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Biomedical subjects

H Tsuchida

Publications and source records attributed to H Tsuchida.

At least 91 records · Page 5Linked to original sources

[Anesthesia combined with profound hypothermia using cardiopulmonary bypass for clipping of giant basilar artery aneurysm].

A 52 year-old female was scheduled for clipping of giant basilar artery aneurysm. This operation needed temporary clipping of the basilar artery for 30-40 minutes, and preoperative examination suggested that some regions would become ischemic by temporary clipping. Therefore profound hypothermia using cardiopulmonary bypass (CPB) and thiamylal loading were planned to prevent cerebral damage during the operation. Anesthesia was induced with thiamylal, fentanyl, and isoflurane in nitrous oxide and oxygen. Following administration of vecuronium, trachea was intubated. Two hours after the start of surgery, thiamylal was titrated to obtain EEG patterns of burst-suppression before CPB and the infusion was continued until CPB was discontinued. With burst-suppression present, CPB was instituted. Hypothermia below 20 degrees C at pulmonary artery temperature was maintained until the aneurysm was clipped and bleeding from the operating site was controlled. Cooling and rewarming by CPB were carried out with ease and uneventfully. The patient had no neurological complications postoperatively.

Basilar Artery↗

Regulation of neutrophil apoptosis--its biological significance in inflammation and the immune response.

Neutrophils play a pivotal role in host defence against bacterial infection. Their life span is short compared with that of leukocytes of other lineages. Neutrophils are programmed to die by apoptosis at the time of differentiation. However, recent studies have demonstrated that environment also has a great influence on apoptosis of these cells. Based on our recent experimental results, we present here a review of studies on the regulation of neutrophil apoptosis and discuss its biological significance in inflammation and the immune response.

Animals↗

In vivo regulation of rat neutrophil apoptosis occurring spontaneously or induced with TNF-alpha or cycloheximide.

We previously demonstrated that human TNF-alpha induces rapid apoptosis of human neutrophils. To understand better the in vivo significance of neutrophil apoptosis, we examined spontaneous, recombinant human and mouse TNF-alpha- or cycloheximide-induced apoptosis of normal peripheral blood neutrophils (PBN), PBN from rats injected i.p. with proteose peptone or a streptococcus preparation, OK-432 (inflammatory PBN), peritoneally exudated neutrophils (PEN) obtained after a proteose peptone injection, and normal bone marrow neutrophils. The following observations were made. 1) Normal PBN responded to TNF-alpha, but PEN, normal bone marrow neutrophils, and inflammatory PBN at 12 h after stimulation did not. 2) The sensitivity to TNF-alpha of the inflammatory PBN started to decrease at 3 h, was lowest at 12 h, and was almost restored at 52 h after stimulation. 3) Spontaneous apoptosis of normal and inflammatory PBN reached 25% at 12 h after in vitro incubation, but that of PEN and normal bone marrow neutrophils was very low over this period. 4) The sensitivity to cycloheximide (6 h incubation) was high for normal PBN and bone marrow neutrophils, but low for PEN and inflammatory PBN after 12 h. 5) 125I-rhTNF-alpha binding of bone marrow neutrophils was significantly lower than that of normal and inflammatory PBN and PEN. 6) TNF-alpha-induced apoptosis of normal or inflammatory PBN and bone marrow neutrophils was enhanced by treatment with low doses of cycloheximide that alone were barely able to induce neutrophil apoptosis; however, apoptosis of PEN was not. The mechanisms and in vivo significance of these phenomena are discussed.

Animals↗

Composite porosity of expanded polytetrafluoroethylene vascular prosthesis.

Polytetrafluoroethylene (PTFE) prostheses were modified to produce two types of composite porosity PTFE grafts: type I--inner 60 microns/outer 20 microns and type II--inner 20 microns/outer 60 microns. These composite porosity PTFE designs were investigated for bleed through, graft healing and patency and compared with high porosity PTFE (60 microns) and standard PTFE (20 microns) grafts. The grafts were implanted into the carotid and femoral arteries of dogs and retrieved after 4, 12 and 18 weeks. Both composite porosity grafts showed significantly less bleed through than standard and high porosity grafts after reperfusion. In composite grafts, the 60-microns layer allowed fibrovascular tissue and histiocyte ingrowth from perigraft tissue, but the 20-microns layer did not. Neointima formation occurred earlier and endothelialization was more extensive in high porosity grafts, but seroma formation occurred in 25% of cases. In type I composite porosity grafts, smooth muscle cells of neointima migrated into the pores of the graft, providing a firmly anchored intima. Type II composite porosity grafts allowed better ingrowth of fibrovascular tissue at the outer layer from the perigraft tissue; however, endothelialization was not completed. Composite porosity grafts should be considered for evaluation in specific clinical situations.

