PubMed Health⌕ Search

Biomedical subjects

K Terasako

Publications and source records attributed to K Terasako.

At least 19 recordsLinked to original sources
PubMed2002

Perioperative plasma concentrations of atrial and brain natriuretic peptides in patients undergoing hip arthroplasty.

Acute hypotension, transient hypoxaemia and elevation of pulmonary artery pressure are well known to occur during cemented arthroplasty. The aim of this prospective clinical study was to characterize the relationship between plasma concentrations of atrial and brain natriuretic peptides (ANP, BNP), and changes in blood pressure in patients undergoing hip arthroplasty. Elevated ANP and BNP levels may be markers of inadequate myocardial reserve. We measured plasma ANP and BNP levels before the operation and 20 minutes after the cementing in 18 patients (54-90 yr). We defined a hypotensive response after cementing as a decrease in systolic blood pressure of more than 15 mm Hg below the pre-cementing value. In the hypotensive group, preoperative values of ANP were 123 +/- 48.5 pg/ml and BNP, 138 +/- 71.7 pg/ml. These values are significantly greater than those in the normotensive group (ANP 35.9 +/- 7.7, and BNP 17.2 +/- 3.2 pg/ml). High preoperative values of ANP and BNP are associated with more hypotension during cemented arthroplasty and could provide an indication of which patients are at risk of this complication.

Aged↗
PubMed2000

Comparison between pentazocine, pethidine and placebo in the treatment of post-anesthetic shivering.

BACKGROUND: We have compared the effects of pethidine, pentazocine and placebo in the treatment of post-anesthetic shivering. METHODS: Forty-five patients who shivered after routine surgery were allocated randomly to receive normal saline (n=15), pentazocine 7.5 mg (n=15) or pethidine 17.5 mg (n=15). RESULTS: After 10 min, 13 patients had stopped shivering in the pethidine group, which was significantly more than the incidence in the two other groups (placebo=2; pentazocine=4) (P<0.01). Pentazocine was not significantly different from normal saline in affecting shivering. CONCLUSION: We conclude that pentazocine 7.5 mg was not effective in the treatment of post-anesthetic shivering.

Adult↗
PubMed1999

Disseminated intravascular coagulation in a patient undergoing removal of humeral head for pain relief.

Disseminated intravascular coagulation (DIC) was recently observed intraoperatively in a patient who required removal of her right humeral head for pain relief. Despite normal preoperative coagulation parameters, the patient developed wound oozing soon after suturing the skin. Coagulation profile revealed decreased platelets, plasma coagulation factors and fibrinogen in association with elevated fibrin degradation products. To manage the DIC, urinastatin and gabexate mesilate, along with blood component replacement, proved effective.

Aged↗
PubMed1998

Platelet transfusion for surgery in the presence of polycythemia vera.

Surgery in the presence of uncontrolled polycythemia vera is associated with a high incidence of perioperative hemorrhage and postoperative venous thromboses. Control prior to surgery reduces the frequency of perioperative complications. A 73-year-old women suffering from polycythemia vera was scheduled for subtotal gastrectomy. Her platelet count before surgery was slightly elevated but bleeding time was prolonged. To manage the current case of polycythemia vera, hydroxyurea was effective for the control of hematocrit and transfusion of platelet concentrates was effective for hemostasis.

Aged↗
PubMed1996

Postoperative seizure-like activity following sevoflurane anesthesia.

Generalized clonic and tonic seizure-like movements were observed during emergence from anesthesia with sevoflurane in a 32-year-old man. The movements lasted 40 sec and necessitated no therapy. There were no significant effects of the incident on the cardiovascular system, such as hypotension, arrhythmia or bradycardia. No neurological abnormalities were obvious after the anesthesia. The movements may have been the result of seizure activity in the central nervous system, or myoclonus of the whole body.

Adult↗
PubMed1995

Identification of the amino acid residues involved in selective agonist binding in the first extracellular loop of the delta- and mu-opioid receptors.

Effects of amino acid substitutions in the first extracellular loop region of the delta- and mu-opioid receptors were examined. Substitution of lysine-108 of the delta-receptor (delta K108) with asparagine improved affinity to [D-Ala2,MePhe4,Gly-ol5]enk ephalin (DAGO), a mu-selective peptide agonist, to be comparable with that of the mu-receptor. On the other hand, replacement of mN127 with lysine decreased the affinity to DAGO by approximately 15-fold. These results suggest that dK108 and mN127, which correspond to each other in the aligned amino acid sequences, mainly determine the difference in DAGO binding affinity between the delta- and mu-receptors.

Amino Acid Sequence↗
PubMed1995

Modification of endothelium-dependent relaxation by propofol, ketamine, and midazolam.

