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Biomedical subjects

F Goto

Publications and source records attributed to F Goto.

At least 91 records · Page 5Linked to original sources
PubMed1998

Reduced pressor activity of midaglizole (selective alpha2-adrenergic antagonist) in hemorrhagic rats.

Midaglizole (DG5128) is a selective alpha2-adrenergic antagonist. However, the hemodynamic effect in hemorrhage remains unclear. The present study examines the effects of 10 mg x kg(-1) midaglizole on mean arterial pressure (MAP) changes following hemorrhagic shock in rats. Hemorrhagic shock was induced by withdrawing blood from the right carotid artery and MAP was maintained at 40 mmHg until 40% of the withdrawn blood had been reinfused. The remaining blood was then slowly infused into the rat. The rats received 10 mg x kg(-1) midaglizole (n = 8) or saline (n = 6) 20 min after reinfusion. Sham-shock rats were observed for 90 min without performing the hemorrhage shock protocol and then administered 10 mg x kg(-1) midaglizole (n = 11). In sham-shock rats, MAP increased maximally 24 s after midaglizole administration, whereas MAP decreased significantly 36-60 s after midaglizole administration in hemorrhagic rats. This difference may result from blockage of peripheral post-synaptic alpha2-adrenoceptors. Thus, vasoconstriction due to post-synaptic alpha2-adrenoceptor activation may play a more important role in maintaining blood pressure during hemorrhagic shock than under normal conditions. Based on the present results, caution is warranted when administering midaglizole in hemorrhagic hypotension.

Adrenergic alpha-Antagonists↗
PubMed1997

Intrathecal neurokinin-1 receptor antagonist reduces isoflurane MAC in rats.

PURPOSE: To study the effects of intrathecal administration of a neurokinin-I(NK-I) receptor antagonist (CP96,345) on the minimum alveolar anaesthetic concentration (MAC) of isoflurane in anaesthetized rats, and on the locomotive activity of conscious rats. METHODS: Wistar rats (n = 36) were fitted with indwelling intrathecal catheters, and the MAC of isoflurane was determined following the intrathecal administration of saline (control group) or the NK-I receptor antagonist CP96,345 (CP) at 1, 10 and 100 micrograms. Subsequently a reversal dose of intrathecal Substance P (SP) at 1, 10 and 100 micrograms was administered and MAC isoflurane was redetermined. Conscious rats (n = 35) were also examined for the presence of locomotor dysfunction following intrathecal administration of CP and SP. Animals were randomly assigned to each treatment group and the investigators were blinded. RESULTS: CP at 10 and 100 micrograms reduced MAC isoflurane by 9.9% and 15.3%, respectively (P < 0.05). Intrathecal administration of SP reversed the decreases in MAC by CP; however, locomotive activity was not changed. CONCLUSION: These results suggest that the NK-1 receptor plays an important role in determining the MAC of isoflurane by inhibition of pain transmission in the spinal cord.

Anesthetics, Inhalation↗
PubMed1997

Production of bioactive salmon calcitonin from the nonendocrine cell lines COS-7 and CHO.

To produce bioactive salmon calcitonin from the conventional nonendocrine cell lines, COS-7 and CHO, we devised a salmon calcitonin expression vector by combining the amino-terminus of human calcitonin precursor with a salmon calcitonin sequence, inserting the efficient furin-cleavable processing sequence Arg-X-Arg-X-Lys-Arg before salmon calcitonin, and deleting the carboxyl-terminal extension peptide. This chimeric calcitonin precursor terminates at glycine to easily receive an amidation reaction. COS-7 and CHO produced a high level of bioactive calcitonin by the resorption pit formation assay. Although amidating activity is highly expressed in CHO, but only a little in COS-7 cells, both cells produced a similar level of bioactive calcitonin. Thus, the engineered salmon calcitonin expression vector enables nonendocrine cells even with low amidation activity to produce bioactive calcitonin.

Animals↗
PubMed1997

Assessment of glycosaminoglycan-protein linkage tetrasaccharides as acceptors for GalNAc- and GlcNAc-transferases from mouse mastocytoma.

