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Biomedical subjects

I Yoshiya

Publications and source records attributed to I Yoshiya.

At least 73 records · Page 4Linked to original sources
PubMed1997

[Hemodynamic effects of amrinone combined with dopamine in patients undergoing living renal transplantation].

Systemic hypertension is a constant feature of chronic renal failure, mediated by renin and exacerbated by salt and fluid loading. Vascular atherosclerosis appears to accelerate in patients on long-term dialysis. Therefore, it is important to control hypertension and keep appropriate renal blood flow during living renal transplantation surgery. Amrinone, a phosphodiesterase inhibitor, produces vasodilation in arterial smooth muscle as well as venodilation in the capacitance bed. By increasing myocardial contractility it increases inotropic effect. Amrinone has potent inodilator effects because of its dual mechanism of action. The current study is aimed to compare hemodynamic effects between amrinone (3-5 mg.kg-1.min-1) (AMR group, n = 4) and nitroglycerin (0.3-1.0 mg.kg-1.min-1) (NTG group, n = 5), combined with dopamine (3-5 mg.kg-1.min-1) in nine patients undergoing living renal transplantation. Increase in cardiac index in AMR group was significantly larger than that in NTG group. Values of systemic and pulmonary vascular resistance in AMR group were significantly smaller than those in NTG group. No significant difference was found in renal function in the post-operative period.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1996

Cardiovascular effects of an ultra-short-acting nitric oxide-releasing compound, zwitterionic diamine/NO adduct, in dogs.

BACKGROUND: This study was conducted to clarify the cardiovascular effects of a new NO-releasing compound, NOC-7, and to compare it with other nitrovasodilators, sodium nitroprusside (SNP) and nitroglycerin, in dogs anesthetized with pentobarbital. METHODS AND RESULTS: A bolus injection of NOC-7 decreased mean aortic blood pressure in a dose-dependent manner. The onset was rapid and the recovery quick. Continuous infusion of NOC-7 decreased mean aortic pressure from 115 +/- 3.9 to 84 +/- 2.9 mm Hg and infusion of SNP, from 118 +/- 3.8 to 87 +/- 3.1 mm Hg. The optimum doses of NOC-7 and SNP were determined to be 2.73 +/- 0.77 and 11.5 +/- 6.1 micrograms.kg-1.min-1, respectively. During infusion of NOC-7, heart rate and cardiac output were increased (P < .05), pulmonary artery pressure was not changed, and systemic and pulmonary vascular resistances were decreased (P < .05). Electromagnetic flowmetry showed that portal venous and internal carotid arterial blood flow were increased (P < .05) and that hepatic and renal arterial blood flows were not changed. These hemodynamic changes during NOC-7 infusion were similar to those with SNP. The plasma level of NO2-/NO3 did not change, but methemoglobin increased slightly (P < .05). Comparison between hypotensive responses before and after a 3.5-hour infusion of NOC-7 or nitroglycerin showed that acute tolerance developed to nitroglycerin but not to NOC-7. CONCLUSIONS: The results indicate that NOC-7 may be useful as an ultra-short-acting nitrovasodilator that has no major adverse effect or tolerance.

Animals↗
PubMed1996

A new nitric oxide donor, NOC-18, exhibits a nociceptive effect in the rat formalin model.

The utility of a new nitric oxide (NO) donor, NOC-18, and the contribution of the neurotransmitter NO to nociception in response to tissue injury in rats, were examined following the subcutaneous injection of formalin into the hindpaw. This model induces biphasic responses in pain-related behavior, such that C-fiber activation during the first phase triggers a state of central sensitization characterized by the second phase. Formalin-induced nociceptive behavior was facilitated by intracerebroventricular administration of NOC-18 in the second phase, but not the first phase. This enhancement was completely abolished by the soluble guanylate cyclase inhibitor, methylene blue. These findings indicate that NO causes nociception via the NO-cGMP pathway in the central nervous system and NOC-18 proved to be a convenient and useful tool for the investigation of nociception-related NO.

Animals↗
PubMed1996

Direct inhibition of the actomyosin motility by local anesthetics in vitro.

