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Biomedical subjects

T Kawazoe

Publications and source records attributed to T Kawazoe.

At least 19 recordsLinked to original sources
PubMed2001

Eyelid reconstruction using a hard palate mucoperiosteal graft combined with a V-Y subcutaneously pedicled flap.

Full-thickness eyelid defects after tumour ablation require the reconstruction of two layers, the anterior and posterior lamellae. Eyelids were successfully reconstructed after removal of malignant tumours in four patients using a hard palate mucoperiosteal graft combined with a curved V-Y subcutaneously pedicled flap. Although there have been some reports of hard palate mucosal grafts for reconstruction of the posterior lamella, the graft is not sufficiently rigid to support the reconstructed eyelid without the aid of supporting materials such as cartilage grafts. The hard palate mucoperiosteal graft seems to be rigid enough to support the reconstructed eyelid without the use of cartilage or other supporting materials. The subcutaneously pedicled V-Y advancement flap is useful for reconstruction of the anterior lamella in partial eyelid defects. We used it with a modified curved design to allow easy advancement and to make postoperative scars inconspicuous.

Basal Cell Carcinoma↗
PubMed2001

[Endotoxin adsorption and continuous hemodiafiltration in three septic patients].

We report 3 patients in septic shock with panperitonitis. Endotoxin adsorption by polymixin B affinity column (PMX) and continuous hemodiafiltration (CHDF) were performed immediately after the surgery. Septic shock was not improved in patient 1 and 2 despite intensive care. Multimodal approach, including complete surgical repair, cardiovascular support and blood purification methods, is essential in treating septic patients.

Adsorption↗
PubMed2001

[Severe pulmonary edema in a preeclamptic patient with peripartum cardiomyopathy].

We report a preeclamptic patient who revealed severe pulmonary edema. A 37-year-old woman, at 32-week gestation, underwent emergency cesarean section under general anesthesia. She had no particular past medical history. SpO2 was 84% (room air) on the arrival at the operating room, and a chest X-ray showed pulmonary edema. She was managed in the intensive care unit postoperatively, she received an intensive treatment (positive pressure ventilation, furosemide, and inotropic support), and was extubated successfully on the third postoperative day. From clinical course and echocardiographic findings, we consider that this pulmonary edema was caused by peripartum cardiomyopathy.

Adult↗
PubMed2000

Acute production of vascular superoxide by angiotensin II but not by catecholamines.

OBJECTIVE: To determine whether vascular superoxide is rapidly released by angiotensin II and is involved in vascular contraction. DESIGN: The effect of superoxide dismutase (SOD) on angiotensin II induced elevation of mean arterial blood pressure was measured. Subsequently, acute production of vascular superoxide by angiotensin II and its effect on isometric tension were measured in rat aortic rings. The effects of catecholamines were concomitantly measured. METHODS AND RESULTS: The acute pressor effects of angiotensin II were significantly reduced when rats were pretreated intravenously with SOD. When angiotensin II was added on aortic segments in the presence of Cypridina luciferin analog, immediate elevations of chemiluminescence were observed which were inhibited by SOD. Furthermore, angiotensin II-induced elevations of isometric tension in aortic rings were significantly reduced by SOD. The effects of epinephrine and norepinephrine were concomitantly measured and were not significant CONCLUSIONS: The acute superoxide producing effect is likely to be specific to angiotensin II, because such a significant modification of the effects was not observed for catecholamines. Our results suggest that angiotensin II causes acute vascular superoxide production, which may be involved in the acute pressor effects.

Angiotensin II↗
PubMed2000

[Depressive effects of propofol on apoptotic injury and delayed neuronal death after forebrain ischemia in the rat--comparison with nitrous oxide-oxygen-isoflurane].