Since volatile anesthetics, barbiturates, and local anesthetics have been reported to inhibit endothelium-dependent relaxation, we hypothesized that any drug with anesthetic action would suppress this relaxation. In the present study, using rat thoracic aortae, we attempted to determine whether nonbarbiturate intravenous anesthetics, including midazolam, propofol, and ketamine, suppress endothelium-dependent relaxation, and to clarify the mechanism(s) involved. Acetylcholine-induced, endothelium-dependent relaxation was significantly attenuated by propofol and ketamine, but was unaffected by midazolam. Sodium nitroprusside (SNP)-induced relaxation was attenuated by propofol, but not by midazolam or ketamine. The acetylcholine-stimulated 3',5'-cyclic guanosine monophosphate (cGMP) level was reduced by pretreatment with propofol and ketamine but not by midazolam, and that stimulated by SNP was reduced by propofol but not by ketamine or midazolam. We conclude that propofol and ketamine suppress endothelium-dependent relaxation, whereas midazolam has no influence. Moreover, the suppressive effect of ketamine on endothelium-dependent relaxation is mediated by suppression of nitrous oxide (NO) formation, whereas that of propofol may be mediated at least partly by suppression of NO function.

Acetylcholine↗
PubMed1995

Vasodilative effect of adrenomedullin in isolated arteries of the dog.

Adrenomedullin is known to induce profound hypotension in vivo, but the direct effect of this peptide on isolated arteries has not been demonstrated. This study estimated the vasodilative effects of adrenomedullin in comparison with those of calcitonin gene-related peptide (CGRP) in basilar, mesenteric, coronary, renal and femoral arteries isolated from the dog. Adrenomedullin (3 to 100 nM) and CGRP (1 to 30 nM) induced concentration-dependent relaxation of these arteries with and without endothelium, and the relaxing effects were slightly greater in endothelium-intact arteries than in denuded ones. The vasodilative potency of adrenomedullin relative to CGRP was smaller in the femoral artery than in basilar, mesenteric, coronary and renal arteries.

Adrenomedullin↗
PubMed1994

Mechanisms of inhibition of endothelium-dependent relaxation by halothane, isoflurane, and sevoflurane.

Volatile anaesthetics inhibit endothelium-dependent relaxation, but the underlying mechanism(s) have not been clarified. In an attempt to elucidate the mechanism(s), we determined the effects of halothane, isoflurane and sevoflurane on relaxation induced by acetylcholine and sodium nitroprusside (SNP) and the cGMP formation elicited by exogenous nitric oxide (NO) and SNP in rat aortas. Acetylcholine (10(-7)-10(-5) M)-induced relaxation was attenuated by halothane (2%), isoflurane (2%) and sevoflurane (4%). SNP (10(-8) M)-induced relaxation was reduced by halothane (2%), but not by isoflurane (2%) or sevoflurane (4%). The cGMP level of NO-stimulated aorta was reduced by halothane (2%) and sevoflurane (4%), but not by isoflurane (2%). The cGMP level of SNP (10(-7) M)-stimulated aorta was reduced by halothane (2%), but not by isoflurane (2%) and sevoflurane (4%). We conclude that the mechanisms responsible for the inhibition of endothelium-dependent relaxation differ among anaesthetics. Isoflurane inhibits the relaxation mainly by inhibiting the formation of NO in the endothelium. In contrast, the effect of halothane on endothelium-dependent relaxation may be largely due to the inhibition of action of NO in the vascular smooth muscle and the effect of sevoflurane may be to inactivate NO or to inhibit the action of NO.

Anesthetics↗
PubMed1994

Halothane and enflurane constrict canine mesenteric arteries by releasing Ca2+ from intracellular Ca2+ stores.

BACKGROUND: Recent studies suggest that volatile anesthetics cause not only vasodilation but also vasoconstriction, depending on the experimental conditions. However, the mechanism of the constrictive effect of volatile anesthetics has not been clarified. The aim of this study was to evaluate the vasoconstrictor effects of halothane, enflurane, and isoflurane and to elucidate the underlying mechanism. METHODS: Vascular rings of canine mesenteric arteries were mounted in organ baths, and isometric tension changes were recorded. Changes in intracellular free Ca2+ concentration of vascular smooth muscle were examined by using the fluorescent Ca2+ indicator fura 2 and a dual-wavelength fluorometer. RESULTS: Halothane (0.75-2.3%) and enflurane (1.7-3.4%), but not isoflurane (1.2-3.5%), induced a concentration-dependent transient contraction, followed by a slight, sustained contraction. Halothane (1.5%)- and enflurane (3.4%)-induced contractions were reduced by endothelial denudation and enhanced by indomethacin (10(-5) M) treatment but were not affected by L-NG-nitroarginine (10(-5) M) or nifedipine (2 x 10(-7) M) treatment. Ryanodine (2 x 10(-5) M) treatment completely abolished the transient increases in tension and Ca2+ concentration. Even in ryanodine-treated arteries, however, both anesthetics induced a slowly developing sustained contraction, and the sustained contraction induced by enflurane (3.4%) was not accompanied by a significant increase in Ca2+ concentration. CONCLUSIONS: Halothane and enflurane, but not isoflurane, induce vasoconstriction by releasing Ca2+ from intracellular stores. Release of a vasodilating prostanoid and endothelium-derived constricting factor may also be involved in the vasoconstrictor effect. Furthermore, increased Ca2+ sensitivity of contractile machinery may be involved in the effect of enflurane.