Two glycosaminoglycan-protein linkage tetrasaccharide-serine compounds, GlcAbeta1-3Galbeta1-3Galbeta1-4Xylbeta1-O-Ser and GlcAbeta1-3Gal(4-O-sulfate)beta1-3Galbeta1-4Xylbeta1-O -Ser, were tested as hexosamine acceptors, using UDP-[3H]GlcNAc and UDP-[3H]GalNAc as sugar donors, and solubilized mouse mastocytoma microsomes as enzyme source. The nonsulfated Ser-tetrasaccharide was found to function as an acceptor for a GalNAc residue, whereas the Ser-tetrasaccharide containing a sulfated galactose unit was inactive. Characterization of the radio-labelled product by digestion with alpha-N-acetylgalactosaminidase and beta-N-acetylhexosaminidase revealed that the [3H]GalNAc unit was alpha-linked, as in the product previously synthesized using serum enzymes, and not beta-linked as found in the chondroitin sulfate polymer. Heparan sulfate/heparin biosynthesis could not be primed by either of the two linkage Ser-tetrasaccharides, since no transfer of [3H]GlcNAc from UDP-[3H]GlcNAc could be detected. By contrast, transfer of a [3H]GlcNAc unit to a [GlcAbeta1-4GlcNAcalpha1-4]2-GlcAbeta1-4-aMan hexasaccharide acceptor used to assay the GlcNAc transferase involved in chain elongation, was readily detected. These results are in agreement with the recent proposal that two different N-acetylglucosaminyl transferases catalyse the biosynthesis of heparan sulfate. Although the mastocytoma system contains both the heparan sulfate/heparin and chondroitin sulfate biosynthetic enzymes the Ser-tetrasaccharides do not seem to fulfil the requirements to serve as acceptors for the first HexNAc transfer reactions involved in the formation of these polysaccharides.

Animals↗
PubMed1997

Regulation of chondroitin sulfate biosynthesis by specific sulfation: acceptor specificity of serum beta-GalNAc transferase revealed by structurally defined oligosaccharides.

The relationship between sulfation and polymerization in chondroitin sulfate (CS) biosynthesis has been poorly understood. In this study, we investigated the specificity of bovine serum UDP-GalNAc: CS beta-GalNAc transferase responsible for chain elongation using structurally defined acceptor substrates. They consisted of tetra- and hexasaccharide-serines that were chemically synthesized and various regular oligosaccharides with a GlcA residue at the nonreducing terminus, prepared from chondroitin and CS using testicular hyaluronidase. The enzyme preparation was obtained from fetal bovine serum by means of heparin-Sepharose affinity chromatography. The preparation did not contain the alpha-GalNAc transferase recently demonstrated in fetal bovine serum (Kitagawa et al., J. Biol. Chem., 270, 22190-22195, 1995), that utilizes common acceptor substrates. The beta-GalNAc transferase used as acceptors, two hexasaccharide-serines GlcA beta 1-3GalNAc beta 1-4GlcA beta 1-3Gal beta 1-3Gal beta 1-4Xyl beta 1-O-Ser and GlcA beta 1-3GalNAc(4-sulfate) beta 1-4GlcA beta 1-3Gal (4-sulfate) beta 1-3Gal beta 1-4Xyl beta 1-O-Ser, but neither the monosulfated hexasaccharide-serine GlcA beta 1-3GalNAc(4-sulfate) beta 1-4GlcA beta 1-3Gal beta 1-3Gal beta 1-4Xyl beta 1-O-Ser nor tetrasaccharide-serines with or without a sulfate group at C-4 of the third sugar residue Gal-3 from the reducing end. The results indicated that the sulfate group at the Gal-3 C-4 markedly affected the transfer of GalNAc to the terminal GlcA. In addition, a sulfate group at C-4 of the reducing terminal GalNAc of regular tetrasaccharides remarkably enhanced the GalNAc transfer, suggesting that the enzyme recognizes up to the fourth saccharide residue from the nonreducing end. The level of incorporation into a tetra- or hexasaccharide containing a terminal 2-O-sulfated GlcA residue was significant, whereas there was no apparent incorporation into tetra- or hexasaccharides containing a terminal 3-O-sulfated GlcA or penultimate 4,6-O-disulfated GalNAc residue. These results indicated that sulfation reactions play important roles in chain elongation and termination.