Animals↗

[A case of nephrotic syndrome mimicking membranoproliferative glomerulonephritis (MPGN) and associated with reactive hemophagocytic syndrome after renal death].

We report a case of nephrotic syndrome which mimicked membranoproliferative glomerulonephritis (MPGN) and was associated with hemophagocytic syndrome after renal death. A 41-year-old Japanese man was referred to our hospital because of nephrotic syndrome in February 1979. He had no signs, symptoms nor laboratory data suggestive of liver damage. He was diagnosed as idiopathic MPGN and administered prednisolone and cyclophosphamide (total dose of about 50,000mg). He developed end-stage renal disease, and dialysis therapy was initiated in February 1992. Simultaneously, he was diagnosed as hepatitis C virus (HCV)-positive liver cirrhosis. In August 1994, he died because of reactive homophagocytic syndrome, which occurred in the setting of immunosuppression due to chronic renal failure, liver cirrhosis, and sesecondary diabetes. In this case, we can not deny the possibility that radical therapeutic intervention against "idiopathic MPGN" had a negative effect on the clinical course of chronic HCV infection.

Cyclophosphamide↗

[Utility of acetated Ringer solution as intraoperative fluids during hepatectomy].

We used acetated Ringer (AR) and lactated Ringer (LR) solutions as an intraoperative fluid during hepatectomy and evaluated their effects on intraoperative and postoperative hemodynamics, metabolism, blood gas and renal as well as liver functions. Twenty patients scheduled for hepatectomy were divided into two groups according to the type of infused solution, AR or LR. The infusion rate was 15 +/- 2 ml.kg-1.min-1 with the first 500 ml and thereafter reduced to 10 +/- 2 ml.kg-1.min-1. Intraoperative serum lactate levels increased significantly in both groups. However, the level of lactate in the LR group (48.6 +/- 16.4 mg.dl-1) was significantly higher than in the AR group (29.1 +/- 14.3 mg.dl-1) at the end of the operation. D-lactate level was significantly higher in the LR group than in the AR group during the operation. Although acetate level increased significantly during the operation in the AR group, it decreased to the normal range at the end of the operation. There were no significant differences in the other parameters between the two groups. These results suggest that AR may be more useful in hepatectomy than LR as an intraoperative fluid.

Adult↗

Differences in immunomodulating effects between wild and cultured Panax ginseng.

The different effects between wild and cultured Panax ginseng on immunological activity were investigated. The extracts of hot water soluble fraction from wild Panax ginseng showed the mitogenic activity to lymphocytes but that from cultured Panax ginseng did not. The mitogenic activity of wild Panax ginseng (100 micrograms/well) was almost equal to Concanavalin A (0.1 microgram/well) which was well-known as one of T cell mitogens. The percentages of Thy 1.2-(pan T cells), L3T4-(helper T cells) and Lyt2-(cytotoxic T cells) positive cell population were significantly increased in the mice orally administered hot water soluble fraction from wild Panax ginseng as compared to control by 31.2, 17.9 and 30.1 percent, respectively.

Adjuvants, Immunologic↗

Clonidine and lidocaine inhibition of isoflurane-induced tachycardia in humans.

