Search PubMed⌕ Search

Biomedical subjects

H Sankawa

Publications and source records attributed to H Sankawa.

At least 19 recordsLinked to original sources
PubMed2000

Difference in glutamate release between retina and cerebral cortex following ischemia.

The difference in ischemic tolerance between the retina and cerebral cortex may be attributable to a difference in glutamate release during ischemia. Glutamate release in the retina and the cerebral cortex was compared in rats. A dialysis electrode for real-time glutamate measurement was perfused with L-glutamate oxidase, and the current evoked between two voltage-clamped electrodes was detected. Two electrodes were implanted in the retina through the choroid and cerebral cortex in 12 anesthetized rats, each mounted on a stereotaxic frame. Global ischemia was induced by ligation on both carotid arteries and hypotension was induced by blood withdrawal. Under control conditions, the glutamate concentration in the retina was 164 +/- 231 (mean +/- standard deviation) microM, being significantly higher (P < 0.05) than that in the cerebral cortex (83 +/- 105 microM). In 10 of the 12 animals, the glutamate concentration in the retina decreased to a minimum of 134 +/- 149 microM (P < 0.01, compared with the value for the cerebral cortex), but that in the cortex increased to 410 +/- 305 microM (averaged highest value). Immediately after the start of reperfusion, the glutamate concentration in the cortex decreased rapidly to 101 +/- 27 microM, but that in the retina increased gradually to almost the control level (148 +/- 204 microM). In the other two animals, the glutamate concentration remained unchanged. In conclusion, glutamate release in the retina does not proceed as rapidly as that in the cerebral cortex during 20 min of ischemia, and in fact decreases. This opposite trend shown by the two organs may be due to the slow depletion rate of ATP in the retina. This may explain the differing neuronal tolerance to ischemia in these two organs.

Animals↗
PubMed2000

The epileptogenic properties of the volatile anesthetics sevoflurane and isoflurane in patients with epilepsy.

UNLABELLED: No study comparing epileptogenicity of sevoflurane to other volatile anesthetics has been performed. We compared the epileptogenic properties of sevoflurane to isoflurane in patients with epilepsy. In 24 mentally and/or physically disabled patients, 12 with epilepsy and 12 without epilepsy, electroencephalograms were recorded under anesthesia with 1.0 minimum alveolar anesthetic concentration (MAC), 1.5 MAC, and then 2.0 MAC sevoflurane or isoflurane under three ventilatory conditions: (A) 100% oxygen, and end-tidal CO(2) partial pressure (ETCO(2)) = 40 mm Hg, (B) 50% oxygen, 50% nitrous oxide, ETCO(2) = 40 mm Hg, and (C) 100% oxygen, ETCO(2) = 20 mm Hg. Spike activity was evaluated as a spike-and-wave index (% durations of spike and wave). The spike-and-wave index increased (P<0.05) from 1.99%+/-0.96% during 1.0 MAC sevoflurane to 6.14% +/- 4.45% during 2.0 MAC sevoflurane in (A) in the epilepsy group, while no spike activity was observed in the nonepilepsy group. Only a few spikes were observed under isoflurane anesthesia, 0.04% +/- 0.04% in (A), with no spikes in (B) and (C). Supplementation with 50% nitrous oxide or hyperventilation (P<0.05) suppressed the occurrence of spikes. Sevoflurane has a stronger epileptogenic property than isoflurane, but nitrous oxide or hyperventilation counteracts this specific epileptogenic property. IMPLICATIONS: The stronger epileptogenicity of sevoflurane than isoflurane was confirmed in a controlled study in patients with epilepsy. Hyperventilation and supplementation of nitrous oxide under sevoflurane anesthesia suppressed epileptogenicity. A combination of sevoflurane and nitrous oxide may be a safer method for seizure-prone patients than the use of sevoflurane alone.

Adolescent↗
PubMed1999

Amino acid release during spreading depression in a flow-compromised cortical area.