Animals↗
PubMed1997

A comparative study of the vasodilator effects of prostaglandin E1 in patients with pulmonary hypertension after mitral valve replacement and with adult respiratory distress syndrome.

UNLABELLED: To determine whether the vasodilator effects of prostaglandin E1 (PGE1) differ according to the etiology and pathophysiology of pulmonary hypertension, we studied 30 patients with pulmonary hypertension after mitral valve replacement (MVR) (n = 16) or with the adult respiratory distress syndrome (ARDS) (n = 14). PGE1 was administered to decrease the mean pulmonary artery pressure to below 30 mm Hg in both groups. Cardiac index and oxygen delivery tended to increase, whereas mean systemic artery pressure, mean pulmonary artery pressure, systemic vascular resistance index (SVRI), and pulmonary vascular resistance index (PVRI) significantly decreased in both groups. A vasodilatory index was defined in this study to allow evaluation of vasodilation relative to PGE1 dose: systemic vasodilatory index (VIs) = SVRI change/PGE1 dose; and pulmonary vasodilatory index (VIp) = PVRI change/PGE1 dose. The VIp was similar in both groups, but the VIs was significantly greater in the ARDS group compared with the MVR group (13.3 +/- 7.8 vs 4.8 +/- 5.1, P < 0.01). A good correlation was found between the pretreatment intrapulmonary shunt fraction (Qs/Qt [%]) value and PGE1 extraction rate in the lung (r = 0.60), and between the pretreatment Qs/Qt value and PGE1 concentration in the radial artery (r = 0.65) in an additional 15 patients. We conclude that the vasodilator effects of PGE1 on the pulmonary circulation are similar in the two groups, whereas the vasodilator effects on the systemic circulation are significantly greater in the ARDS group and that significant reduction in VIs in the ARDS group was associated with decreased PGE1 extraction in the lung. IMPLICATIONS: Pulmonary hypertension after mitral valve replacement, or with adult respiratory distress syndrome, is a major medical problem. The authors found that administration of prostaglandin E1 significantly dilated the pulmonary circulation with a concomitant decrease in pulmonary artery pressure. Because the systemic vasodilatory effect was greater in the adult respiratory distress syndrome group, the authors concluded that prostaglandin E1 concentrations in the systemic circulation depend on the severity of lung injury.

Adult↗
PubMed1997

The differential effects of prostaglandin E1 and nitroglycerin on regional cerebral oxygenation in anesthetized patients.

UNLABELLED: We evaluated the effects of prostaglandin E1 (PGE1) and nitroglycerin (NTG) on regional tissue oxygenation and use in the brain using near infrared spectroscopy (NIRS). Twenty-four patients who underwent elective cardiac surgery were randomly divided into two groups. The study was performed after the induction of anesthesia and before the start of the surgical procedure. After measuring arterial and jugular venous blood gases, cardiovascular hemodynamics, and relative cerebral oxyhemoglobin (HbO2), deoxyhemoglobin, and cytochrome aa3 at the baseline, PGE1 (n = 12) or NTG (n = 12) was infused intravenously at a rate of 0.3 g/kg or 5 g/kg, respectively. Thirty minutes after the start of drug infusion, administration of the drugs was stopped. Both PGE1 and NTG reduced mean arterial pressure to approximately 70% of the baseline value 10, 20, and 30 min after start of drug infusion (P < 0.05). Internal jugular venous pressure increased significantly during NTG but not during PGE1 infusion (P < 0.05). PGE1 increased HbO2 concentration, which was sustained for 30 min after discontinuing the drug. NTG increased HbO2 concentration, but this gradually returned to the baseline level after discontinuation of the drug. Baseline value of jugular oxygen saturation was 64.5% +/- 2.1%, and there was no significant changes during the infusion of PGE1 or NTG. These results demonstrate that both NTG and PGE1 increased cerebral oxygen saturation as measured by NIRS. This may be explained by local cerebral hyperemia without major alteration in flow/metabolism coupling of brain. The onset of this increase was slower and the duration of this effect after discontinuation of the drug was more prolonged with PGE1. These phenomena occurred despite the relatively similar time course of the effect of these two drugs on systemic hemodynamic values. IMPLICATIONS: The cerebrovascular effects of vasodilators used for induced hypotension are not fully understood. In this study, we used near infrared spectrometry and jugular oxygen saturation measurement to assess the effects of prostaglandin E1 and nitroglycerin on cerebral perfusion. We found that nitroglycerin and prostaglandin E1 increase cerebral oxygen saturation as measured by near infrared spectrometry, but with different time courses. This information will hopefully help anesthesiologists to better maintain adequate regional cerebral oxygenation.

