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Biomedical subjects

T Sakabe

Publications and source records attributed to T Sakabe.

At least 91 records · Page 5Linked to original sources
PubMed1986

Nicardipine increases cerebral blood flow but does not improve neurologic recovery in a canine model of complete cerebral ischemia.

The effects of the calcium entry blocker nicardipine on CBF, CMRO2, and neurologic outcome following 10 min of complete cerebral ischemia were examined in dogs. In CBF and CMRO2 studies, the CBF in the untreated group (seven dogs) and the nicardipine group (seven dogs; 20 micrograms kg-1 at 30 min postischemia and a subsequent infusion of 2 micrograms kg-1 min-1 for 90 min) initially increased to 300-400% and then returned to preischemic values at 30 min postischemia. Thereafter the CBF in the untreated group significantly decreased to 50% of preischemic values for the following 90-min period (hypoperfusion), while the CBF in the nicardipine group did not differ from preischemic values. The CMRO2 in both groups decreased to approximately 50-80% of preischemic values after 15 min postischemia and did not differ between the groups throughout the study. In neurologic outcome studies, 18 dogs were divided into three groups (of six dogs each): untreated; saline infusion only, posttreated; nicardipine as in CBF and CMRO2 studies, pretreated; nicardipine 20 micrograms kg-1 at 2 min preischemia and a subsequent infusion of 2 micrograms kg-1 min-1 from immediately postischemia to 120 min postischemia. Nicardipine treatment initiated either before or after ischemia failed to improve neurologic outcome at 48 h postischemia. Thus, the increase of postischemic global CBF by nicardipine is not accompanied by neurologic recovery in a canine model of complete cerebral ischemia.

Animals↗
PubMed1986

[Effect of S-adenosyl-L-methionine on cerebral monoamine turnover after hypoxia in rats].

The effects of S-Adenosyl-L-methionine (SAMe) on cerebral monoamine turnover at 60 min of reoxygenation after hypoxia (PaO2, 31-35 mmHg) for 15 min were studied in 44 rats anesthetized with nitrous oxide. The accumulations of monoamine metabolites: 3-methoxy 4-hydroxyphenylglycol (MHPG), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were determined after probenecid. The accumulations of noradrenaline (NA) and dopamine (DA) were also determined after pargyline. In the non-treated group, there was an impairment of degradation of NA to MHPG and of DA to DOPAC or HVA in the control group (no hypoxia). These changes were accompanied by higher levels of NA and DA in the cerebral cortex, hypothalamus and striatum than those of the control group. In the group treated with 100 mg/kg SAMe plus 38 mg/kg mannitol 3 min after the start of reoxygenation, there were no significant changes in these metabolites and amines. Mannitol alone did not cause significant changes. There were no changes in serotonin and 5-HIAA in any of the groups studied. The effects of SAMe were studied in an additional 16 awake rats. MHPG in all regions measured after probenecid in the rats treated with SAMe was higher than that without SAMe. It appears that SAMe ameliorates perturbation of cerebral catecholamine turnover produced by reoxygenation after hypoxia.

Animals↗
PubMed1986

[Diagnosis and treatment of anal carcinoma].

Because of several different histological types of epithelium in the anal canal, various kinds of carcinomas such as adenocarcinoma, squamous carcinoma, cloacogenic carcinoma arise from this region, and carcinoma related to fistula in-ano is one of the characteristic malignancies. Though the fundamental treatment of anal carcinoma is rectal amputation, prophylactic gland dissection of inguinal lymph-node is not necessary except a case with definite metastasis. Numerous kinds of adjuvant chemotherapy to radical operation have been tried, however, selection of antitumor drugs, method of administration are not settled yet, and, at present, long term clinical effects are unknown.

Adenocarcinoma↗
PubMed1985

Responses of EEG, cerebral oxygen consumption and blood flow to peripheral nerve stimulation during thiopentone anaesthesia in the dog.