Animals↗
PubMed1994

Barbiturates inhibit endothelium-dependent and independent relaxations mediated by cyclic GMP.

The inhibitory effects of volatile and local, but not intravenous, anesthetics on endothelium-dependent relaxations of blood vessels have been demonstrated in vitro by several investigators. The aim of this study was to determine the effects of barbiturates on endothelium-dependent arterial relaxation and elucidate the mechanism(s) responsible. Canine mesenteric arteries and rat aortae were isolated, and tension changes in helical strips were recorded. Endothelium-dependent relaxations elicited by acetylcholine and bradykinin in canine mesenteric arteries, and those by acetylcholine in rat aortae, were significantly attenuated by thiopental (3 x 10(-4) M) pretreatment. Sodium nitroprusside (SNP)-induced, endothelium-independent relaxations were significantly attenuated by thiopental (10(-4)-3 x 10(-4) M). The effects of pentobarbital were less marked than those of thiopental. Acetylcholine (10(-5) M)-stimulated levels of 3',5'-cyclic guanosine monophosphate (cGMP) in rat aortae were reduced significantly by thiopental and pentobarbital (both 10(-3) M), and SNP (3 x 10(-7) M)-stimulated levels were reduced by thiopental (3 x 10(-4)-10(-3) M) and pentobarbital (10(-3) M). We conclude that barbiturates inhibit cGMP-mediated endothelium-dependent and independent arterial relaxations. Inhibition of endothelium-dependent relaxation by barbiturates may be mediated by their effects on vascular smooth muscle itself and not on endothelium.

Acetylcholine↗
PubMed1994

Inhibitory effects of anesthetics on cyclic guanosine monophosphate (cGMP) accumulation in rat cerebellar slices.

General anesthetics, including halothane, isoflurane, and barbiturates, suppress endothelium-dependent formation of 3',5'-cyclic guanosine monophosphate (cGMP) in the systemic and cerebral vasculature. The present study was conducted to determine whether these anesthetics have similar effects on the nitric oxide (NO)-cGMP system in the brain, and to elucidate the mechanism responsible. In rat cerebellar slices, formation of cGMP was suppressed by halothane after stimulation by N-methyl-D-aspartate (NMDA, 0.1 mM) and D-aspartate (1.0 mM) but not after stimulation by sodium nitroprusside (SNP, 0.3 mM). Isoflurane (2%) suppressed NMDA (0.1 mM)-stimulated, but not D-aspartate (1.0 mM)- and nitroprusside (0.3 mM)-stimulated formation of cGMP. In contrast, thiopental (0.1-1.0 mM) suppressed NMDA (0.1 mM)-, D-aspartate (1.0 mM)-, and nitroprusside (0.3 mM)-stimulated formation of cGMP. Treatment with aminophylline (0.1 mM), a phosphodiesterase inhibitor, did not influence the effect of thiopental, suggesting that the effect of thiopental was not mediated by activation of phosphodiesterase. D-Aspartate increases intracellular calcium, which in turn activates NO synthase, and nitroprusside generates NO without activation of NO synthase. Therefore, the present findings strongly suggest that halothane inactivates NO synthase (or related cofactors) without marked interaction with the NMDA receptor, that isoflurane may interact with the NMDA receptor, receptor-coupled G-protein, or calcium channels, and that thiopental suppresses guanylate cyclase activity.

2-Amino-5-phosphonovalerate↗
PubMed1994

[Low dose dibutylic cyclic AMP administration during coronary artery bypass graft surgery].

To evaluate the effectiveness of low dose dibutylic cyclic AMP (DBcAMP) during coronary artery bypass graft surgery, we compared circulatory and endocrine-metabolic parameters among the three different doses: (1) DBcAMP 10 microg.kg-1.min-1 (A-10 group), (2) DBcAMP 20 microg.kg-1.min-1 (A-20 group), and (3) control (A-0 group). In the A-10 group, perfusion pressure was significantly higher than in the A-0 group at the point of maximum cooling and at the start of warming during cardiopulmonary bypass (CPB), while peripheral vascular resistance was significantly lower than in the A-0 group at the closing of CPB. On the contrary, in the A-20 group, perfusion pressure was significantly lower than in the A-0 group at the point of maximum cooling and the start of warming during CPB, while peripheral vascular resistance was significantly lower than in the A-0 group at the start of warming and the closing of CPB. Among these groups, the hourly urine volume during CPB was significantly largest in A-10 group. Endocrine-metabolic parameters showed no statistic difference among these groups. These results suggest that the administration of DBcAMP 10 microg.kg-1.min-1 during CPB might improve the cardiac performance and maintain the tissue perfusion without the endocrine-metabolic deterioration.

Aged↗