BACKGROUND: A rapid increase in isoflurane concentration can induce tachycardia and hypertension and increase plasma catecholamine concentrations. To investigate a possible mechanism, we measured hemodynamic responses to isoflurane administered via mask; we also administered clonidine for premedication, lidocaine topically to the nasal mucosa, or lidocaine intravenously to evaluate the effect of these drugs on the hemodynamic responses. METHODS: Forty ASA physical status 1 patients (aged 20-30 yr) scheduled for elective oral surgery participated in the study. Thirty patients were randomly allocated to one of three groups: a control group, a group receiving 3-4 micrograms.kg-1 of oral clonidine for premedication, and a group receiving 2 ml of 4% lidocaine spray to the nasal mucosa. Ten patients were assigned nonrandomly to a group receiving intravenous lidocaine continuously (0.4 mg.kg-1 bolus followed by 30 micrograms.kg-1.min-1) after the initial randomized experiments were done to test whether systemic lidocaine blunts the responses to inhaled isoflurane. Anesthesia was induced with thiamylal, after which inhalation of 1% isoflurane in 100% oxygen via mask was begun. The inspired concentration of isoflurane was increased by 1% every 5 min to a maximum of 4%. During normocapnia and without surgical stimulation, heart rate and systolic blood pressure were measured every minute for 20 min before and during isoflurane inhalation. Plasma catecholamine concentrations were measured before and at each isoflurane concentration. RESULTS: In the control and intravenous lidocaine groups, an increase in isoflurane concentration from 2% to 3% significantly increased systolic blood pressure (peak changes of 16 +/- 5 and 15 +/- 6 mmHg, respectively) and heart rate (peak changes of 23 +/- 3 and 13 +/- 4 beats.min-1, respectively). A change in concentration to 4%, however, did not significantly alter hemodynamics. Blood pressure and heart rate responses to a change to 3% isoflurane were significantly blunted in the groups receiving clonidine (peak changes of 4 +/- 4 mmHg and 8 +/- 3 beats.min-1, respectively) or nasal lidocaine (peak changes of 2 +/- 1 mmHg and 4 +/- 2 beats.min-1, respectively) compared with the control group. In all groups, plasma epinephrine and norepinephrine concentrations increased after administration of 2% and 1% isoflurane, respectively. Plasma lidocaine concentrations were 0.3-1.3 micrograms.kg-1 in the nasal lidocaine group and 0.6-1.5 micrograms.kg-1 in the intravenous lidocaine group. CONCLUSIONS: Stepwise increases in isoflurane concentration elicited hypertension and tachycardia as well as increments in plasma catecholamine concentrations during mask anesthesia. Nasal administration of lidocaine and clonidine premedication significantly blunted the circulatory responses to isoflurane. Intravenous lidocaine did not significantly weaken the responses to changes in isoflurane concentration.

Administration, Topical↗

Role of intracellular Ca2+ pools in the effects of halothane and isoflurane on vascular smooth muscle contraction.

We examined the effect of halothane and isoflurane on contraction in the vascular smooth muscle of rat thoracic aorta simultaneously with the cytosolic Ca2+ levels ([Ca2+]i). Isolated spiral strips of rat thoracic aorta were suspended for isometric tension recordings in physiologic salt solution. The [Ca2+]i was measured concomitantly using fura-2-Ca2+ fluorescence. Muscle tension was elicited either by 51 mM K+ solution or 30 nM norepinephrine, and the muscle was exposed to 0%, 1%, 2%, 3% halothane or 0%, 1%, 2%, 3%, 4% isoflurane. The effects of the anesthetics were compared with the effects of verapamil, an L-type voltage-dependent Ca2+ channel blocker, also administered during K(+)-induced muscle contraction. In another series, the effects of the anesthetics on caffeine- or norepinephrine-induced muscle contraction were determined in Ca(2+)-free solution. Finally, 3% halothane or 4% isoflurane was administered during K(+)-induced contraction in muscle strips pretreated with ryanodine and caffeine. During K(+)-induced contraction, halothane evoked a transient increase followed by a decrease in both muscle tension and [Ca2+]i. The biphasic change in muscle tension was not elicited by isoflurane or by any agent under norepinephrine-induced contraction. Both halothane and isoflurane ultimately suppressed both K(+)- and norepinephrine-induced increases in muscle tension and the [Ca2+]i in a concentration-dependent manner. The slopes of the [Ca2+]i-tension regression lines under the two anesthetics were significantly steeper than that under verapamil during K(+)-induced contraction. Halothane, but not isoflurane, augmented 4 mM caffeine-induced tension and [Ca2+]i transients in the Ca(2+)-free solution in a concentration-dependent manner. However, neither anesthetic influenced norepinephrine-induced tension and [Ca2+]i transients. In the muscle strips pretreated with ryanodine and caffeine, the difference observed between the anesthetics was abolished. In conclusion, halothane, but not isoflurane, enhances Ca2+ release predominantly from the caffeine-releasable Ca2+ stores in vascular smooth muscle; this release may modify the effect of halothane. The intracellular Ca2+ pools can be affected differently by volatile anesthetic drugs, depending on the nature of the stimulus for smooth muscle contraction.

Animals↗

[Hemodynamic responses to nitrous oxide during isoflurane anesthesia in humans].

