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Biomedical subjects

M Yanagimoto

Publications and source records attributed to M Yanagimoto.

17 recordsLinked to original sources
PubMed2005

Chilling-injury and disturbance of ion homeostasis in the coxal muscle of the tropical cockroach (Nauphoeta cinerea).

Adults of warm- and cold-acclimated tropical cockroaches, Nauphoeta cinerea were exposed to low temperatures of 0 or 5 degrees C for various time intervals (hours to days). Development of chilling-injury (defects in crawling and uncoordinated movements) and mortality during the exposure were assessed and correlated with the changes in concentrations of metal ions (Na(+), K(+) and Mg(2+)) in the haemolymph and coxal muscle tissue. Warm-acclimated insects entered chill-coma at both low temperatures. In their haemolymph, the [Na(+)] and [Mg(2+)] linearly decreased and [K(+)] increased with the increasing time of exposure. The rate of concentration changes was higher at 0 than at 5 degrees C. The concentration changes resulted in gradually dissipating equilibrium potentials across the muscle cell membranes. For instance, E(K) decreased from -49.8 to -20.7 mV during 7 days at 5 degrees C. Such a disturbance of ion homeostasis was paralleled by the gradual development of chilling-injury and mortality. Most of the cockroaches showed chilling-injury when the molar ratio of [Na(+)]/[K(+)] in their haemolymph decreased from an initial of 4.4 to 2.1-2.5. In contrast, the cold-acclimated cockroaches did not enter chill-coma. They maintained constant concentrations of ions in their haemolymph, constant equilibrium potentials across muscle cell membranes and the development of chilling-injury was significantly suppressed at 5 degrees C for 7 days.

Acclimatization↗
PubMed1999

Excitation of oxytocin cells in the hypothalamic supraoptic nucleus by electrical stimulation of the dorsal penile nerve and tactile stimulation of the penis in the rat.

In urethane-anaesthetized male rats, electrical stimulation of the dorsal penile nerve (DPN) excited 29 of 48 (60%) oxytocin cells in the contralateral supraoptic nucleus, whereas only 5 of 28 (18%) vasopressin cells were excited by the stimulation. The stimulus applied to the ipsilateral DPN to the recorded neurone also excited a similar proportion of oxytocin cells (25 of 43; 58%). Tactile stimulation of the glans penis excited 7 of 12 (58%) oxytocin cells, whereas the same stimulation excited only 3 of 16 (19%) vasopressin cells. The results suggest that sensory information arising from the penis preferentially excites oxytocin cells in the supraoptic nucleus.

Animals↗
PubMed1999

Relation with preoperative fructosamine and autonomic nerve function and blood pressure during anesthesia in diabetics: a retrospective study.

Many diabetics may have a high risk involving the cardiovascular system. In an attempt to predict the intraoperative risks of diabetics during anesthesia, we evaluated retrospectively the relationship among the biochemical assay or autonomic nerve function obtained as parts of the preoperative examination, and the blood pressure changes relating to the stimulation of intubation and extubation for anesthesia. In 40 diabetic surgical patients examined the biochemical assay (HbA1c, fructosamine level and blood glucose level) beforehand, the autonomic nerve function was quantified preoperatively by analysis of ECG R-R variability recorded in supine and subsequent standing position using an HRV analyzer, and some parameters of autonomic nerve function especially responsive sympathetic nerve activities were obtained. We assessed the correlation with systolic blood pressure changes in these cases at intubation for general anesthesia comparing to similar conditioned 40 non-diabetics. A diabetics with low vagal activity became larger systolic blood pressure afterdrop at tracheal intubation for anesthesia (r=0.513, p<0.001). Otherwise the blood pressure afterdrop at extubation became larger in a non-diabetics with high sympathetic activity (r=0.502, p<0.001). The preoperative fructosamine concentration in diabetics correlated positively with the responsive sympathetic nerve irritability index; "mRR(sup)-RRmin(std)" (r=0.432, p<0.05) and the responsive sympathetic nerve excitability index; "mRR(sup-std)" (r=0.448, p<0.05). However HbA1c had no correlation with these parameters of autonomic nerve function and blood pressure rise at tracheal intubation. Because of above correlation with blood pressure rise at intubation for anesthesia induction, the preoperative fructosamine examination and the responsive sympathetic nerve function test must be useful preoperative examination for detection of the unexpected heart events of diabetic patients during operation.