We investigated the brain protection effects of propofol anesthesia and nitrous oxide-oxygen-isoflurane anesthesia (GOI) using forebrain ischemic model of male Sprague-Dawley rats. Propofol group (P, n = 15) was anesthetized with propofol, oxygen and nitrogen (FIO2 = 0.33), and isoflurane group (GOI, n = 15) with 66% nitrous oxide, 33% oxygen and 1.2% isoflurane under mechanical ventilation. The anesthesia was deepened until electroencephalographic burst suppression appeared in each group. The bilateral common carotid arteries were, then, occluded for 10 minutes while the blood pressure was maintained at about 40 mmHg by venesection. The venesected blood was returned at the end of ischemic period. The animals were kept and fed in cage after emergence. On the day 2, 4, and 7, five animals of each group were sacrificed and the microscopic samples were obtained. The CA-1 cells of hippocampus were then stained with hematoxylin and eosin for the delayed neuronal death (DND) and with TUNEL method for the apoptosis. Propofol reduced the apoptosis, i.e., reduced the TUNEL positive cell count (GOI = 121.2 +/- 25.2.mm-1; P = 53.8 +/- 11.4.mm-1; P < 0.01; mean +/- SD) on the day 2 after ischemia, and also reduced the delayed neuronal death (alive CA-1 cell count; GOI = 18.1 +/- 8.9.mm-1; P = 33.1 +/- 12.8.mm-1; P < 0.01) on the day 7 after ischemia. It is important to determine the recovery interval after brain ischemia in detection of DND and apoptosis. We conclude that propofol inhibits neuronal apoptosis after brain ischemia and consequently reduces the delayed neuronal death in the CA-1 pyramidal cell layer of the hippocampus.

Anesthesia, Inhalation↗
PubMed2000

[A review of correlation between transfusion rate of irradiated blood and potassium load].

Transfusion of the irradiated blood has become popular in Japan to prevent the graft-versus-host disease. Case reports, however, of hyperkalemic death or lethal ECG change have been increasing since the irradiated blood was introduced nation-wide. The potassium concentration of the supernatant of irradiated blood becomes about 60 mEq.l-1 by the end of storage period. If the potassium concentration is 60 mEq.l-1, the estimated safe transfusion rate would be 6 ml.min-1 and this can not be agreed with by clinicians who transfuse daily in cases of massive bleeding. The calculated safe transfusion rate (10 mEq.hr-1 of potassium load) ranges from 6 to 72 ml.min-1 considering the storage period from the day of gathering and irradiation. This difference could affect the survival rate. On the other hand, only the difference of the potassium concentration in the supernatant between the irradiated blood and the non-irradiated blood could not explain the increasing number of hyperkalemic case report. The mechanical factors may be related to hemolysis that causes extreme hyperkalemia. Control studies of proper transfusion rate of irradiated blood should be performed to establish a safety guideline for rapid transfusion of irradiated blood.

Arrhythmias, Cardiac↗
PubMed2000

[Anesthesia for emergency surgery in 2 extremely low birth weight infants with ileus].

Two extremely-low-birth-weight infants, weighing each 684 and 975 g at birth, underwent emergency surgery because of ileus. Our previous experience with an extremely low birth weight infant, whose hemodynamic control during the surgery had been difficult without administering extra preoperative fluid and transfusion, made us administer enough fluid and transfusion during operation although their urine output was more than 2 ml.kg-1.hr-1. We gave intravenous volume to the present 2 cases before the operations despite the level of preoperative urine output and made their hemodynamic situation more stable during surgeries. We conclude it is very important to administer some amounts of intravenous volume (approximately 8-12 ml.kg-1.hr-1) in extremely low birth weight infants for emergency surgery with ileus regardless of their preoperative urine output.

Anesthesia↗
PubMed1999

Reaction of neuronal nitric oxide synthase with the nitric oxide spin-trapping agent, iron complexed with N-dithiocarboxysarcosine.

A water-soluble iron complex with N-dithiocarboxysarcosine (Fe-DTCS) has been developed as an ESR spin-trapping agent for NO and successfully applied to ESR imaging of endogenous NO production in mice. We attempted to measure NO produced by purified neuronal NO synthase (nNOS) by this method, but could not detect NO. We speculated that Fe-DTCS inhibits NOS activity. In fact, it markedly inhibited NOS activity with an IC50 value of 9.7 +/- 0.7 microM in the citrulline-formation assay. DTCS alone did not inhibit the activity. An iron complex with N-methyl-D-glucamine dithiocarbamate, a similar spin-trapping agent for NO, also inhibited the activity, with an IC50 value of 25.1 +/- 2.9 microM. Fe-DTCS suppressed cytochrome c and ferricyanide reductase activities of nNOS, and markedly increased nNOS-mediated NADPH oxidation. Concomitantly, it accelerated oxygen consumption caused by activated nNOS. These results suggest that the ESR spin-trapping agent Fe-DTCS inhibits NO synthesis by interfering with the physiological electron flow from NADPH to nNOS heme iron.

