Changes in plasma concentrations of free amino acids during and after the anhepatic period.
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Journal Article↗
Biomedical subjects
J Yoshitake
Publications and source records attributed to J Yoshitake.
Effects of lidocaine on intracellular Ca2+ and tension in airway smooth muscle.
BACKGROUND: Many studies have demonstrated that lidocaine directly relaxes airway smooth muscle. The underlying mechanisms, especially in relation to Ca2+ mobilization, remain to be elucidated. METHODS: Using front-surface fluorometry and fura-2-loaded porcine tracheal smooth muscle strips, intracellular Ca2+ concentration ([Ca2+]i) and isometric tension were simultaneously measured. RESULTS: In cases of 40 mM K(+)-induced contraction and 1 microM acetylcholine (ACh)-induced contraction, the cumulative application of lidocaine (10(-6) approximately 3 x 10(-3) M) caused a concentration-dependent decrease in [Ca2+]i and tension, and almost complete relaxation. To examine the effect of lidocaine on Ca2+ sensitivity of the contractile apparatus, the [Ca2+]i-tension relationship was determined by changing the extracellular Ca2+ concentration during 40 mM K+ induced depolarization, with and without treatment with lidocaine. Although treatment with 1 mM lidocaine inhibited increases in both [Ca2+]i and tension induced by extracellular Ca2+, it had little effect on the [Ca2+]i-tension relationship. In the presence of 1 microM ACh, the [Ca2+]i-tension relationship shifted markedly to the left, thereby indicating an increase in Ca2+ sensitivity of the contractile apparatus; this shift was inhibited by 1 mM lidocaine. In the absence of extracellular Ca2+, 1 mM lidocaine inhibited the release of stored Ca2+ induced by 1 microM ACh, but not that by 20 mM caffeine. CONCLUSIONS: Lidocaine directly relaxes airway smooth muscle by decreasing [Ca2+]i. In addition, lidocaine inhibits the ACh-induced increase of Ca2+ sensitivity of the contractile apparatus, although it has little effect on Ca2+ sensitivity during high K+ depolarization. The decrease in [Ca2+]i is attributed to inhibition of the influx of extracellular Ca2+, as induced by high K+ depolarization and by ACh, and to the inhibition of the ACh-induced release of stored Ca2+.
Animals↗
Effects of ketamine on contraction and synthesis of inositol 1,4,5-trisphosphate in smooth muscle of the rabbit mesenteric artery.
BACKGROUND: Ketamine acts directly on vascular smooth muscle, causing relaxation. It has been suggested that the mechanism underlying this action involves an interference with transmembrane Ca2+ influx and an inhibition of Ca2+ release from intracellular Ca2+ stores. In vascular smooth muscle cells, agonist-induced Ca2+ release is thought to be mediated by an intracellular second messenger, inositol 1,4,5-trisphosphate (InsP3). To investigate the site at which ketamine acts on agonist-induced contraction, the authors studied the effects of ketamine on contraction and on the synthesis of InsP3 in smooth muscles of the rabbit mesenteric artery. METHODS: Changes in isometric tension of smooth muscle fibers were measured by attaching a thin circular strip from the rabbit mesenteric artery to a strain gauge. To measure the norepinephrine (NE)-induced production of InsP3, smooth muscle strips of the rabbit mesenteric artery were exposed to the agents and homogenized. Inositol 1,4,5-trisphosphate in the supernatant fractions was then assayed. RESULTS: Ketamine dose-dependently inhibited contractions induced by high K+, NE, and histamine in normal Krebs solution. Ketamine also inhibited the NE- or histamine-induced contraction in Ca(2+)-free solution containing 2 mM ethylene-glycol bis-(beta-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA), indicating that this drug inhibits agonist-induced Ca2+ release from intracellular stores. Norepinephrine (10 microM) transiently increased the synthesis of InsP3 in Ca(2+)-free solution, and ketamine (0.1-1.0 mM) inhibited this effect, in a dose-dependent manner. CONCLUSIONS: These results indicate that, in the rabbit mesenteric artery, ketamine inhibits agonist-induced Ca2+ release through its inhibitory action on the agonist-induced synthesis of InsP3. Thus, it is possible that ketamine interferes with the synthesis of intracellular second messengers.