Aged↗
PubMed1998

[Intraoperative CT imaging system using a mobile CT scanner gantry mounted on floor-embedded rails for neurosurgery].

Many neurosurgeons prefer to use intraoperative computed tomographic (CT) scanning, when possible, to check whether there is residual lesion or unexpected bleeding. We report a practical intraoperative CT imaging system using a high-speed CT scanner installed in the operating room along with a digitally controlled neurosurgical operating table. We designed a rail-track system to mobilize the CT gantry. The gantry is fixed onto a motorized carrier that can be moved smoothly on a rail-track embedded in the floor and with a maximum reach of 2.85 m from the room's wall to the operating table. The longitudinal motion of the operating table is easily adjusted by a foot switch from manual control to automatic control directly from the CT scanner's computer like an ordinary CT scanner bed in increments of 2, 5 or 10 mm during CT scanning. Either a carbon-made radiolucent head frame or carbon-made head plate is used as a headrest. Using this CT scanner system, pre- and intraoperative CT scannings were performed on 46 patients with brain tumors, cervical lesions or other intracranial lesions. We could operate on the patient with enough working space between the mobile CT gantry and the operating table for microneurosurgery. We could obtain intraoperative CT imaging of a patient on the operating table while the surgical wound remained open, the surgical drapes kept in place, and the surgical position unchanged, saving time in intraoperative CT scanning and preparation for further surgery when needed. This intraoperative CT imaging system installed in the operating room should be useful for neurosurgery.

Brain↗
PubMed1997

Effects of growth hormone-releasing hormone (GRF) analogs, bovine and rat GRF on growth hormone secretion in cattle in vivo.

Effects of bovine and human growth hormone-releasing hormone (GRF) analogs (bGRF(1-29)-NH2: bGRF-29, [D-Ala2, Ala15]-bGRF-29, [D-Ala2]-hGRF(1-29)-NH2: [D-Ala2]-hGRF-29), bovine GRF (bGRF(1-44)-NH2: bGRF-44), as well as rat GRF (rGRF) on GH release were studied in female calves. Intravenous (i.v.) bolus injections of 0.25 microg/kg BW of bGRF-29, [D-Ala2, Ala15]-bGRF-29, and [D-Ala2]-hGRF-29 stimulated GH release. Plasma GH levels began to rise 10 min after the injection of each peptide, and significant increases in GH concentrations were obtained at 60, 180 and 150 min after the injection of bGRF-29, [D-Ala2, Ala15]-bGRF-29 and [D-Ala2]-hGRF-29, respectively. The concentrations of GH 80 min after the injection of [D-Ala2, Ala15]-bGRF-29 were significantly higher than those after the injection of [D-Ala2]-hGRF-29 (except at 80 and 90 min) or bGRF-29. The i.v. bolus injections of 0.25 microg/kg BW of bGRF-44 and rGRF stimulated GH release, and the GH-releasing potency of rGRF was approximately equal to that of bGRF-44. The plasma GH responses to the repeated i.v. injection of bGRF-29 or [D-Ala2, Ala15]-bGRF-29 at 2-h intervals were examined. bGRF-29 acutely increased plasma GH levels after each injection, and the high GH levels decreased to the basal values within 2 h. In contrast, high GH levels induced by [D-Ala2, Ala15]-bGRF-29 were gradually decreased but not lowered to basal values throughout the experiment. These results show that [D-Ala2, Ala15]-bGRF-29 has longer-lasting and greater GH-releasing activity than the other GRF analogs in female calves, and the GH-releasing potency of rat GRF is approximately equal to that of bovine GRF in cattle in vivo.

Animals↗
PubMed1996

Afferents originating from the dorsal penile nerve excite oxytocin cells in the hypothalamic paraventricular nucleus of the rat.

Electrical stimulation of the dorsal penile nerve (DPN) produced orthodromic excitation in about half of oxytocin cells in the paraventricular nucleus (PVN). In contrast, less than 10% of vasopressin cells were excited. Tactile stimulation of the glans penis by a paintbrush produced excitation in 40% of oxytocin cells. Castration did not prevent activation of oxytocin cells. These results suggest that somatosensory information from the penis is transmitted to the PVN through the DPN and that such afferent input preferentially innervates oxytocin cells.