Animals↗
PubMed1999

Involvement of superoxide in acute reaction of angiotensin II in mesenteric microcirculation.

Superfusion of angiotensin II (Ang II) ceased blood flow in rat mesenteric microcirculation, however, successive reflow occurred. When nitric oxide synthase inhibitor was present, the stoppage of flow occurred by the lower concentration of Ang II. Superoxide dismutase (SOD) significantly delayed the stoppage by Ang II and restored the successive reflow earlier. The acute reaction between Ang II and mesenteric artery induced immediate superoxide (O(2)(-)) production when observed by a chemiluminescence method using the Cypridina luciferin analog. The acute vascular O(2)(-) production on the addition of Ang II contributed to in vitro vascular contraction as it was significantly attenuated by SOD. The acute superoxide-producing effect is likely to be specific to Ang II because such significant modification by SOD was not observed for norepinephrine.

Angiotensin II↗
PubMed1998

Two-dimensional configuration of the myoneural junctions of human masticatory muscle detected with matrix electrode.

Motor unit action potentials (MUAPs) propagate bidirectionally from the myoneural junction along the muscle fibre. The propagation of excitation within single motor units can be detected during sustained isometric contraction using a surface electrode array. Electromyographic (EMG) signals from an adjacent pair of contacts along the muscle fibres show a very similar wave form with a time shift. In the present study, EMG signals of the masseter and the temporal muscles were obtained from two male adults during clenching in the intercuspal position using the multichannel surface electrode with 17 x 11 contacts. The two-dimensional location of the myoneural junction for each column from the source of the propagation was estimated. Each of the myoneural junctions was located in the lower portion of the masseter muscle and in the upper portion of the temporal muscle. However, the junction was distributed within 10 mm along the muscle fibres at different contraction levels in each muscle. This noninvasive technique of multiple surface electrodes enabled us to add to knowledge of the anatomical structure of the masticatory muscles examined.

Action Potentials↗
PubMed1998

The stress-bearing ability of mucosa in complete denture-wearers.

OBJECTIVE: The purpose of this study was to investigate the stress-bearing ability of mucosa in complete denture-wearers. METHODS: The maximum bite force (MBF) was obtained in 31 voluntary complete denture-wearers with a miniature bite force instrument and a set of central bearing devices. The projective stress-bearing area in the mandible (PAM) was measured through the impression surface of the mandibular complete denture. The authors evaluated the stress-bearing ability (SBA) of mucosa in complete denture-wearers by the formula MBF/PAM. RESULTS: The results showed that there was a significant positive correlation between the MBF (the mean was 15.13 kg in men and 11.39 kg in women) and the PAM (the mean was 17.15 cm2 in men and 14.46 cm2 in women) and that there was no significant difference between the mean of the SBA in men (0.89 kg/cm2) and the mean of the SBA in women (0.79 kg/cm2). The mean value of the maximum pressure borne by the mandibular edentulous region was 82 kPa (0.84 kg/cm2). CONCLUSIONS: The SBA may become a valuable parameter for the design of both occlusion and reinforcement in the denture construction and for the selection of the maximum load in mechanical tests of complete dentures.

Aged↗
PubMed1997

Effect of a prostaglandin I2 analogue, beraprost sodium, on burn-induced gastric mucosal injury in rats.