Using a recently developed in vitro motility assay, we have demonstrated that local anesthetics directly inhibit myosin-based movement of single actin filaments in a reversible dose-dependent manner. This is the first reported account of the actions of local anesthetics on purified proteins at the molecular level. In this study, two tertiary amine local anesthetics, lidocaine and tetracaine, were used. The inhibitory action of the local anesthetics on actomyosin sliding movement was pH dependent; the anesthetics were more potent at higher pH values, and this reaction was accompanied by an increased proportion of the uncharged form of the anesthetics. QX-314, a permanently charged derivative of lidocaine, had no effect on actomyosin sliding movement. These results indicate that the uncharged form of local anesthetics is predominantly responsible for the inhibition of actomyosin sliding movement. The local anesthetics inhibited sliding movement but hardly interfered with the binding of actin filaments to myosin on the surface or with actomyosin ATPase activity at low ionic strength. To characterize the actomyosin interaction in the presence of anesthetics, we measured the binding and breaking force of the actomyosin complex. The binding of actin filaments to myosin on the surface was not affected by lidocaine at low ionic strength. The breaking force, measured using optical tweezers, was approximately 1.5 pN per micron of an actin filament, which was much smaller than in rigor and isometric force. The binding and breaking force greatly decreased with increasing ionic strength, indicating that the remaining interaction is ionic in nature. The result suggests that the binding and ATPase of actomyosin are governed predominantly by ionic interaction, which is hardly affected by anesthetics; whereas the force generation requires hydrophobic interaction, which plays a major part of the strong binding and is blocked by anesthetics, in addition to the ionic interaction.

Actins↗
PubMed1996

Ketamine inhibits nitric oxide production in mouse-activated macrophage-like cells.

We have investigated the effects of ketamine on nitric oxide produced by activated macrophages using a murine macrophage-like cell line, J774. Cells were incubated for 18 h under stimulation with lipopolysaccharide and interferon-gamma or lipoteichoic acid and interferon-gamma, with various concentrations of ketamine (6-600 mumol litre-1). Nitric oxide production was assessed by measuring nitrite, a stable by-product of nitric oxide breakdown, in the medium. Other N-methyl-D-aspartate receptor antagonists, MK-801 (150 mumol litre-1) and dextromethorphan (150 mumol litre-1) were also tested. In addition, we studied the effects of ketamine on production of tumour necrosis factor-alpha by activated macrophages. Ketamine inhibited nitrite production dose-dependently with both lipopolysaccharide- and lipoteichoic acid-activated macrophages by up to approximately 65% at the highest ketamine concentration (600 mumol litre-1). Neither MK-801 nor dextromethorphan had an inhibitory effect. Ketamine also suppressed production of tumour necrosis factor-alpha. The data show that ketamine inhibited nitric oxide production by activated macrophages probably, in part, via inhibition of production of tumour necrosis factor-alpha, an autocrine stimulatory factor for nitric oxide production, but not via the NMDA receptor pathway, which is involved in neuronal nitric oxide production.

Anesthetics, Dissociative↗
PubMed1996

Mode and site of analgesic action of epidural buprenorphine in humans.

This study was designed to clarify the site of analgesic action of epidural buprenorphine and its spinal segmental analgesia. Fifty patients undergoing gastrectomy were randomly assigned to five groups according to the dose of buprenorphine and route of administration: epidural saline group, epidural buprenorphine 2- and 4-micrograms/kg groups, and intravenous buprenorphine 2- and 4-micrograms/kg groups. The changes in pressure pain threshold (PPT) and visual analog scale (VAS) were compared within groups of patients receiving either buprenorphine, 2 or 4 micrograms/kg epidurally, and between groups of patients receiving buprenorphine 2 or 4 micrograms/kg either epidurally or intravenously. The PPT near the surgical incision was significantly greater (P < 0.05) in the epidural buprenorphine group compared to the intravenous group during the middle period (between 2 and 6 h after administration) of analgesia obtained after administration of buprenorphine. VAS response significantly (P < 0.05) decreased in the epidural group compared to the intravenous group at the same dose. In the smaller dose buprenorphine epidural group, PPT at the forehead (an index of systemic analgesia) exceeded the preoperative value during the 12 h after administration of buprenorphine. PPT near the surgical incision decreased by 30% from the preoperative value and did not exceed the preoperative value throughout the study. PPT at the forehead significantly exceeded the PPT changes measured near the surgical incision (an index of regional analgesia) (P < 0.05). In the larger dose buprenorphine epidural group, during the early period (up to 2 h after administration), PPT at the forehead increased by 30%-40%, while PPT near the surgical incision decreased by 10%-25% compared to the preoperative value (P < 0.01). However, in the middle period, there were no significant differences in the changes between PPT at the forehead and near the surgical incision. In the late period (more than 6 h after administration), PPT at the forehead maintained the level of preoperative value, whereas PPT near the surgical incision decreased by more than 25% from the preoperative value (P < 0.01). VAS value significantly (P < 0.01) decreased in the larger dose buprenorphine epidural group compared with that in the smaller dose group during the middle period. The larger dose of epidural buprenorphine provided better analgesia than the smaller dose. We conclude that epidural buprenorphine acts predominantly at the supraspinal region and produces spinal segmental analgesia in a dose-related manner.