The glutamate concentrations in dialysate samples obtained from microdialysis probe implanted in the cortex were assayed during artificially induced spreading depression (SD) and SD with hypoperfusion. The glutamate concentrations did not differ even after SD induction with hypoperfusion (all p>0.05 cf. control), whereas anoxic depolarization caused significantly high glutamate release. Prolonged SD in hypoperfused area did not expose cerebral neurons to high glutamate concentrations.

Alanine↗
PubMed1998

High oxygen delivery and extraction by perfluorocarbon-primed extracorporeal membrane oxygenation do not prevent anaerobic metabolism in rabbits.

PURPOSE: This study was designed to evaluate the advantage of perfluorocarbon (PFC) emulsion priming for venoarterial extracorporeal membrane oxygenation (ECMO) by comparison with hydroxyethyl starch (HES) solution in rabbits (2.8 to 3.9 kg). RESULTS: ECMO initiation was accompanied by a profound decrease in hematocrit (from 40.1% to 14.9%) in both groups. The arterial and the right atrial oxygen contents in the PFC group (n = 4; 38.5 and 11.5 mL/dL) were greater than in the HES group (n = 5; 7.0 and 5.1 mL/dL). Right atrial oxygen tension in the PFC group increased at the beginning of ECMO (from 38.4 to 51.2 mm Hg; P = .031) and remained higher than in the HES group for 60 minutes. These results indicate that oxygen supply and extraction in the PFC group were much greater than in the HES group. However, plasma lactate increased progressively during the 120-minute ECMO procedure in both groups (from 1.8 to 14.5 in the HES group, and from 2.3 to 12.2 in the PFC group). CONCLUSION: Perfluorocarbon priming for ECMO, although providing high oxygen delivery and extraction, does not prevent anaerobic metabolism.

Anaerobiosis↗
PubMed1998

Relationships between glutamate release, blood flow and spreading depression: real-time monitoring using an electroenzymatic dialysis electrode.

Spreading depression (SD) in a flow-restricted area of the brain may be prolonged and may become potentially harmful by releasing glutamate. We induced SD in an oligemia model and examined the subsequent glutamate release. In 18 anesthetized male Fischer rats, a laser Doppler flowmeter, an electroenzymatic electrode for continuous measurement of glutamate, and a calomel electrode for measuring DC potential were placed through a cranial window positioned 3 mm away from a second window where KCl-soaked cotton was placed to initiate SD. The left carotid artery or both the common carotid arteries were ligated to suppress reactive hyperemia of SD. SD produced an increase in glutamate from 24.8 +/- 13.8 to 33.5 +/- 25.3 microM (peak value) (P < 0.0001). After ligation of both carotid arteries, the duration of SD increased from 1.5 +/- 0.6 min (before ligation) to 6.4 +/- 5.1 min (P < 0.05). Glutamate reached a peak level of 63.9 +/- 72.3 microM, then quickly returned to the control value. However, there was no positive correlation between the duration of SD and glutamate concentration. It is concluded that prolonged SD is not accompanied by a progressive increase in glutamate. Therefore, glutamate release induced by SD may not exert harmful effects on neurons.

Animals↗
PubMed1998

Spreading depression induces depletion of MAP2 in area CA3 of the hippocampus in a rat unilateral carotid artery occlusion model.

Traumatic brain injury (TBI) induces neuronal cell loss in area CA3 of the hippocampus. However, it has not yet been established why traumatic injury of the cortex induces neuronal damage in more remote areas. Spreading depression (SD) may be one potential mechanism for this pathophysiology. The present study evaluated whether SD on the cortex evokes a pathological change in the hippocampus. Forty-two Fisher rats were assigned to four groups: Group I: sham operation (n = 7), Group II: right carotid occlusion (UO) for 7 days (n = 7), Group III: repeated induction of SD by KCl application on dura for 7 days (n = 7), Group III' for 3 h (n = 7), Group IV: SD induction and UO for 7 days (n = 14) Group IV' for 3 h (n = 7). In 5 out of 7 animals in Groups III' and IV', cerebral blood flow (CBF) was monitored using laser Doppler flowmetry for 3 h during the passage of SD. The brains were processed for immunohistochemical analysis of microtubule-associated protein 2 (MAP2). Reactive hyperemia induced by SD was not significantly suppressed by right carotid occlusion (194 +/- 25% and 181 +/- 42% UO in Groups III and IV, respectively). In 6 out of 7 animals in a 7-day model of Group IV, and 3 animals in a 7-day model of Group III, MAP2 depletion in the CA3 area of the hippocampus (partly including CA2) was observed, although no change in the hippocampus was observed in other groups. In conclusion, SD in combination with UO yielded reproducible lesions in CA3. Neuronal injury in the hippocampus after brain trauma may be attributable to SD in combination with the blood flow restriction.