Afferent Pathways↗
PubMed1994

Brain energy metabolism and blood flow during sevoflurane and halothane anesthesia: effects of hypocapnia and blood pressure fluctuations.

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (31P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a Paco2 of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a Paco2 of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50% of the control value when Paco2 was < or = 2.7 kPa with 2 MAC of sevoflurane and < or = 4.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a Paco2 of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane. The hypocapnia-induced abnormality during exposure to 2 MAC of either agent was due to decreased CBF associated with low perfusion pressure, indicating that there was no direct effect of these anesthetics on cerebral energy metabolism.

Adenosine Triphosphate↗
PubMed1994

Retinal complications with elevated circulating plasma C5a associated with interferon-alpha therapy for chronic active hepatitis C.

Retinal hemorrhage is a complication of interferon therapy of unknown pathogenesis. We report two chronic active hepatitis C patients who developed retinal hemorrhage and/or cotton wool patches during interferon-alpha therapy 4 and 12 wk after beginning treatment. At the time of the hemorrhage, plasma-activated complement 5, a known potent intravascular aggregator of granulocytes, increased to 54 ng/ml in one patient and to 29 ng/ml in the other patient. When the hemorrhage resolved, it decreased to under 5 ng/ml. Our cases suggest that complement activation occurs in patients treated with interferon-alpha and that activation of complement 5 can lead to retinal capillary infarction and retinal hemorrhage. High levels of activated complement 5 may predict retinal artery infarction or perhaps microvascular emboli in the other organs.

Complement Activation↗
PubMed1994

[Brain fat embolism: an experimental model from MR imaging in rats].

Recently CT and MR imaging have demonstrated that cerebral edema is present in cases of fat embolism syndrome. To simulate this we have made a model of brain-fat embolism in rats under MR imaging. In 20 rats, we did intravenous injection of heparinized blood, 1.5 ml.kg-1 taken from femoral bone marrow cavity. Twenty four hours after the injection, we examined the MR images (1.5 tesla, spin-echo method) of brains and histologic findings of brains and lungs were obtained. In 5 of 20 rats, high signal intensity on T2-weighted images and low signal intensity on T1-weighted images were observed in the area of the unilateral cerebral cortex or hippocampus. These findings showed edema of the brains. They disappeared, however, one week later. Histologic examinations showed massive micro-fat emboli in capillaries of the deep cerebral cortex and substantia nigra, but no edematous findings of the brain were revealed in HE staining. In pulmonary arteries, we also found large fat emboli. We conclude that our model is a useful one for the study of brain fat embolism.

Animals↗
PubMed1993

Brain energy metabolism and blood flow during sevoflurane and halothane anesthesia: effects of hypocapnia and blood pressure fluctuations.

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (31P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a PaCO2 of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a PaCO2 of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50% of the control value when PaCO2 was < or = 2.7 kPa with 2 MAC of sevoflurane and < or = 4.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a PaCO2 of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1993

[An analysis of the status of surgical transfusion and a trial of maximum surgical blood order schedule (MSBOS) in Fukui Medical School Hospital].

To evaluate the present status of surgical transfusion during operations, we computed the amount of preoperative preparation and intraoperative use of blood. And we examined cross-match to transfusion ratio (C/T ratio) and maximum surgical blood order schedule (MSBOS) based on the statistical data in our hospital. The result revealed that too much blood was prepared in our hospital. The amount of prepared blood was 12,825 units of which 2,419 units were transfused (1 unit = 200 ml of whole blood). The mean C/T ratio was 5.30. And a trial of MSBOS revealed that we could save 70% of the blood presently prepared. We are sure that the introduction of T & S and MSBOS will lead to more efficient transfusion in our hospital.

Blood Loss, Surgical↗
PubMed1992

[The effects of sevoflurane/halothane anesthesia during normo- and hyperventilation on the energy metabolism of the cat brain].