Adult↗
PubMed1996

Antiarrhythmic action of rilmenidine on adrenaline-induced arrhythmia via central imidazoline receptors in halothane-anaesthetized dogs.

1. To elucidate the role of central imidazoline receptors in the genesis of adrenaline-induced arrhythmias under halothane anaesthesia, we investigated the effects of rilmenidine, a selective agonist at imidazoline receptors, on this type of arrhythmia in dogs. Rilmenidine (1, 3, 10 micrograms kg-1, i.v.) did not affect basal haemodynamic parameters (heart rate and blood pressure), but dose-dependently inhibited adrenaline-induced arrhythmias under halothane anaesthesia. 2. Although, rilmenidine has a weak affinity for alpha(2)-adrenoceptors, pretreatment with idazoxan (10 micrograms kg-1, intracisternally i.c.), an imidazoline receptor antagonist which has also alpha(2)-adrenoceptor blocking potency, blocked the antiarrhythmic effect of rilmenidine (10 micrograms kg-1, i.v.). In contrast, pretreatment with rauwolscine (20 micrograms kg-1, i.c.), a classical alpha(2)-adrenoceptor antagonist with little affinity for imidazoline receptors, did not affect the effect of rilmenidine (10 micrograms kg-1, i.v.). Furthermore, bilateral vagotomy completely blocked the antiarrhythmic action of rilmenidine (10 micrograms kg-1, i.v.). 3. It is suggested that the antiarrhythmic action of rilmenidine is due to the activation of central imidazoline receptors and that vagal tone is critical for this action of rilmenidine.

Adrenergic alpha-Agonists↗
PubMed1996

Fucoidin, a potent inhibitor of leukocyte rolling, prevents neutrophil influx into phorbol-ester-induced inflammatory sites in rabbit lungs.

The polysaccharide fucoidin, a homopolymer of sulfated L-fucose, is known, by interfering with the function of L-selectin, to inhibit leukocyte rolling, which is an early and essential step in the process of leukocyte extravasation into inflamed sites. We tested the inhibitory effect of fucoidin on neutrophil accumulation in lung inflammation induced by phorbol myristate acetate and peritoneal inflammation induced by thioglycollate in rabbits. Pretreatment (10 mg/kg) followed by continuous administration (10 mg/kg/h) of fucoidin dramatically reduced the number of neutrophils recruited into the lungs (determined by neutrophil counts in bronchoalveolar lavage fluid; 97.7 +/- 0.52% reduction) and peritoneal cavity (determined by neutrophil counts in peritoneal lavage fluid; 98.4 +/- 1.29% reduction). Fucoidin treatment also increased the systemic neutrophil count. These results suggest that the inhibition of leukocyte rolling, which may be a primary function of fucoidin, leads to a reduction of neutrophil accumulation at inflammatory sites, which may be beneficial for attenuating neutrophil-mediated tissue injury.

Animals↗
PubMed1996

[Pharmacokinetics of propofol during liver transplantation in small pigs].