Animals↗
PubMed1998

Circulating blood volume measured by pulse dye-densitometry: comparison with (131)I-HSA analysis.

BACKGROUND: Pulse dye-densitometry (PDD) is a newly developed technique for monitoring the arterial concentration of indocyanine green. Using this method, circulating blood volume (CBV) can be calculated without using radioisotopes. In this study, the CBV value obtained by PDD was validated by comparison using the human serum albumin ((131)I-HSA) dilution method. METHODS: Eleven healthy volunteers underwent placement of cannulae into the radial artery and antecubital vein for withdrawal of blood samples and injection of indicator. Probes for PDD were attached to the right nostril and the right index finger. Indocyanine green (20 mg), dissolved in 4 ml water, and 25 microCi (131)I-HSA in 1 ml distilled water were injected simultaneously into the left antecubital vein. Blood samples were withdrawn 3, 6, 10, 20, 30, and 45 min after injection, then processed for spectrophotometric measurement of indocyanine green and scintillation counting. RESULTS: The blood dye concentration correlated well with the values obtained by PDD (r=0.986, imprecision 0.04+/-0.11 mg/l, 10.0+/-31%. The imprecision of the CBV value obtained by PDD (nose probe) and by the (131)I-HSA dilution method was 3.99+/-10.54%, 0.259+/-0.593 l. The imprecision of the CBV obtained by in vitro spectrophotometry compared with PDD was 2.47+/-9.00%, 0.100+/-0.446 l. CONCLUSIONS: This newly developed, less invasive method can measure CBV with an imprecision of 3.99+/-10.54%, 0.259+/-0.593 l (nose probe), and thus is also as accurate as the conventional radioisotope method.

Adult↗
PubMed1997

Cardiac output and circulating blood volume analysis by pulse dye-densitometry.

OBJECTIVE: Pulse dye-densitometry (PDD) is a newly developed method for monitoring the indocyanine green (ICG) concentration in an artery with which cardiac output (CO) and circulating blood volume (CBV) can be determined. We evaluated its accuracy for clinical use. METHODS: In 7 patients under general anesthesia, ICG-sensitive optical probes (805 and 890 nm) were attached to a finger. Following injection of ICG, the arterial concentration of dye was recorded optically by the non-invasive test instrument and sampled arterial blood ICG concentration was also measured photometrically for comparison. In order to validate the PDD analysis, CO was also measured by both the dye dilution cuvette method and by thermodilution in 8 patients scheduled for coronary artery bypass grafting. In 30 other patients, CBV assessed by PDD was compared with its value estimated from body size. RESULTS: The blood dye concentration correlated well with the values obtained by PDD (r = 0.953, p < 0.01). Mean bias for the test PDD CO was +0.15 +/- 0.72 min l-1 (not significant (n.s.)) compared with the cuvette method while the mean bias of the thermodilution method vs the cuvette method was +0.79 +/- 0.84 min l-1 (p < 0.0001.). The average value of CBV obtained by PDD was 3.81 +/- 1.39 L compared with that estimated value, 3.72 +/- 0.77 L (n.s.). CONCLUSIONS: CO determined by PDD agrees well with cuvette densitometry, and somewhat less well with CO by thermodilution. The new method, by not requiring a pulmonary arterial catheter, is less invasive than either older method, and yields in addition a value of CBV.