The effects of sciatic nerve stimulation on the electroencephalogram (EEG), cerebral metabolic rate for oxygen (CMRO2) and cerebral blood flow (CBF) were investigated during thiopentone anaesthesia in dogs. Anaesthetic levels at 15, 35, 65, 95 and 125 minutes after the start of thiopentone infusion (23 mg X kg-1 X hr-1) were designated levels I, II, III, IV and V, respectively. The effects of stimulation for 5 min were tested at each level. At level I (plasma thiopentone concentration; 15 +/- 2 micrograms X ml-1), the EEG was activated with stimulation and CMRO2 and CBF increased by a maximum of 16 and 15 per cent, respectively. The increase in CMRO2 and CBF was significant for five and four minutes, respectively, though the increase became less with time. At level II (27 +/- 3 micrograms X ml-1), the CMRO2 and CBF increased at one minute by eight and nine per cent, the increase being accompanied by transient EEG activation. At the three deepest levels III, IV and V (37 +/- 6, 42 +/- 6, 49 +/- 6 micrograms X ml-1), the EEG, CMRO2 and CBF remained unchanged with stimulation. The results suggest the existence of the tight coupling between the EEG, CMRO2 and CBF and of a threshold level of thiopentone to block the response to peripheral stimulation during thiopentone anaesthesia.

Anesthesia↗
PubMed1985

Local cerebral glucose utilization during nitrous oxide and pentobarbital anesthesia in rats.

Local cerebral glucose utilization was measured in rats during nitrous oxide and pentobarbital anesthesia, using the 2-[14C]-deoxyglucose method. During nitrous oxide anesthesia, 67%, marked heterogeneity of glucose utilization was observed. During pentobarbital anesthesia (30 mg/kg), glucose utilization decreased, the decrease being pronounced in the structures where glucose utilization was high during nitrous oxide anesthesia. During combined use of nitrous oxide and pentobarbital (30 mg/kg), with an electroencephalogram (EEG) consisting of 4-6 Hz wave super-imposed by 10-15 Hz wave, glucose utilization was higher in many brain structures, including the midbrain reticular formation, than that observed during pentobarbital (30 mg/kg) anesthesia alone. With pentobarbital, 125 mg/kg, the EEG became nearly flat and a dose-related decrease in glucose utilization was observed in the cerebral cortices and inferior colliculus but not observed in any other structures. During the combined use of nitrous oxide and pentobarbital (125 mg/kg), the EEG was nearly flat, and no statistically significant differences in glucose utilization were observed as compared with those during pentobarbital (125 mg/kg) anesthesia in any of the structures examined. The results suggest that nitrous oxide and pentobarbital affect local cerebral glucose metabolism differently and that nitrous oxide acts as cerebral metabolic stimulant in the presence of cortical function during pentobarbital anesthesia.

Animals↗
PubMed1985

[Comparative clinical study of aspoxicillin and sulbenicillin in postoperative wound infections].

A well-controlled comparative study was performed to evaluate efficacy, safety and utility of aspoxicillin (ASPC) as compared with sulbenicillin (SBPC) in the treatment of postoperative wound infections. Either 2 g of ASPC or 2 g of SBPC was administered to patients by intravenous drip infusion twice a day for 7 days. The following results were obtained: Overall clinical effectiveness rates were 82.5% (66/80) in ASPC group and 77.0% (57/74) in SBPC group, with no statistically significant difference between 2 groups. Final overall clinical improvement rates were 83.8% (67/80) in ASPC group and 81.1% (60/74) in SBPC group, with no statistically significant difference between 2 groups. As to bacteriological effectiveness, eradication rates of clinical isolates were 70.4% (38/54) in ASPC group and 74.4% (32/43) in SBPC group. There was no statistically significant difference in 2 groups. Side effects and abnormal laboratory findings were observed in 6 cases (6.7%) and 11 cases (12.4%) in ASPC group (89 cases) respectively, and 4 cases (4.4%) and 7 cases (7.8%) in SBPC group (90 cases) respectively. Especially severe adverse reactions were not observed, and there was no significant difference in the incidences of side effects and abnormal laboratory findings between 2 groups. As to overall clinical utility, utility rates were 77.5% (62/80) in ASPC group and 70.3% (52/74) in SBPC group. There was no statistically significant difference between 2 groups. These results may be indicated that ASPC is as useful as SBPC in the treatment of postoperative wound infections.

Adolescent↗
PubMed1985

[A cooperative study of alternating immunochemotherapy with futraful and PSK (second report)--3-year survival rate].

Patients who had undergone gastrectomy for stomach cancer were placed on adjuvant chemotherapy two weeks after surgery. They were divided into three groups according to the following regimen in order to compare the 3-year survival rate : in the first group, administration of futraful was carried out for 3 consecutive months and followed by administration of PSK for 2 consecutive months. This course was repeated for more than 2 courses. Administration of futraful in the second group was repeated for 3 consecutive months with 2 months of withdrawal and repeated for more than 2 courses. The third group received surgery alone. When all the patients of each group were compared, there was no difference in 3-year survival rate, but the group receiving alternating therapy with futraful and PSK showed a significantly high survival rate for the first year only. Further, among patients having stage III carcinoma, those with n2 + n3 or poorly differentiated adenocarcinoma had a remarkably high survival rate.