A study using 14C propofol showed that the liver is the main eliminating organ for the agent. The current study was designed to clarify pharmacokinetics of propofol during liver transplantation in pigs. Five small pigs weighing 25.4 +/- 2.5 kg were anesthetized with isoflurane (0.5-1.5%) and mechanically ventilated under muscle paralysis with pancuronium. In the anhepatic phase, veno-veno bypass was placed from the inferior vena cava and portal vein to the superior vena cava. We studied pharmacokinetic parameters following an intravenous bolus injection of propofol at 2 mg.kg-1 in each phase, i.e. the pre-anhepatic, anhepatic and post-anhepatic phase during liver transplantation. Pharmacokinetic analysis showed that total plasma clearance of propofol in the anhepatic phase was significantly lower than that in the post-anhepatic phase. The results suggest that propofol may be metabolized extrahepatically and can be used at reduced doses in the anhepatic phase during liver transplantation.

Anesthetics, Intravenous↗
PubMed1996

Adrenoceptor mechanism involved in thiopental-induced potentiation of halothane-epinephrine arrhythmias in dogs.

Although thiopental is known to potentiate halothane-epinephrine arrhythmias, the precise mechanism of this potentiation is obscure. The authors investigated the comparative role of alpha 1 and beta adrenergic actions in the thiopental-induced potentiation of halothane-epinephrine arrhythmias in dogs. Adult mongrel dogs were anesthetized with halothane alone (1.3%) or thiopental (20 mg kg-1) plus halothane and monitored continuously for systemic arterial pressures and for premature ventricular contractions. The arrhythmogenic doses of phenylephrine and isoproterenol were determined during the two anesthetic methods and the effect of thiopental on the arrhythmogenic action of alpha 1 and beta agonists was examined. Thiopental failed to exert a significant potentiation of arrhythmogenic effect of phenylephrine or isoproterenol, when these agents were administered separately. On the other hand, the potentiation of arrhythmogenicity by thiopental was remarkable in the case of combined administration of both the agonists, that is, thiopental enhanced the synergistic interaction between phenylephrine and isoproterenol for inducing arrhythmias during halothane anesthesia. In addition, the potentiation was more prominent when a low dose of isoproterenol and a high dose of phenylephrine was combined than that when a high dose of isoproterenol and a low dose of phenylephrine was given in combination. The results indicate that thiopental significantly potentiates the arrhythmogenic interaction of alpha 1 and beta adrenergic agonists administered concurrently, although individual potentiation of these agonists is not significant.

Anesthetics↗
PubMed1996

[Sevoflurane inhalation reduced bronchospasm after extubation].

A 73-year-old female was scheduled for left upper lobectomy. She had no history of asthma or chronic obstructive pulmonary disease. During the operation, respiratory sound was clear. As spontaneous breathing was regular and stable after the reversal of neuromuscular blockade, an endotracheal tube was extubated. But soon after the extubation, wheezing and gasping respiration occurred and she complained of dyspnea. Therefore, we administered aminophylline and steroid intravenously, and the patient's lungs were ventilated manually with 100% oxygen. But after 10 minutes, there was no improvement in symptoms, and sevoflurane inhalation was started immediately. Inspiratory sevoflurane concentration was 4% at first, and was decreased to 2%. About 20 minutes after starting sevoflurane inhalation, wheezing was reduced. Sevoflurane may be useful in the treatment of bronchospasm after extubation.

Administration, Inhalation↗
PubMed1996

[Anesthetic management of a patient complicated with restrictive cardiomyopathy for gastrectomy].

Restrictive cardiomyopathy is a rare condition characterized with endomyocardial fibrosis, which interferes diastolic ventricular filling. A 52-year-old man with a 38 year history of dyspnea on effort presented with advanced gastric cancer. Subtotal gastrectomy under general anesthesia was scheduled. Preoperative examination showed biventricular dysfunction, impaired liver function and chronic renal failure. General anesthesia was induced using fentanyl, pancuronium and isoflurane, and maintained with nitrous oxide/oxygen, isoflurane and fentanyl. Extensive invasive monitoring included arterial blood pressure, central venous pressure, pulmonary artery pressure and oxygen saturation of mixed venous blood as indices of left-sided pump function. Dopamine and nitroglycerin infusion was also started after the tracheal intubation. Although a transient improvement of cardiac function was noted after the removal of ascites 5 liter, restricted fluid administration induced desaturation of mixed venous blood and tachycardia. The start of low dose prostaglandin E1 markedly improved cardiac output without hypotension, while an increase of intravenous nitroglycerin did not prove to be beneficial. PGE1 was more selective in decreasing left ventricular afterload, while nitroglycerin produces greater decrease of preload.