Aged↗
PubMed1997

Factors affecting neostigmine reversal of vecuronium block during sevoflurane anaesthesia.

We examined the influence of the concentration of sevoflurane and the degree of muscle block at the time of reversal on the activity of neostigmine. Ninety ASA 1-2 patients were anaesthetised with 0.2, 0.7 or 1.2 MAC of sevoflurane (30 patients each) in 66% nitrous oxide in oxygen. The electromyographic (EMG) response of the adductor digiti minimi was monitored at 20-s intervals after train-of-four stimulation of the ulnar nerve. The initial neuromuscular block was produced by vecuronium 100 micrograms.kg-1. When the amplitude of the first response (T1) values had recovered to 10%, 25% or 40% of the control, neostigmine 40 micrograms.kg-1 was administered. The train-of-four ratio values were recorded at 1-min intervals during the subsequent 15-min period. Higher endtidal concentrations (p < 0.0001) and more pronounced block at the time of reversal (p < 0.0001) were associated with a delayed recovery in the train-of-four ratio. In addition, the train-of-four ratio 15 min after neostigmine administration was more dependent on the sevoflurane concentration than on the degree of block present (p < 0.0001). These results confirm that neostigmine (40 micrograms.kg-1) can reverse vecuronium-induced but not sevoflurane-induced neuromuscular block.

Adult↗
PubMed1997

Nitric oxide metabolite in pregnant women before and after delivery.

BACKGROUND: During pregnancy, systemic vascular resistance as well as vascular sensitivity to vasoconstrictive agents decreases in pregnant women. METHODS AND MATERIALS: The vascular resistance of the fetus is also maintained in the presence of low blood pressure. We believe that the main factors in this phenomenon are nitric oxide (NO), along with prostaglandin. NO is an unstable compound with a short half-life;it is easily converted to nitrite (NO2) and nitrate (NO3). Since NO cannot be precisely quantified, we measured the NO2 concentration in maternal blood just before and after delivery and compared in with the values of non-pregnant women. RESULTS: NO2 concentrations in the 13 women who received cesarean deliveries under epidural anesthesia were not significantly changed by the anesthesia. Before anesthesia the NO2 concentration was 216 +/- 115 pmol/mg protein, and after the induction of anesthesia, but before surgery, it was 218 +/- 112 pmol/mg protein. The NO2 concentration then fell significantly after the surgery to 174 +/- 75 pmol/mg protein (p < 0.05). In addition, after vaginal delivery, in 17 other patients we observed marked decreases in NO2 concentration, falling from 160 +/- 82 to 125 +/- 61 pmol/mg protein (p < 0.05). These values were significantly higher than those of non-pregnant women (3.4 +/- 2.1 microM, 33 +/- 22 pmol/mg protein) (p < or = 0.0001). CONCLUSION: These results suggest that NO contributes to the low vascular resistance observed in the mother and fetus during pregnancy.

Adult↗
PubMed1997

[Fatal pulmonary embolism during knee surgery under epidural anesthesia].