Isoflurane often produces tachycardia during clinical anesthesia. We examined the effect of a stepwise increase of isoflurane concentration on hemodynamic parameters in the absence or presence of nitrous oxide (N2O). After induction with thiamylal (3 mg.kg-1), isoflurane in oxygen or in 66% N2O-oxygen was administered with mask ventilation. Inspired isoflurane concentration was increased in a stepwise fashion (1, 2, 3 and 4%) every 5 minutes and manual ventilation was performed to maintain ETCO2 within 35-40 mmHg. Blood pressure (BP), heart rate (HR) and cardiac output (CO) were measured before and at every minute after isoflurane administration until 20 minutes. Systolic BP decreased gradually with increasing isoflurane concentration, but was transiently elevated for 3%. HR increased in a dose-related manner. CO decreased significantly at 1-3%. N2O and this seemed to magnify the isoflurane-induced decrease in BP and increase in HR at 1% and 2%. CO increased from baseline at 4%. Isoflurane tended to increase HR in a dose-related manner and induced a hyperdynamic response during rapid increasing of isoflurane concentration. This response may have beed caused by the irritating effect of isoflurane on the airways. Addition of N2O attenuated this response because it increases the speed of induction and the depth of anesthesia.

Adult↗

[Epidural anesthesia for a patient with Charcot-Marie-Tooth disease, mitral valve prolapse syndrome and IInd degree AV block].

A 24-year-old, 48 kg female with Charcot-Marie-Tooth disease, mitral valve prolapse syndrome and IInd degree AV block was scheduled for emergency cesarean section under epidural anesthesia. This anesthesia was chosen because she had heart disease. Furthermore, the combination of general anesthesia with neuromuscular blockade posed the risk of a prolonged response to muscle relaxants and resulting respiratory insufficiency. Surgery lasted 50 min and proceeded uneventfully. A normal female infant was delivered with Apgar scores of 9 at 1 min and 10 at 5 min. Epidural anesthesia was safely performed during the operation. Postoperatively, there were no signs of respiratory or neurologic dysfunction. In conclusion, epidural anesthesia seems to be a good choice for a patient with Charcot-Marie-Tooth disease.

Adult↗

Effects of halothane and isoflurane on cytosolic calcium ion concentrations and contraction in the vascular smooth muscle of the rat aorta.

BACKGROUND: Halothane and isoflurane have been reported to suppress the contraction of vascular smooth muscle, although the exact mechanism has not been explained fully. This study examined the effect of halothane and isoflurane on cytosolic calcium ion (Ca2+) concentrations ([Ca2+]cyt), which was measured simultaneously with muscle tension in the vascular smooth muscle of the rat aorta to improve the understanding of the anesthetic's effect on vascular smooth muscle. METHODS: Isolated spiral strips of rat thoracic aorta were suspended for isometric tension recordings in physiologic salt solution. The [Ca2+]cyt was measured concomitantly by using fura-2-Ca2+ fluorescence. During exposure to 0%, 1%, 2%, or 3% halothane or 0%, 2%, or 4% isoflurane, increases in muscle tension and [Ca2+]cyt induced by 32.8 mM K+ or 30 nM norepinephrine were measured and compared with the reference values. In the other series, the 3% halothane-induced increase in [Ca2+]cyt was measured in Ca2+)-free solution without and with a pretreatment of ryanodine, caffeine, or norepinephrine. RESULTS: Halothane and isoflurane increased resting-state [Ca2+]cyt, although only 3% halothane elicited a transient increase in muscle tension during the resting state. By contrast, both anesthetic agents attenuated the high K(+)- and norepinephrine-induced increases in [Ca2+]cyt and muscle tension in a concentration-dependent manner. During 3% halothane or 4% isoflurane exposure, the pretreatment of the muscle strip with a 10(-6)-M dose of Bay K 8644 augmented the high K(+)-induced increase in [Ca2+]cyt to the level observed in the control (0% anesthetic exposure) state. However, the increase in muscle tension in the presence of Bay K 8644 was low; it was still attenuated from the control level during 3% halothane or 4% isoflurane administration. These results indicate that, not only [Ca2+]cyt-dependent, but also [Ca2+]cyt-independent, mechanisms are involved in the anesthetic-induced suppression of smooth muscle contraction. A 3% halothane-induced increase in [Ca2+]cyt was observed in the Ca(2+)-free solution even when the muscle strip was pretreated with a 10(-6)-M dose of ryanodine and a 20-mM dose of caffeine, whereas it was abolished completely after the muscle strip was pretreated with ryanodine, caffeine, and 100 nM norepinephrine. These results indicate that halothane can release Ca2+ from an intracellular Ca2+ store other than the caffeine-releasable site. CONCLUSIONS: Halothane and isoflurane have multiple effects on the [Ca2+]cyt and induce [Ca2+]cyt-dependent and [Ca2+]cyt-independent suppression of the contraction in the vascular smooth muscle.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

High porosity PTFE improves endothelialization of arterial grafts without increasing early thrombogenicity.