Animals↗
Heparin prevents the vasodilating actions of protamine on human small mesenteric arteries.
Despite the wide clinical use of protamine, the precise mechanisms of its hypotensive effects during reversal of heparin anticoagulation have not been elucidated fully. We, therefore, investigated the effects of protamine on isolated human small mesenteric arteries, both in the absence and presence of heparin, employing the isometric tension recording method. Protamine exerted vasodilating actions in the absence of heparin: 1) protamine (> or = 50 or 150 micrograms/mL) inhibited (P < 0.05) both norepinephrine (1 microM)- and high K+ (40 mM)-induced contractions in the presence of extracellular Ca2+ both in endothelium-intact and -denuded tissues; and 2) protamine inhibited (P < 0.05) norepinephrine (1 microM)-induced, but not caffeine (10 mM)-induced, contractions in the absence of extracellular Ca2+. Such vasodilating actions were blocked almost completely in the presence of heparin. We conclude that only protamine, but not a heparin-protamine complex, has a vasodilating action on the human arteries.
Aged↗
Increase in the plasma concentration of reduced glutathione observed in rats with liver damage induced by lipopolysaccharide/D-galactosamine: effects of ulinastatin, a urinary trypsin inhibitor.
The changes in plasma concentrations of reduced glutathione were investigated in rats with endotoxin hepatitis. An increase in serum alanine aminotransferase activity and in serum total bilirubin concentration was observed 12 hr after the intraperitoneal co-administration of small doses of Escherichia coli lipopolysaccharide and D-galactosamine in starved rats. At the same time, an increase in the plasma concentration of reduced glutathione was also observed. The increase in reduced glutathione from 14 +/- 2 to 20 +/- 9 microM (n = 11, P < 0.05) correlated well with that in serum alanine aminotransferase activity. Ulinastatin, a potent inhibitor of polymorphonuclear leukocyte elastase, partially counteracted all of these changes. Ulinastatin also reduced histological liver damage induced by endotoxin. We conclude that the increase in the plasma concentration of reduced glutathione reflects hepatocellular damage associated with endotoxin hepatitis. The partial reversal of the damage by ulinastatin is consistent with the proposal that the activation of polymorphonuclear leukocytes is involved in endotoxin hepatitis.
Animals↗
Changes in end-tidal CO2 level following tourniquet deflation during orthopedic surgery.
We studied the changes in end-tidal CO(2) (ET(CO)(2)) and systemic responses after tourniquet deflation in spontaneously breathing and ventilation-controlled patients during orthopedic surgery of both the upper and/or the lower extremities. In most patients, increases in ET(CO)(2), heart rate, and Pa(CO)(2), as well as decreases in blood pressure and pH were observed. In every spontaneously breathing patient, the respiratory rate began to increase before the ET(CO)(2) reached a maximum. Arterial blood gas analysis suggested that the increase in ET(CO)(2) closely reflected the increase in Pa(CO)(2). Our study yielded new information on the ET(CO)(2) changes as follows: 1) the time for ET(CO)(2) level to reach a peak (peak time) was almost constant despite the considerable differences in the increases in ET(CO)(2) both in spontaneous breathing and ventilation-controlled groups and the peak time in the former group was shorter than that in the latter group; and 2) it was suggested that the increase in ET(CO)(2) in the spontaneously breathing patients was smaller than that in ventilation-controlled patients when both patients were subjected to the same conditions on tourniquet time and tourniqueted area. Our data showed that the increase in ET(CO)(2) (or Pa(CO)(2)) can be large and prolonged in some situations. Thus, we recommend continuous ET(CO)(2) monitoring and the proper hyperventilation at tourniquet deflation in order to minimize any adverse effects of acidosis.
Journal Article↗
Effects of prostaglandin E1 on left ventricular performance in dogs; comparisons with trinitroglycerin and adenosine triphosphate.