Adjuvants, Immunologic↗
PubMed1984

Antesternal pharyngogastrostomy by oral insertion of a stapler.

Cancer of the hypopharynx and cervical esophagus involve problems such as removal of the cervical region, resection of the esophagus and also esophageal reconstruction. A standard surgical procedure has not been established. In our clinic, surgery is performed by two teams; one for head and neck and the other for the digestive tract. Since 1963, we have performed 22 operations on patients with such cancers; resection of the cancer and reconstruction of the alimentary tract were performed in sixteen 16 patients and palliative operations in six. As procedures of reconstructive surgery, antesternal pharyngogastrostomy was performed in ten patients, and antesternal esophagogastrostomy in one. Six of these reconstructions were carried out with oral insertion of a stapler. In this paper, we present the surgical techniques and some of the problems involved in total esophagectomy without thoracotomy, i.e., blunt dissection of the esophagus and antesternal pharyngogastrostomy, particularly pharyngogastrostomy, using a stapler inserted orally.

Aged↗
PubMed1983

Cerebral circulation and metabolism during enflurane anesthesia in humans.

The effects of enflurane anesthesia on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) were studied in 17 patients. The patients were divided into two groups according to the depth of anesthesia. Cerebral perfusion pressure was maintained above 60 mmHg with phenylephrine. In Group 1 (arterial enflurane concentration, 15 mg/dl), patients were studied before surgery, while in group 2 (enflurane concentration, 27 mg/dl), the measurements were performed before and during surgery. In Group 1, mean CBF and CMRO2 were 53 and 2.8 ml X 100 g-1 X min-1, respectively. These values were not significantly different from CBF (46 ml X 100 g-1 X min-1) and CMRO2 (3.1 ml X 100 g-1 X min-1) values previously obtained in awake patients. In Group 2 before surgery, mean CBF and CMRO2 were 61 and 2.6 ml X 100 g-1 X min-1, respectively, and were significantly different from the awake values, while the EEG showed frequent spikes and suppression. In Group 2 during surgery, mean CBF and CMRO2 did not differ from the values obtained before surgery, despite significant EEG changes. The results indicate that enflurane is a cerebral vasodilator and causes an increase in CBF and a decrease in CMRO2 in humans at an anesthetic level characterized by frequent spikes and suppression on the EEG.

Adult↗
PubMed1982

Effect of diazepam on cerebral monoamine synthesis during hypoxia and hypercapnia in the rat.

In view of the fact that diazepam has been shown to prevent an increase in catecholamine synthesis and/or turnover rates in stressful situations, and to modify the cerebral metabolic (and circulatory) response to hypoxia and hypercapnia, the influence of the drug on synthesis rates of DOPA and 5-HTP in three regions of the rat brain were studied under normoxic-normocapnic conditions, as well as in hypoxia and hypercapnia. In order to exclude a modifying influence of variations in tissue pO2 during hypercapnia, cerebral venous pO2 was kept at control values by moderate arterial hypoxia. When compared to the control state (paralyzed animals maintained on 70% N2O) normoxic and normocapnic animals given diazepam (in the absence of N2O) showed a slightly enhanced DOPA synthesis in limbic structures and reduced 5-HTP synthesis in limbic structures and striatum. In hypoxia, the drug considerably curtailed DOPA synthesis in limbic structures and striatum but had no effect on synthesis rate in cortex. The drug also appeared to exaggerate the generalized reduction in 5-HTP synthesis observed under 70% N2O. In hypercapnia, diazepam reduced the enhanced rate of DOPA synthesis (observed under 70% N2O) in striatum but left that in the cortex unchanged. The drug prevented the hypercapnia-induced increase in 5-HTP synthesis, observed under 70% N2O. It is concluded that diazepam significantly alters dopamine and serotonin synthesis in hypoxia and hypercapnia. Probably an indirect action, perhaps related to the stress-alleviating effect of diazepam, is involved. The results suggest that the effect of the drug on cerebral metabolic rate and blood flow in hypoxia and hypercapnia is unrelated to changes in noradrenaline synthesis or turnover. Furthermore, although the results demonstrate that diazepam modulates dopamine metabolism in hypoxia and hypercapnia it seems questionable that this influence can explain the metabolic and circulatory effects of diazepam in these conditions.