OBJECTIVE: High porosity (HP) (90 micron internodal distance) PTFE grafts were implanted into the carotid and femoral arteries of dogs to investigate early thrombogenicity, patency, and endothelialization. EXPERIMENTAL DESIGN: Standard PTFE (STD) grafts (30 micron internodal distance) were used as controls. 12 HP and 12 STD grafts were implanted into 6 dogs. Indium-111 labeled platelets were infused intravenously after graft implantation. A graft platelet accumulation index (GPAI) was calculated as the ratio of radioactive emission from the PTFE grafts excised at 48 hours to the emission from a native arterial segment. Another 12 HP and 12 STD grafts were implanted into femoral and carotid arteries to assess patency and endothelialization at 4 and 18 weeks. RESULTS: There was no significant difference in the GPAI of the HP and STD grafts at either the carotid (HP = 31.5 +/- 9.7, STD = 30.6 +/- 11.8; p > 0.05) or femoral (HP = 34.0 +/- 5.0, STD = 31.5 +/- 7.9; p > 0.05) positions. Combined data (carotid and femoral HP vs. carotid and femoral STD) also did not demonstrate a difference in GPAI (HP = 32.8 +/- 7.5, STD = 31.1 +/- 9.6; p > 0.05). Patency rates were the same at 4 weeks (75%), but greater in the HP grafts at 18 weeks (HP = 75%, STD = 37%; p > 0.05). No difference was noted in the percentage of graft endothelialization at 4 weeks (HP = 5.2 +/- 5.8, STD = 5.0 +/- 4.0; p > 0.05), however, at 18 weeks the HP graft had significantly more endothelial coverage compared to STD grafts (HP = 75.2 +/- 13.9, STD = 22.6 +/- 9.5; p < 0.01). CONCLUSIONS: Given that HP PTFE is no more thrombogenic than STD PTFE, and that it provides superior endothelialization, HP grafts should continue to be developed and studied for potential clinical use.

Animals↗

[Maintenance therapy on the anemia in continuous ambulatory peritoneal dialysis (CAPD) patients using subcutaneous administration of recombinant human erythropoietin fortnightly--a multicenter trial].

Eighty-seven CAPD patients whose hematocrit (Ht) level was maintained by recombinant human erythropoietin (rHuEPO) were enrolled in this trial for a new formulation of rHuEPO suitable for subcutaneous injection. 6000IU rHuEPO was administered every 2 weeks for 12 weeks. Fortnightly doses were increased to 9000IU or 12000IU at 4 or 6 weeks if the Ht level decreased by 2% or more. During the study period, Ht values were maintained at the appropriate level in 88% of patients. 6000IU or lower was selected as a maintenance dose given every 2 weeks in 57 (76.0%) patients, 9000IU was selected in 8 patients and 12000IU was chosen in one patient. In 9 patients, the Ht could not be maintained during the study and the appropriate dose, therefore, remained unclear. Hypertension was observed in 2 patients as a side effect, and headache occurred in 2 other patients during the trial. Cutaneous abnormalities were not observed in the course of the subcutaneous injections. We conclude that anemia in most CAPD patients could be controlled with fortnightly injections in the dose range of 6000 to 12000IU rHuEPO given subcutaneously.

Adult↗

[Mechanisms of action of volatile anesthetics on smooth muscle].

The development of intracellular Ca2+ fluorescent indicators and specific enzymatic substances as well as the application of the patch-clamp method have made it possible to clarify the mechanisms of action of volatile anesthetics inhibit smooth muscle contraction in part by decreasing intracellular Ca2+ concentration ([Ca2+]i); this effect is mediated by blocking calcium channels, especially the L-type voltage-operated channel, and by raising the intracellular cyclic AMP and cyclic GMP levels. Volatile anesthetic-induced suppression of smooth muscle contraction is also attributable to mechanisms independent of [Ca2+]i, which involve the depression of Ca2+ sensitization mediated by C kinase.

Anesthesia, Inhalation↗