To examine the cardiovascular response to prostaglandin E1 infusion, we observed hemodynamic changes including left ventricular diameter (an ultrasonic crystal pair) during PGE(1)-induced hypotension in anesthetized open-chest dogs. Left ventricular contractility was assessed primarily by measuring the slope of the left ventricular endsystolic pressure-diameter relation (ESPDR) determined by combining end-systolic points from a vena caval occlusion. The cardiovascular effects of induced hypotension by infusions of trinitroglycerin and adenosine triphosphate were also examined at the equivalent magnitude of hypotension. Approximately 25% reduction of systemic blood pressure was produced by the three agents. PGE(1) significantly increased cardiac output from 1200 +/- 132 to 1439 +/- 162 ml.min(-1) (mean +/- SE, P < 0.05), stroke volume from 9.1 +/- 1.1 to 10.0 +/- 1.0 ml (P < 0.05), and %-diameter shortening from 10.4 +/- 0.8 to 14.4 +/- 0.8% ( P < 0.01), but the slope of ESPDR was unchanged. Similar changes were also observed during adenosine triphosphate-induced hypotension. PGE(1) significantly decreased end-diastolic diameter in a similar manner to trinitroglycerin. Thus PGE(1) appears to have little influence on left ventricular contractility aside from its effects on afterload and preload, indicating that it is a useful agent for producing controlled hypotension during anesthesia.
Journal Article↗
Retrospective study of post-anesthetic mild liver disorder associated with inhalation anesthetics, halothane and enflurane.
The incidence of post-anesthetic mild liver disorder (PAMLD) was compared between 928 patients administered halothane and 1766 patients administered enflurane. They were selected from 19 504 surgical patients administered general anesthesia at Kyushu University Hospital over the past 6 years and 4 months. They had had normal liver function before operation and had no history of blood transfusion. Alanine aminotransferase (ALT) levels exceeding 70 IU. l(-1) within 180 days after operation were found in 226 patients in the halothane group (24.4%), and in 250 patients in the enflurane group (14.2%) ( P < 0.01). Both maximum ALT levels and duration of ALT elevation were higher and longer in the halothane group ( P < 0.01). These results suggest that, not only in the development of fulminant hepatitis but also in PAMLD, enflurane is less hepatotoxic than halothane.
Journal Article↗
Paraplegia associated with hyperthermia during repair of coarctation of the aorta.
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Journal Article↗
Coronary artery spasm immediately following extubation of the trachea.
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Journal Article↗
VO2 and VCO2 following tourniquet deflation.
We examined changes in O2 uptake, CO2 output, blood pressure and heart rate following tourniquet deflation in 23 patients undergoing orthopaedic surgery of the lower extremities. A pneumatic tourniquet was applied for periods ranging from 21 to 106 min (mean 51 min). Prerelease values of VO2 (O2 uptake at each min) and VCO2 (CO2 output at each min) were 201 (37) and 174 (38) (mean (SD)) ml.min-1, respectively. Significantly, VO2 and VCO2 increased by 55% and 80%, respectively, at 2 min after tourniquet release and returned to prerelease values within 8 min. The blood pressure fell significantly and the heart rate rose significantly. The increases in CO2 output and O2 uptake were dependent on the length of tourniquet inflation time; Y = 4.7 x (tourniquet time) + 54, r = 0.88, (p less than 0.001) for CO2, and Y = 1.3 x (tourniquet time) + 99, r = 0.52, (p less than 0.05) for O2. The slope of the increase in CO2 output as a function in inflation time was 3.6 times greater than that of O2 uptake. In conclusion, CO2 output and O2 uptake increased transiently after tourniquet deflation and the extent of the increase in CO2 output is more than threefold as compared with that in O2 uptake.
Adolescent↗
Cardiac beriberi (shoshin beriberi) caused by excessive intake of isotonic drink.
A 21 month old female had voluntarily ingested 0.5-1.51 of isotonic sports drink daily from 10 months of age. She developed hyponatremia and beriberi heart disease, which resulted in metabolic acidosis and cardiogenic shock (shoshin beriberi). Mechanical ventilation was applied for pulmonary edema. Right heart failure was improved after administering vitamin B1. However, 5 days after the shock, hypoxemia and diffuse radiographic infiltrates progressed, and a diagnosis of adult respiratory distress syndrome (ARDS) was made. After the occurrence of an air leak, the patient died of respiratory failure. The cardiogenic shock and pulmonary edema due to cardiac beriberi may have triggered the ARDS.