Energy metabolism of the cat brain was studied using phosphorous-31 nuclear magnetic resonance (31P-NMR) during sevoflurane/halothane anesthesia with normo- and hyperventilation. Under normocapnia, the findings associated with abnormal energy metabolism were not observed at concentration of sevoflurane/halothane up to 2 MAC. Meanwhile under hypocapnia by hyperventilation, the value of phosphocreatine began to decrease at and below 20 mmHg of PaCO2 (2 MAC sevoflurane) and 30 mmHg of PaCO2 (2 MAC halothane) respectively. These abnormal findings of brain metabolism were limited to the cases with cerebral blood flow (CBF) of less than a half of control state (nonanesthetized and normoventilated), and they were normalized with increased CBF by the vasoconstrictor, metaraminol. From the above data, it was concluded that the deteriorated energy metabolism by hyperventilation was due to decrease in CBF with hypotension and there was no direct effect on cerebral metabolism with less than 2MAC of both sevoflurane and halothane.

Anesthesia, Inhalation↗
PubMed1990

[Epilepsy after operation for ruptured intracranial aneurysm].

Fifty-five patients who underwent surgery for ruptured aneurysm of the anterior circulation were evaluated with respect to postoperative epilepsy. Prophylactic treatment with anticonvulsants had been carried out in all patients. The overall incidence of the postoperative epilepsy was 23.6% (13/55). The mean latency between the operation and the first seizure was 11 months (range, 8 days to 5 years). The most important risk factors by statistical analyses were multiple aneurysms, preoperative severity, severe subarachnoid hemorrhage, intracerebral hematoma, normal pressure hydrocephalus, EEG abnormalities in the chronic stage, intracerebral low density area on CT-films and neurological deficit. Other risk factors were aneurysm of MCA and early operation for aneurysm. Our opinions concerning postoperative anticonvulsant therapy for aneurysmal patients are as follows. 1) Prophylactic treatment with anticonvulsant should be administered to all patients who have undergone aneurysm surgery. 2) The risk factors should be considered in determining the duration of medication with the anticonvulsant. 3) The treatment with the anticonvulsant should be performed while monitoring the clinical course, EEG findings, plasma concentration level of the anticonvulsant and side effects of the drugs.

Adult↗
PubMed1989

Identification of binding protein of virginiae butanolide C, an autoregulator in virginiamycin production, from Streptomyces virginiae.

In Streptomyces virginiae, production of virginiamycin is triggered by signal molecules named virginiae butanolide A, B or C (VB-A, B or C: Yamada, Y. et al. J. Antibiotics 40: 496-504, 1987). We have found a specific VB-C binding protein from S. virginiae, and characterized it by using a tritium-labeled VB-C analogue as a ligand. By equilibrium dialysis in the absence and presence of radio-inert VB-C, a crude extract from 1 g of wet mycelia specifically bound 3.5 pmol of [3H]VB. The binding disappeared after pronase digestion and showed ligand specificity toward cis VB-C (cis VB-C greater than trans VB-C much greater than A-factor type), indicating that binding was due to a cis VB-C specific binding protein. Scatchard analysis of the binding demonstrated a single class of high affinity binding sites (Kd 1.1 nM) and low number of the binding sites (30-40 sites/genome DNA). By gel filtration on Sephadex G-75 and molecular sieve HPLC, the binding protein was shown to have an Mr of about 20,000. These results indicate that the substance is a novel VB-C binding protein and suggest that it is a VB-receptor mediating the pleiotropic signal transmitted by VBs in S. virginiae.

4-Butyrolactone↗
PubMed1987

The structure of inducing factors for virginiamycin production in Streptomyces virginiae.

Virginiamycin inducing factors (inducing material or inducing factor) of Streptomyces virginiae were isolated from the culture broth of this microbe and separated into three closely related compounds. They were named virginiae butanolides A, B and C and their structures were determined as 2-(1'-hydroxy-5'-methylhexyl)-3-(hydroxymethyl)butanolide (6), 2-(1'-hydroxy-4'-methylhexyl)-3-(hydroxymethyl)butanolide (7) and 2-(1'-hydroxyhexyl)-3-(hydroxymethyl)butanolide (8), respectively. Part of their stereochemistry was also determined. Racemic virginiae butanolide C was synthesized to confirm their structures.

4-Butyrolactone↗