7 min after administration of ISDN. The antihypertensive effect of ISDN was dose-dependent, but there was no significant difference between two groups of patients given 20 or 40 micrograms.kg-1, or between those anesthetized with NLA or GOE. ISDN did not significantly alter heart rate, thereby causing a significant decrease in rate pressure product which reflects myocardial oxygen demand. The results suggest that a bolus injection of ISDN is a simple, practical and effective means of controlling hypertension during general anesthesia.

Adult↗
PubMed1991

Phenytoin prevents epinephrine-induced arrhythmias through central nervous system in halothane-anesthetized dogs.

The authors investigated the effect of phenytoin through the central nervous system on epinephrine-induced arrhythmias in halothane-anesthetized dogs. The arrhythmogenic dose (AD) of epinephrine during halothane anesthesia was determined in the presence of phenytoin (1 mg/kg), vehicle, and saline, which were administered directly into the cisterna magna. Phenytoin increased the AD of epinephrine as compared with vehicle or saline. The cerebrospinal and plasma concentration of phenytoin during the arrhythmias were 23.6 and less than 0.5 micrograms/ml, respectively. There was no significant difference in AD between the vehicle and saline groups. The same dose of phenytoin (1 mg/kg) administered intravenously did not affect the AD of epinephrine, and the plasma concentration of phenytoin during the arrhythmias was 1.2 micrograms/ml. These findings suggested that phenytoin exerts a protective effect against halothane-epinephrine arrhythmias through a central mechanism and that the central nervous system may be involved, at least in part, in the myocardial sensitization by halothane.

Anesthesia↗
PubMed1991

The effect of prostaglandin E1 on local cerebral blood flow during cerebral-aneurysm clip ligation.

Prostaglandin E1(PGE1) was administered for deliberate hypotension during general anaesthesia in 27 patients undergoing cerebral-aneurysm clip ligation, and the effect of the drug on local cerebral blood flow was studied. Local cerebral blood flow measurements were made using a thermal-gradient blood flowmeter. Control measurements were made immediately before administration of the drug. Local cerebral blood flow was measured 10, 30, 60 and 120 min after starting the drug infusion and 10, 30 and 60 min after discontinuation. The mean blood pressure was reduced significantly by the administration of PGE1. Urine output was increased after commencement of the drug infusion. Local cerebral blood flow did not change. These results suggest that PGE1 may be an appropriate hypotensive drug for use during cerebral-aneurysm clip ligation, because the cerebral blood flow remains within the normal range and the urine output is increased.

Alprostadil↗
PubMed1990

Immunohistochemical distribution of calcium-activated neutral proteinases and endogenous CANP inhibitor in the rabbit hippocampus.

Intracellular accumulation of Ca2+ after brain ischemia is regarded as one of the principal causes of neuronal death, but details of the intracellular events occurring after Ca2+ accumulation have not yet been described. We propose that a calcium-activated neutral proteinase which can degrade neuronal cytoskeletal proteins might link Ca2+ accumulation and irreversible injury of the neuronal intracellular structure. First, therefore, we examined the distribution of calcium-activated neutral proteinase in normal brains. Immunohistochemical distribution of calcium-activated neutral proteinases (CANP) with high and low sensitivity to Ca2+ (muCANP and mCANP) and of endogenous CANP inhibitor was investigated in the dorsal hippocampus of the rabbit. muCANP-immunoreactivity was detected in almost all of the pyramidal cells and granule cells and in some other neurons. A full-length staining from perikarya to dendrites was shown in muCANP-positive neurons. mCANP-immunoreactivity was found mainly in four kinds of hippocampal interneurons: 1) basket cells in the stratum oriens of Ammon's horn, 2) pyramidal basket cells at the boundary of pyramidal cell layer and stratum oriens, 3) polymorphic cells in the hilar region of dentate gyrus, and 4) pyramidal or fusiform basket cells at the inner boundary of the granule cell layer and the hilar region. The distribution of these four kinds of neurons was similar to that of parvalbumin-containing GABAergic neurons. CANP inhibitor immunoreactivity was confined to pyramidal cells in the CA3-CA3c region and some hilar neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Fine structure of noradrenergic terminals and their synapses in the rat spinal dorsal horn: an immunohistochemical study.

Noradrenergic fibers in the spinal dorsal horn originate from neurons in the A5-7 cell groups, and may participate in the modulation of pain. Here we studied the fine structure of noradrenergic terminals in the rat by immunohistochemistry using antiserum against dopamine-beta-hydroxylase (DBH). We also investigated the relationship between such terminals and primary afferent terminals. DBH-like immunoreactive terminals were found in lamina I and the outer layer of lamina II of the dorsal horn and they contained many clear round vesicles and some large granular vesicles. More than half of these terminals made synaptic contact with other neuronal elements with membrane specialization. Most of the postsynaptic structures of these terminals were small dendrites (69%); 28% were spines, and no synaptic contact was made with primary afferent terminals. These findings suggest that noradrenaline acts on the spinal dorsal horn neurons postsynaptically mainly via a direct synaptic mechanism.

Animals↗
PubMed1990

Calcium-binding proteins calbindin and parvalbumin in the superficial dorsal horn of the rat spinal cord.

Neurons containing the calcium-binding proteins, calbindin or parvalbumin, were studied by immunohistochemistry in the superficial dorsal horn of the rat spinal cord. Calbindin-containing cells were found in laminae I, II and III, being more abundant in laminae I and II. Some of the neurons in lamina I containing calbindin projected to the supraspinal area. Parvalbumin-containing neurons were mainly distributed in laminae IIi and III. Calbindin and parvalbumin were not detected in the same cells. Some 75% of the neurotensin-like immunoreactive neurons contained calbindin, which corresponded to 13% of the calbindin-containing neurons. Calbindin was sometimes found in the same cells with substance P, enkephalin or somatostatin but less frequently (44-46% of the peptide-containing neurons). Parvalbumin was not found together with these peptides. Electron microscopy showed that the immunoreactive products of calbindin or parvalbumin were mostly in the dendrites or cell bodies. Immunoreactive axon terminals were relatively few. In rhizotomized animals, neurons containing one of these proteins in laminae II and III were found to receive direct inputs of primary afferent fibers. These findings indicate that neurons containing these two proteins belong to different subpopulations of dorsal horn neurons. They may be important in primary afferent processing.

Animals↗
PubMed1990

Comparison of flow-resistive work load due to humidifying devices.

There are many kinds of humidifying devices. We evaluated six humidifiers from the viewpoint of AWLs. The AWL was obtained by calculating the area difference between pressure-volume tracings obtained without and with humidifiers. To examine the effect of pressure monitoring sites on AWL when a humidifier is placed, we measured AWL at three different pressure monitoring sites. The AWL was affected significantly by the pressure monitoring site for the ventilator. When a pressure monitor sensor was placed on the inspiratory limb between the inspiratory valve and humidifiers, the ventilator was not able to compensate for the pressure drop caused by impedance characteristics of the humidifier equipment. This resulted in significant inspiratory AWL on the patient. Thus, humidifying devices should be carefully selected from the viewpoint of not only humidifying capability but also AWL. Furthermore, we must recognize the importance of the pressure monitoring site for the ventilator.

Airway Resistance↗