A 36 year old male patient suddenly died of pulmonary embolism during the second application of a pneumatic tourniquet undergoing tibial fracture repair. Pulmonary artery angiography using Swan-Ganz catheter demonstrated that the left and right pulmonary arteries were occluded except the partial left upper lobe. PaO2 was below 7 mmHg, and cardiopulmonary resuscitation was not possible. Autopsy showed massive emboli completely blocking the both pulmonary arteries.

Adult↗
PubMed1996

Role of tachykinins in enhancement of bradykinin-induced bronchoconstriction by captopril.

In anesthetized, mechanically ventilated guinea pigs, infusion of captopril (1 mg/kg/h), an angiotensin converting enzyme inhibitor, significantly enhanced bronchoconstriction induced by intravenous injection of bradykinin (BK; 0.1-30 nmol/kg). Pretreatment of guinea pigs with capsaicin (100 mu g/kg) slightly suppressed the bronchoconstriction by BK alone and almost all of the enhancement of BK-induced bronchoconstriction by captopril was suppressed. Intravenous injection of substance P (SP; 0.1-100 nmol/kg), neurokinin A (NKA; 0.1-30 nmol/kg) and neurokinin B (NKB; 0.1-30 nmol/kg) also induced dose-dependent bronchoconstriction but captopril treatment enhanced only the bronchoconstriction induced by SP. BK degradation in bronchoalveolar lavage fluid (BALF) in vitro was significantly suppressed by captopril (p < 0.05). Captopril infusion to guinea pigs significantly increased the levels of BK, SP, and NKA in BALF after BK injection (p < 0.05). FK224, an NK1 and NK2 receptor antagonist and SR 48968, an NK2 receptor antagonist, significantly suppressed the bronchoconstriction induced by BK alone (p < 0.01 and p < 0.05, respectively) as well as the enhancement by captopril (p < 0.01). It can be concluded that the enhancement of BK-induced bronchoconstriction by captopril was attributable to inhibition of the degradation of BK itself and thereby enhanced release of NKA and partly of SP from sensory nerves by BK.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Malignant hyperthermia during epidural anesthesia.

We anesthesized a patient susceptible to malignant hyperthermia (MH) three different times by epidural anesthesia with different types of local anesthetics. His skinned fiber test showed a marked acceleration of calcium (Ca2+)-induced Ca2+ release (CICR). When ester type local anesthetic was used for ankle contracture repair, MH signs appeared following the release of the tourniquet. CICR test is reliable for diagnosing different types of MH.

Adolescent↗
PubMed1996

Radiographic findings of unilateral epidural block.

In 236 consecutive lumbar epidural anesthesia patients, epidurography was performed in seven patients who developed unilateral loss of cold sensation to clarify the cause of unilateral block. Epidurography demonstrated the epidural catheter tip location in the anterior epidural space in four patients (57%) and in the transforaminal passage in three patients (43%). In all seven patients, successful bilateral epidural anesthesia was obtained by a second puncture using another catheter. Our results showed that the most frequent cause of unilateral epidural blockade was the misplacement of the catheter into the anterior epidural space.

Adult↗
PubMed1996

Treatment of postoperative pain with thoracic epidural morphine in oral malignant tumor patients.

CASE REPORT: Thoracic epidural morphine was administered to five patients who underwent radical resection and reconstructive surgery for oral malignant tumors. METHODS AND RESULTS: In case 1, an epidural catheter was inserted at the T3-T4 interspace, and 4 mg morphine was administered through the catheter approximately 5 h before the end of surgery. Forty-five minutes after the end of surgery, a total of 10 mg morphine was continuously infused over a 2-day period using a balloon infusion system. The patient did not complain of pain, and no other analgesics were necessary. There were no serious side effects throughout the treatment of postoperative pain. Good control of pain was obtained by this method in four similar cases. CONCLUSION: Thoracic epidural morphine was effective in the relief of postoperative pain following oral surgery in five cases.

Adult↗
PubMed1996

Effect of eel ventricular natriuretic peptide on the kidney and cardiovascular system in the dog.