Blood Volume↗
PubMed1997

[Effect of dibucaine and lidocaine on histamine release from mouse bone marrow-derived cultured mast cells].

We examined the effects of dibucaine and lidocaine on histamine release from mouse bone marrow-derived cultured mast cells. The effects of these drugs on intracellular calcium were also monitored by assessing Fura-2 signals. Additionally, the inhibitory effects of lidocaine on IgE dependent and independent stimuli were examined. Though dibucaine induced histamine release and increases in intracellular calcium from mast cells dose-dependently, lidocaine did not. Lidocaine inhibited both the IgE-dependent and independent histamine release from mast cells in a dose dependent manner. However, the ability of lidocaine to inhibit the IgE-dependent response was greater. Lidocaine also inhibited increases in intracellular calcium to a greater extent after IgE-dependent stimulation as compared with IgE-independent stimulation. The degree of the inhibition of histamine release by lidocaine appeared to parallel decreases in calcium mobilization.

Anesthetics, Local↗
PubMed1996

Thromboxane synthetase inhibitor ameliorates delayed neuronal death in the CA1 subfield of the hippocampus after transient global ischemia in gerbils.

Thromboxane A2 accumulates in the hippocampus after global ischemia and may play a key role in postischemic hypoperfusion. Thromboxane synthetase inhibitor (OKY-046) inhibits the accumulation of thromboxane A2 and promotes prostacycline production. Therefore, we set out to determine whether the inhibition of thromboxane synthesis would ameriolate postischemic neuronal death. Three groups of six Mongolian gerbils were subjected to different treatments: untreated control, untreated ischemia, and treated ischemia. Immediately after forebrain ischemia, OKY-046 (10 mg/kg) was injected intraperitoneally into the treated group. After 7 days of survival, the histopathology of the brain was examined. Pyramidal cell density in the CA1 sector in the treated group was 147 +/- 70 nuclei/mm (mean +/- SD), which was significantly (p < 0.05) higher than than in the untreated group (33 +/- 10 (nuclei/mm). The findings were 231 +/- 7 nuclei/mm for the control group. No significant difference was seen in the profile of temporal muscle temperature before and after ischemia between the groups. Ultrastructurally, the vessels in the CAI sector showed lumen patency in the treated group, whereas occluded vessels with an extended perivascular space were observed in the untreated group. Thromboxane synthetase inhibitor thus partly ameliorates the selective vulnerability of the hippocampus after forebrain ischemia, suggesting that thromboxane A2 is involved in the development of delayed neuronal death, independently of any thermal effect.

Animals↗
PubMed1996

Effect of lidocaine on histamine release and Ca2+ mobilization from mast cells and basophils.

BACKGROUND: Various anesthetic drugs have been known to induce allergic reactions, which have been caused by histamine release from mast cells/basophils. Although lidocaine is reported to suppress allergic reactions, there have been no reports about lidocaine's direct effects to inhibit histamine release from mast cells/basophils. METHODS: We examined the effect of lidocaine on histamine release in vitro from freshly extracted as well as cultured mast cells and basophils. Additionally, the effects of lidocaine on intracellular calcium concentration were monitored by assessing Fura-2 signals in cultured cells. RESULTS: Lidocaine (10(-3)-10(-2) M: approximately 234-2340 micrograms/ ml) inhibited both the IgE-dependent and IgE-independent histamine release from all mast cells/basophils in a dose-dependent manner. However, lidocaine inhibited the IgE-dependent response more than the IgE-independent response (P < 0.01). Lidocaine also inhibited increases in intracellular Ca2+ to a greater extent after IgE-dependent stimulation as compared with IgE-independent stimulation. The degree of the inhibition of histamine release by lidocaine appeared to parallel decreases in Ca2+ mobilization. CONCLUSIONS: Our results indicate that lidocaine directly inhibits histamine release from both rodent mast cells and human basophils in vitro at concentrations from 10(-3) to 10(-2) M (234 to 2340 micrograms/ml). That may be influenced by Ca2+ mobilization. Although these results are not immediately relevant to clinical practice, allergic reaction caused by direct effect of lidocaine seems to be impossible.