Beriberi↗
Effects of CGRP on baroreflex control of heart rate and renal sympathetic nerve activity in rabbits.
We examined the effects of intravenous infusion of calcitonin gene-related peptide (CGRP) and sodium nitroprusside (SNP) on baroreceptor afferent nerve activity, renal sympathetic efferent nerve activity (RSNA), and heart rate in alpha-chloralose-anesthetized rabbits. Baroreceptor afferent nerve activity was measured from aortic nerves during CGRP- and SNP-induced hypotension. Decreases in aortic nerve activity in response to decreases in mean arterial pressure were not different during CGRP and SNP infusion. Progressive infusion of CGRP (12-120 pmol.kg-1.min-1) increased RNSA by 83 +/- 14 (mean +/- SE), 175 +/- 26, 246 +/- 36, and 343 +/- 41%, and heart rate by 8 +/- 2, 24 +/- 3, 37 +/- 4, and 47 +/- 6 beats/min during falls of blood pressure of 5, 10, 15, and 20 mmHg, respectively. These increases in RSNA and heart rate produced by CGRP were significantly greater than those produced by SNP. The alterations in heart rate and RSNA with CGRP were reversed by restoring blood pressure with phenylephrine HCl. In rabbits with sinoaortic and vagal deafferentation, the responses of heart rate and RSNA to a fall of blood pressure were abolished during both CGRP and SNP infusion. Therefore, it is suggested that the facilitated responses of heart rate and RSNA during CGRP infusion occurred by way of the arterial baroreflex arc.
Administration, Topical↗
Clinical management of boric acid ingestion: pharmacokinetic assessment of efficacy of hemodialysis for treatment of acute boric acid poisoning.
Seven hours after suicidal ingestion of about 21 g of boric acid, a 26-year-old female admitted to our hospital in a state of slightly impaired consciousness, with frequent vomiting, shivering, fever and skin flush. Immediately, gastric lavage, followed by administration of activated charcoal and laxative (MgSO4), was performed. In order to ensure her urination, fluid infusion therapy was conducted with the aid of diuretics (furosemide). Since the serum concentrations of boric acid was very high, hemodialysis was carried out twice during the first 39 h. She responded well to the above mentioned treatment and was discharged 12 d post-admission without any sequelae. The concentrations of boric acid in serum and urine were measured in appropriate intervals with our modified Miyamoto's method, and the pharmacokinetics of boric acid were analyzed. The concentration of boric acid in serum and urine at the beginning of treatment was 465 micrograms/ml and 3.40 mg/ml, respectively. The half-life of boric acid in serum was 13.46 h, whereas it was shortened to 3.76 h during hemodialysis. The total body clearance was 0.99 l/h, while it increased to 3.53 l/h by hemodialysis. The additional removal of boric acid by hemodialysis was estimated to be about 5 g. It was concluded that the hemodialysis was very useful in the treatment of boric acid poisoning, because it accelerated the elimination of boric acid about four times faster than with conventional treatment.
Acute Disease↗
Protection of cellular and mitochondrial functions against anoxic damage by fructose in perfused liver.
In anoxic perfused liver, conversion of fructose to lactate was greatly increased to about 3 mumol/min per g liver. This increase in lactate implied that the same amount of ATP was also produced. The rate of metabolism of glucose was less than 10% of that of fructose, as judged by rate of production of lactate. In anoxic liver perfused with fructose, the ATP levels of both the tissue and mitochondria remained high, despite lack of oxygen, thus preventing enzyme leakage and preserving processes requiring ATP, such as bile excretion and urea formation. The mitochondrial oxidative phosphorylation capacity of anoxic liver perfused with fructose was also unimpaired. Spectral analysis of light transmitted through the liver revealed that the mitochondrial electron transfer system was in the completely reduced state during anoxia, indicating that the mitochondria were incapable of synthesizing ATP. These results suggest that fructose metabolism during anoxia resulted in sufficient production of ATP for maintaining the physiological functions of the cells and the oxidative phosphorylation capacity of their mitochondria.