Alprostadil↗
PubMed1995

NOC, a nitric-oxide-releasing compound, induces dose dependent apoptosis in macrophages.

The ability of exogenous nitric oxide (NO) to induce apoptosis in macrophages was analyzed using NOC, a NO-releasing compound, as a source of NO. Exogenous NO was shown to induce apoptosis in a dose dependent manner. Quantitative analysis revealed that the amount of NO required to induce apoptosis in more than half of macrophages exposed was 100 times larger than that for endogenous NO-induced apoptosis. NOC proved to be a convenient and useful tool for investigation of apoptosis related to NO.

Animals↗
PubMed1995

Intracerebroventricular administration of a nitric oxide-releasing compound, NOC-18, produces thermal hyperalgesia in rats.

This study was undertaken to define the role of nitric oxide (NO) in central nociceptive mechanisms by intracerebroventricular injection of an NO-releasing compound, NOC-18, in rats. The nociceptive threshold was evaluated by the radiant heat tail-flick test. Sixty-nine rats were divided into the seven groups, and the following drugs were injected intracerebroventricularly in 5 microliters of saline: no drug (control) (n = 13), 15 micrograms of NOC-18 (n = 15); 150 micrograms of NOC-18 (n = 9); 100 micrograms of N-nitro-L-arginine methyl ester (L-NAME) (n = 8); 15 micrograms of NOC-18 + 100 micrograms of L-NAME (n = 8); 10 micrograms of methylene blue (MB) (n = 8); 15 micrograms of NOC-18 + 10 micrograms of MB (n = 8). NOC-18 caused a dose-dependent curtailment (7% and 23% decreases for 15 micrograms and 150 micrograms of NOC-18, respectively) of the tail-flick latency during the period from 15 to 120 min. L-NAME caused prolongation (15% maximum) of the tail-flick latency during the period from 15 to 150 min. However, NOC-18-induced hyperalgesia was not influenced by L-NAME. MB also caused prolongation (9% maximum) of the tail-flick latency during the period from 15 to 150 min, and completely blocked the hyperalgesia induced by 15 micrograms of NOC-18. These findings indicate that the NO-cGMP pathway is directly involved in thermal hyperalgesia in the brain.

Animals↗
PubMed1995

Pulmonary resistance in dogs: a comparison of xenon with nitrous oxide.

Xenon (Xe) may cause an increase in airway resistance due to its high density and viscosity. The object of this study was to examine the effects of Xe on pulmonary resistance using dog models with normal and methacholine-treated airways. During anaesthesia 22 mongrel dogs' tracheas were intubated and the lungs were mechanically ventilated with 70% N2/30% O2 as a control gas. The gases 70% nitrous oxide (N2O), 50% N2O, 70% Xe and 50% Xe were administered in a random order for 25 min. Bronchoconstriction was produced by a continuous infusion of methacholine, 0.22 mg.kg-1.hr-1. Pulmonary resistance (RL) was calculated by the isovolume method using flow at the airway opening, volume and transpulmonary pressure. In normal dogs, RL breathing 70% Xe (mean +/- SEM, 0.84 +/- 0.12 cm H2O.L-1.sec-1) was greater (P < 0.05) than with 70% N2O, 50% N2O or control gas (0.61 +/- 0.08, 0.59 +/- 0.06 and 0.62 +/- 0.06 cmH2O.L-1.sec-1). Breathing 50% Xe the RL (0.77 +/- 0.10 cmH2O.L-1.sec-1) was not different from 50% N2O or control. Methacholine infusion increased RL 3.92 +/- 1.98 (mean +/- SD) times. The RL breathing 50% Xe (2.55 +/- 0.44 cmH2O.L-1.sec-1) was not greater than during 50% N2O or control (2.08 +/- 0.33 and 2.13 +/- 0.33 cmH2O.L-1.sec-1) in methacholine-treated dogs. The data suggest that inhalation of high concentrations of Xe increases airway resistance, but only to a modest extent in dogs with normal or methacholine-treated airways.

Airway Resistance↗