Anesthetics, Local↗
PubMed1995

The effect of ketamine or thiamylal on succinylcholine-induced myoglobinemia under halothane anesthesia in adults.

We studied the effect of intravenous (IV) thiamylal or ketamine on the increases in serum myoglobin, creatine kinase (CK), and potassium induced by succinylcholine under halothane anesthesia. Ninety patients were divided into three groups. In Group O, succinylcholine (1.0 mg/kg) was administered after an the inhaled induction of anesthesia with halothane. In Group T, thiamylal (4.0-5.0 mg/kg), and in Group K, ketamine (1.5-2.0 mg/kg) was injected prior to succinylcholine administration. Anesthesia was maintained with halothane, nitrous oxide, and oxygen. Myoglobin increased in Group O at 60 min to 855 ng/mL (median) and CK to 98.6 IU/L. These increases were significantly higher than those of Group T (110 ng/mL and 66.4 IU/L) and Group K (110 ng/mL and 57.0 IU/L). Potassium increased in Group O only. There was no significant difference between Groups T and K for any of the three values. These results indicate that IV thiamylal and ketamine both suppress the increases of myoglobin, CK, and potassium, and that in cases when succinylcholine is used, both drugs can help to avoid myoglobinemia and limit the increases of CK and potassium.

Adolescent↗
PubMed1994

Blood-brain barrier opening following transient reflex sympathetic hypertension.

Numerous researchers have shown that experimentally induced hypertension opens the blood-brain barrier (BBB), whereas physiologically induced hypertension is accompanied by sympathetic activation, which exerts a protective effect on the BBB via cerebral vasoconstriction. It has not yet been established that transient reflex sympathetic hypertension can open the BBB. In this study, 14 lightly-anesthetized adult cats were subjected to electrical stimulation of a tooth and transient reflex sympathetic hypertension (duration of less than 60 s) was elicited repeatedly. Continuous flowmetry of the cerebral blood flow showed that autoregulation breakthrough occurred. Light halothane anesthesia supplemented with 30 or 60% nitrous oxide, or 1.2% halothane anesthesia occasionally suppressed the elicited pressor response and prevented such breakthrough. Leakage of Evans blue (EB), which was administered before the hypertensive insult, was confirmed in the marginal and suprasylvian gyri in 5 cats. The EB positive cats reached a significantly (p < 0.05) higher mean arterial blood pressure (198 +/- 16 mmHg) during reflex sympathetic hypertension than EB negative cats (189 +/- 19 mmHg). Breakthrough occurred 16 times in EB positive, but only 8 times in EB negative cats. In conclusion, transient reflex sympathetic hypertension can elicit cerebrovascular autoregulation breakthrough and if the breakthrough occurs repeatedly it is followed by the opening of the BBB.

Animals↗
PubMed1991

[Does methylprednisolone potentiate the effects of dobutamine during thoracic epidural analgesia?].

The cardiovascular effects of dobutamine (DOB) combined with methylprednisolone (MP) were studied during thoracic epidural analgesia (TEA) in 59 patients undergoing operations on upper abdomen. To establish TEA, 8-10 ml of lidocaine 20 mg.ml-1 was injected into the epidural space through the T8-T9 interspace. The patients was intubated after fentanyl 0.2 mg, thiopental 3 mg.kg-1 and vecuronium 0.2 mg.kg-1. Anesthesia was maintained with 67% N2O, 33% O2 and 0.6% enflurane and DOB was infused at a rate of 5 micrograms.kg-1.min-1 during the surgical operation. Systolic blood pressure and urinary output after TEA did not decrease in the two groups, pretreated with MP 5 mg.kg-1 one hour or immediately before TEA, but decreased in the control group without MP injection. Heart rate showed no significant changes after TEA in all groups. We conclude that MP may potentiate the cardiovascular effects of DOB during TEA.

Anesthesia, Epidural↗