5-Hydroxytryptophan↗
PubMed1981

Cerebral blood flow and oxygen consumption in the rat brain after lesions of the noradrenergic locus coeruleus system.

The effect of lesions of the locus coeruleus neuron system on cerebral metabolic rate for oxygen (CMRO2) and blood flow (CBF) was evaluated in paralyzed and mechanically ventilated rats, using a 133xenon modification of the Kety-Schmidt inert gas technique. Bilateral electrothermic lesions of its ascending bundle caused no significant change in CBF or CMRO2. The 6-hydroxydopamine lesions did not influence the CBF and CMRO2 responses to hypercapnia and hypoxia. It is concluded that the locus coeruleus does not exert any resting tone on CBF and CMRO2 and that no influence on the CBF and CMRO2 responses to hypercapnia and hypoxia is mediated via its ascending projections.

Animals↗
PubMed1981

The influence of hypoxia on the concentrations of cyclic nucleotides in the rat brain.

In order to study the influence of hypoxia on cyclic nucleotides in the brain, we reduced arterial Po(2) for 15-30 min in lightly anaesthetised and artificially ventilated rats to obtain values ranging from about 45 to about 10 mm Hg. In an additional group (arterial Po(2) 18-22 mm Hg), the tissue hypoxia was aggravated by moderate arterial hypotension (mean arterial blood pressure about 80 mm Hg). In all animals, electrocortical activity was recorded. Cyclic GMP concentrations in cerebral cortex were unchanged in all groups but one. In that group, in which tissue hypoxia was severe enough to induce a suppression-burst EEG pattern and a measurable reduction in the adenylate energy charge, cyclic GMP concentrations were slightly increased (p less than 0.05). Cyclic AMP concentrations remained unaltered at all degrees of hypoxia studied. It is concluded that changes in cyclic nucleotides in brain tissue occur first at such severe degrees of hypoxia of the duration studied that function and metabolism are profoundly altered.

Animals↗
PubMed1981

The effect of indomethacin on cerebral blood flow and oxygen consumption in the rat at normal and increased carbon dioxide tensions.

The effect of the fatty acid cyclo-oxygenase inhibitor indomethacin on cerebral blood flow (CBF) and the metabolic rate for oxygen (CMRO2) was studied in paralyzed and artificially ventilated rats. In normocapnic animals, the drug (10 mg.kg-1i.v.) reduced CBF to 50% of control without a measurable effect on CMRO2. During hypercapnia (PaCO2 70-80 mmHg) the increase in CBF was reduced by about 80% but CMRO2 remained unchanged. Autoradiographic evaluation of local CBF in 20 brain structures indicated that the reduction in CBF was relatively uniform throughout the brain. Dose response curves showed that an effect on CBF was evident already at an indomethacin dose of 1 mg.kg-1 and maximal effects were obtained with 3-5 mg.kg-1. Following i.v. injection of the drug reduction in CBF was observed already after 10 s and the full response occurred after 1-2 min. It is concluded that metabolites of arachidonic acid, possibly mainly prostacyclin, are powerful modulators of normal cerebrovascular tone, and help to mediate the CBF response to increased CO2 tensions. However, since indomethacin does not modify the circulatory response in other conditions with increased CBF these substances do not qualify as general coupling factors controlling CBF in physiological or pathological states.

Animals↗
PubMed1978

Cerebral effects of nitrous oxide in the dog.

The cerebral effects of nitrous oxide, 60 per cent, were examined in 27 dogs. During administration of halothane, 0.2 per cent, nitrous oxide increased cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMR02) to a maximum of 203 and 121 per cent of control, respectively. Cerebrospinal fluid pressure paralleled the change in CBF. The electroencephalogram (EEG) showed low-voltage slow-wave activity. With halothane, 0.8 per cent, nitrous oxide increased CBF and CMR02 to maximum values of 164 and 108 per cent of control, respectively. After administration of thiamylal, 8 mg/kg, intravenously, nitrous oxide did not increase CBF or CMR02 for the first 30-min period, but thereafter, CMR02 increased to 11 per cent above control. Pretreatment with reserpine, 0.5 mg/kg, intramuscularly, for two days did not modify the cerebral circulator and metabolic responses to nitrous oxide. These results indicate that nitrous oxide causes cerebral metabolic stimulation accompanied by an increase in CBF and slowing of the EEG. Sympathoadrenal stimulation would appear not to be the mechanism for the increases in CBF and CMR02. The cerebral effects of nitrous oxide are modified by the background anesthesia.

Animals↗