Ventricular natriuretic peptide (VNP), a possibly new type of natriuretic peptide with an extended C-terminal tail, has been isolated from eel cardiac ventricles. We investigated the effects of eel VNP on the kidney and cardiovascular system and compared these results with those of mammalian peptides in dogs. Eel VNP, human (dog) ANP, human and dog BNPs were infused into the renal artery at non-hypotensive doses. All peptides produced similar diuresis and natriuresis, but cardiac output and the left and right ventricular stroke work were decreased by BNPs, but ANP and eel VNP did not change these parameters. Systemic vascular resistance was increased by BNPs, but unaffected by other peptides. These results show that eel VNP has renal effects similar to ANP and BNP, but it elicits responses in the heart different from those of BNPs in anesthetized dogs.

Animals↗
PubMed1995

N-acetylgalactosamine (GalNAc) transfer to the common carbohydrate-protein linkage region of sulfated glycosaminoglycans. Identification of UDP-GalNAc:chondro-oligosaccharide alpha-N-acetylgalactosaminyltransferase in fetal bovine serum.

During the course of a study of elucidate the role of modification of the common polysaccharide-protein linkage structure, GlcA beta 1-3Gal beta 1-3Gal beta 1-4Xyl beta 1-O-Ser, in biosynthetic sorting mechanisms of the different sulfated glycosaminoglycan chains, a novel N-acetylgalactosamine (GalNAc) transferase was discovered in fetal bovine serum. The enzyme catalyzed the transfer of [3H]GalNAc from UDP-[3H]GalNAc to linkage tetrasaccharide and hexasaccharide serines synthesized chemically and to various regular oligosaccharides containing terminal D-glucuronic acid (GlcA), which were prepared from chondroitin and chondroitin sulfate using testicular hyaluronidase digestion. The labeled products obtained with the linkage tetra- and hexasaccharide serines and with the tetrasaccharide (GlcA beta 1-3GalNAc)2 were resistant to digestion with chondroitinase AC-II and beta-N-acetylhexosaminidase but sensitive to alpha-N-acetylgalactosaminidase digestion, indicating that the enzyme is an alpha-N-acetylgalactosaminyltransferase. This finding is in contrast to that of Rohrmann et al. (Rohrmann, K., Niemann, R., and Buddecke, E. (1985) Eur. J. Biochem., 148, 463-469), who reported that a corresponding product was susceptible to digestion with beta-N-acetylhexosaminidase. The presence of a sulfate group at C4 of the penultimate GalNAc or Gal units markedly inhibited the transfer of GalNAc to the terminal GlcA, while a sulfate group at C6 of the GalNAc had little effect on the transfer. Moreover, a slight but significant transfer of [3H]GalNAc was observed to an oligosaccharide containing terminal 2-O-sulfated GlcA as acceptor, whereas no incorporation was detected into oligosaccharides containing terminal unsaturated or 3-O-sulfated GlcA units. These results suggest that this novel serum enzyme is a UDP-GalNAc:chondro-oligosaccharide alpha 1-3- or 1-4-N-acetylgalactosaminyltransferase. The possibility of involvement of this enzyme in glycosaminoglycan biosynthesis is discussed.

Acetylgalactosamine↗
PubMed1995

Autogenous production of hydroxyl radicals from thiopental.

It is generally believed that barbiturates can protect neural tissues from the damage induced by cerebral hypoxia. One of the mechanisms for protecting neurons is through the inhibition of lipid peroxidation (LPO). We therefore examined LPO in rat brain, liver and kidney by measuring the accumulation of thiobarbituric acid-reactive substances (TBAR) after thiopental administration under 21% O2. We also designed an in vitro study to gain insight into free radical generation leading to the formation of LPO from thiopental by electron spin resonance (ESR). An accumulation of TBAR in the rat liver was observed after the administration of a large dose of thiopental (70 mg/kg intraperitoneally). However, no change in LPO in the brain and kidney was observed. In the in vitro study, thiopental could scavenge superoxide (O2-.) radicals, while it spontaneously generated hydroxyl radicals (.OH) in solution. We conclude that thiopental can scavenge O2-., while producing .OH, subsequently resulting in membrane lipid peroxidation under physiologic O2 conditions. This formation of .OH may damage cell membrane lipids.

Animals↗