Stress ulcers still have a high mortality in critically burned patients and the pathophysiology remains relatively unknown. Impaired gastric mucosal perfusion is one of the factors contributing to gastric mucosal ulceration. Burn injury causes thrombosis and vascular occlusion by increasing the blood viscosity, resulting in decreased organ perfusion. Reduced blood flow is one of the most important factors in gastric mucosal ulceration. Beraprost sodium is a chemically stable prostaglandin I2 (PGI2) analogue with antiplatelet, vasodilator and cytoprotective actions. In the present study, we examined the effects of a PGI2 analogue, beraprost sodium (Procylin, Kaken Pharmaceutical Company, Tokyo, Japan) on burn-induced gastric mucosal changes in rats. Twenty male Sprague-Dawley rats weighing an average of 400 g were burned with hot water (90 degree C) and then divided into two groups of 10 animals. One group received 0.015 mg of beraprost sodium intraperitoneally immediately after burn injury, while the control group received the same volume of saline. Gastric mucosal blood flow was measured with a laser Doppler flowmeter and the area of mucosal necrosis was also determined macroscopically and histologically. Gastric mucosal damage was significantly reduced in the beraprost sodium-treated rats and gastric mucosal blood flow was significantly improved (p < 0.05). These findings demonstrate that PGI2 plays a very important role in the pathophysiology of burn-induced Curling's ulcer and that beraprost sodium can improve gastric mucosal blood flow and reduce mucosal damage.

Animals↗
PubMed1997

Reduction of burn-induced gastric mucosal injury by an endothelin receptor antagonist in rats.

Burn-induced stress ulcers may be a major complication in critically burned patients. The pathophysiology of gastric mucosal ulceration is relatively unknown, however reduced gastric mucosal blood flow is one contributing factor. Endothelin (ET) is a well known vasoconstrictor peptide produced by vascular endothelial cells. Endothelin has been reported to have a fundamental role in the regulation of the systemic circulation. The plasma ET level is increased by burn injury, which also causes thrombosis and vessel occlusion. Endothelin has potent ulcerogenic and vasoconstrictor actions in the stomach where it induces gastric mucosal damage and increases gastric vascular tone. In the present study, we examined the effects of a new non-selective ET receptor antagonist, TAK-044, on burn-induced gastric mucosal injury in rats. Twenty male Sprague-Dawley rats weighting an average of 400 g were burned with hot water (90 degrees C) and then divided into two equal groups. The treatment group received 1 mg/kg of TAK-044 via the dorsal vein of the penis immediately after burn trauma, while the control group received the same volume of saline. Gastric mucosal blood flow was measured with a laser Doppler flowmeter and the area of mucosal necrosis was also determined macroscopically and histologically. Inhibition of ET activity by TAK-044 after burn injury significantly improved microvascular perfusion in the gastric mucosa and prevented the progression of mucosal damage in the stomach (P < 0.05). The present study supports the role of ET in burn-induced gastric ulceration (Curling's ulcer).

Animals↗
PubMed1997

A new experimental model of a true myocutaneous flap in the rat: the gluteus maximus myocutaneous flap.

Rat myocutaneous flap models are relatively rare. The authors describe the development of a new myocutaneous flap model using the gluteus muscle in rats. A description of the anatomy of the gluteus maximus is included, along with a method of producing skin-island gluteus maximus myocutaneous flaps that can be pedicled or free. This flap model may serve as a useful tool in laboratory studies of the physiologic or pathologic changes in myocutaneous flaps, and may help to narrow the gap between experimental and clinical applications.

Animals↗
PubMed1997

Reduction of progressive burn injury by using a new nonselective endothelin-A and endothelin-B receptor antagonist, TAK-044: an experimental study in rats.