Adenine Nucleotides↗
Hypervolaemic haemodilution before major surgery.
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Blood Volume↗
Effects of protamine on vascular smooth muscle of rabbit mesenteric artery.
Systemic hypotension is commonly observed in association with protamine administration after cardiopulmonary bypass. However, little information is available concerning the action of protamine on vascular smooth muscle. Thus, we investigated the action of protamine on vascular tissues using tension recording and microelectrode methods. Protamine (5-500 micrograms/ml) inhibited contractions induced by norepinephrine (NE)- or elevated K+ in a concentration-dependent manner in both endothelium-intact and -denuded strips. Protamine inhibition of NE contractions was less profound after endothelial denudation, whereas protamine inhibition of K(+)-induced contractions was less affected by prior denudation. In endothelium-intact strips, the protamine-induced inhibition was significantly reduced by inhibitors of the endothelium-derived relaxing factor pathway, including oxyhemoglobin, methylene blue, or NG-nitro-L-arginine, whereas the contractile inhibition was enhanced by superoxide dismutase. In endothelium-denuded strips, protamine inhibited Ca(2+)-induced contraction evoked in Ca(2+)-free solution containing 100 mM K+ and inhibited the NE-induced contraction under the following conditions: 1) in Ca(2+)-free solution; 2) after nifedipine treatment; and 3) after depletion of stored Ca2+ by A23187 or ryanodine. In membrane-permeabilized strips, protamine did not modify Ca(2+)-induced contraction. Protamine (50-500 micrograms/ml) did not modify the membrane potential of either endothelium-intact or -denuded strips. Furthermore, protamine irreversibly impaired acetylcholine-induced endothelium-dependent relaxant response, implying a toxic effect of protamine on the endothelium. We conclude that protamine exerts its inhibition on vascular smooth muscles in both an endothelium-dependent and -independent manner; i.e., the endothelium-dependent component is mediated probably by endothelium-derived relaxing factor, and direct smooth muscle effects are due to the inhibition of both Ca(2+)-influx and the NE-induced Ca2+ release from intracellular stores.
Animals↗
Effects of augmenting cardiac contractility, preload, and heart rate on cardiac output during enflurane anesthesia.
Changes in cardiac output in response to augmenting cardiac contractility, preload, and heart rate during enflurane anesthesia were examined in 12 open-chested dogs. Cardiac contractility was assessed by the slope of the end-systolic pressure-volume relation (Emax). Dobutamine (3, 6, and 9 micrograms.kg-1.min-1) was administered to augment cardiac contractility. Autologous blood (5.0 and 10 mL/kg) was infused to increase preload. Atrial pacing was used to increase the heart rate by about 30%. Cardiac output decreased from 96 +/- 4 (0% enflurane) (mean +/- SE) to 73 +/- 5 (1.7% enflurane) and to 46 +/- 7 mL.kg-1.min-1 (3.4% enflurane), concomitantly with decreases in Emax from 6.0 +/- 1.2 (0% enflurane) to 4.5 +/- 1.2 (1.7% enflurane) and to 2.5 +/- 0.5 mm Hg/mL (3.4% enflurane). Dobutamine (3, 6, and 9 micrograms.kg-1.min-1) increased Emax from 69% +/- 7% (compared to 0% enflurane with no dobutamine) to 139% +/- 15%, 167% +/- 25%, and 183% +/- 35% at 1.7% enflurane, and from 43% +/- 8% to 78% +/- 7%, 137% +/- 20%, and 157% +/- 22% at 3.4% enflurane, respectively. The decreases in cardiac output by 1.7% and 3.4% enflurane were reversed by the intravenous administration of 3 micrograms.kg-1.min-1 of dobutamine. Cardiac output was significantly increased by administration of 10 mL/kg of autologous blood at 1.7% enflurane, but did not significantly increase at 3.4% enflurane. Increasing the heart rate did not significantly increase cardiac output at 1.7% and 3.4% enflurane. The results of this study suggest that increasing cardiac contractility is the most effective therapeutic means of reversing circulatory depression during enflurane anesthesia.
Anesthesia↗