Endothelins are well-known vasoconstrictor peptides produced by vascular endothelial cells that have been reported to have a fundamental role in regulation of the systemic blood circulation. Plasma levels of endothelins are increased by burn injury, which also causes thrombosis and occlusion of vessels in the dermis as well as a vascular response in the adjacent uninjured dermis. Diminished blood flow leads to progressive ischemia and necrosis of the dermis beneath and around the burn (zone of stasis). If blood flow could be restored in this zone, secondary tissue damage would be minimized. In this study we examined the effects of a new nonselective endothelin receptor antagonist, TAK-044 (Takeda Chemical Industries, Ltd., Osaka, Japan), on burn trauma in rats. Fifty male Sprague-Dawley rats weighing an average of 450 gm were burned with a brass probe that produced a row of three burns 10 x 30 mm in size and two intervening unburned areas 5 x 30 mm in size. Rats were divided into five groups of 10 animals. Four groups received 0.01, 0.1, 1 or 10 mg/kg of TAK-044 via the dorsal vein of the penis immediately after burn trauma, while the control group received the same volume of saline. Skin blood flow was measured with a laser-Doppler flowmeter, and the development of edema and the area of necrotic tissue also were determined. Inhibition of endothelin activity by TAK-044 after burn injury improved microvascular perfusion in the zone of stasis and prevented the progression of tissue damage in this zone. This supports the role of endothelins in the progression of burn injury in the zone of stasis. TAK-044 was most effective in preventing progressive burn damage at a dose of 1 mg/kg. The extent of necrosis and edema was reduced significantly, and blood flow in the zone of stasis was increased in the treated rats.

Animals↗
PubMed1997

[The effects of premedication on induction doses of propofol and hemodynamic responses during induction].

We chose five sedatives for premedication and investigated the effect of these drugs on the induction doses of propofol. One hundred patients were allocated into one of five groups of 20. These groups consisted of control group (C) given only atropine 0.5 mg i.m.; CL group (plus clonidine 0.15 mg orally); H group (plus hydroxyzine 25 mg i.m.); M group (plus midazolam 3 mg i.m.) and D group (plus diazepam 10 mg orally). The induction dose was measured using loss of count technique. Arterial pressure and heart rate were measured, before and after propofol induction as well as after intubation. We also calculated rate pressure products (RPP) at each point. The induction doses were significantly lower in M-group than those in C-group. On the other hand, in hemodynamic responses, RPP was unchanged in any groups after propofol induction and after the intubation. Both propofol and midazolam have been known to have a depressive effect on the central nervous system via GABA-A receptor-mediated inhibition, although the exact receptor for propofol is unknown. We thought, therefore, that when the interaction occurred, both midazolam and propofol had the same effect on the GABA-A receptor and increased chloride ion flux through the channels. Hydroxyzine and clonidine, however, do not share a common receptor or exert effect on the GABA-A receptor. We consider that this was one of the reasons why induction doses of both H and CL group could not decrease significantly. We concluded that midazolam 3 mg decreased propofol induction dose significantly. Both midazolam 3 mg and clonidine 0.15 mg decreased RPP before induction and hemodynamic responses to induction and intubation were stable.

Adult↗
PubMed1996

Reduction of progressive burn injury by a stable prostaglandin I2 analogue, beraprost sodium (Procylin): an experimental study in rats.

Beraprost sodium is a chemically stable prostaglandin I2 analogue with antiplatelet and vasodilator actions. Burn injury causes thrombosis and vessel occlusion by increasing the blood viscosity and by thermal damage to the vascular network in the dermis. A vascular response also occurs in the uninjured dermis surrounding the site of injury. Diminished blood flow and spreading tissue oedema lead to progressive ischaemia and necrosis around the burn site (zone of stasis), with the final necrotic tissue area being larger than the initial one. If blood flow could be restored in the zone of stasis, secondary tissue damage would be minimized. In this study, we examined the effects of a prostaglandin I2 analogue, beraprost sodium (Procylin, Kaken Pharmaceutical Company, Tokyo, Japan) on burn injury in rats. Twenty male Sprague-Dawley rats weighing an average of 450 g were burned with a comb-shaped brass probe that produced a row of three burns measuring 10 x 30 mm each and two intervening unburned areas measuring 5 x 30 mm each. The rats were divided into two groups of 10 animals. One group received 0.015 mg of beraprost sodium intraperitoneally immediately after burn injury, while the control group received the same volume of saline. Skin blood flow was measured with a laser Doppler flowmeter, and the development of oedema as well as the area of necrotic tissue were also determined. The extent of skin necrosis and oedema were significantly reduced in the beraprost sodium-treated rats, and blood flow in the zone of stasis was increased. These findings demonstrate that prostaglandin I2 plays an important role in burn injury and that beraprost sodium can reduce secondary necrosis in the zone of stasis.

Animals↗