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Biomedical subjects

T Shibamoto

Publications and source records attributed to T Shibamoto.

At least 73 records · Page 4Linked to original sources
PubMed1995

No effects of large doses of catecholamines on vascular permeability in isolated blood-perfused dog lungs.

Neurogenic pulmonary oedema (NPO) is believed to be induced by intense activation of the sympathetic nervous system, characterized by massive secretion of catecholamines into the blood stream. There is a possibility that NPO is partly the result of increased vascular permeability. However, the mechanism for an increase in pulmonary vascular permeability is not known. The present study was designed to test the hypothesis that large doses of catecholamines increase pulmonary microvascular permeability directly. Adrenaline or noradrenaline (100 and 300 micrograms) was injected as a bolus into isolated dog lungs perfused with heparinized autologous blood at constant pressure. Adrenaline or noradrenaline produced sustained lung weight loss although both catecholamines increased pulmonary capillary pressure, assessed by double occlusion pressure, by 2-5 mmHG above baseline. Vascular permeability, as measured by the capillary filtration coefficient and the isogravimetric capillary pressure, did not change significantly from baseline at 30 and 60 min after catecholamine. Finally, the final-to-initial wet lung weight ratio of the catecholamine-treated lungs did not differ from that of saline-injected control lungs. Thus, we conclude that circulating catecholamines, even at supraphysiological doses, do not increase permeability in isolated blood-perfused dog lungs.

Animals↗
PubMed1995

Suppression of sympathetic nervous system is involved in hypotension and bradycardia during hemofiltration in anesthetized dogs.

Hypotension occurring during hemodialysis is often accompanied by paradoxical bradycardia. However, the mechanism is poorly understood. This study was designed to determine the role of the sympathetic nervous system in hemodialysis-induced hypotension and bradycardia. We measured efferent sympathetic nerve activities to the heart (CNA), kidney (RNA), liver (HNA), spleen (SpNA), and adrenal gland (AdNA), along with heart rate (HR), blood pressure (BP), central venous pressure (CVP), and left atrial pressure (LAP) during hemofiltration performed at a rate of 0.3 mL .center dot Kg(-1) center dot min(-1) for 30 min in anesthetized dogs. The response to hemorrhage was also studied at the same bleeding speed. Hemorrhage caused a decrease in BP (-18 +/- 1 mmHg; 1 mmHg = 133.3 Pa) with reflex increases in HR (7 +/- 2 beats/min) and sympathetic nerve activities. In contrast, hemofiltration caused a decrease in CNA (85 +/- 18%), HNA (86 +/- 11%), and SpNA (88 +/- 11%) with greater decreases in BP (-43 +/- 10 mmHg) and HR (-27 +/- 14 beats/min) than hemorrhage. During hemofiltration, the decreases in BP, HR, CNA, HNA, and SpNA were attenuated after vagotomy. Hematocrit increased by 6.5% at 30 min after hemofiltration, whereas it decreased by 4.3% after hemorrhage. These results suggest that hemofiltration suppresses the sympathetic nervous system, resulting in decreases in HR and BP. Furthermore, this sympathetic suppression during hemofiltration is mediated by vagal afferents.

Animals↗
PubMed1995

Baroreflex attenuation after hypotension induced by vena caval occlusion in anesthetized dogs.

We determined effects of vena caval occlusion-induced systemic hypotension of 50 mmHg lasting 10 min (VCO) on efferent sympathetic nerve activity (SNA) and sympathetic baroreflex responsiveness. We recorded simultaneously SNA to the kidney (RNA), heart (CNA), spleen (SpNA), and liver (HNA) in anesthetized dogs. Baroreflex sensitivity was assessed using the ratio of a reflex SNA increase to a mean arterial pressure fall, which was also induced by caval occlusion. During VCO, SNA initially and equivocally increased, followed by recovery toward baseline. Cervical vagotomy attenuated the VCO-induced initial sympathoexcitation and subsequently maintained SNA at higher levels than those of intact animals, a finding basically similar to hemorrhagic hypotension [S. Koyama, F. Sawano, Y. Matsuda, Y. Saeki, T. Shibamoto, T. Hayashi, Jr., Y. Matsubayashi, and M. Kawamoto. Am. J. Physiol. 262 (Regulatory Integrative Comp. Physiol. 31): R579-R585, 1992]. At 5 min after releasing VCO, the baroreflex responsiveness was significantly attenuated: RNA, 79 +/- 11%; CNA, 78 +/- 8%; HNA, 60 +/- 16%; SpNA, 81 +/- 13% of the corresponding baseline. Fifteen minutes after VCO, this attenuation disappeared. Either vagotomy or pretreatment with intravenous vasopressin V1 receptor antagonist abolished this baroreflex attenuation. In conclusion, systemic hypotension to 50 mmHg for 10 min causes transient attenuation of sympathetic baroreflex sensitivity due to circulating vasopressin released by unloading of cardiopulmonary receptors during hypotension.

Animals↗
PubMed1994

Volatile carbonyl levels in tissues of transgenic mice with nerve sheath tumors.

Volatile carbonyl compounds in homogenates prepared from various tissues of tumor-bearing transgenic mice were determined. Formaldehyde and acetaldehyde were derivatized to thiazolidines. Malonaldehyde was derivatized to 1-methylpyrazole. The derivatives were quantified by gas chromatography with a highly sensitive and specific nitrogen-phosphorus detector. The limits of quantitation of formaldehyde and malonaldehyde were 2 micrograms/ml of homogenate and 27 ng/ml of homogenate, respectively. Levels of malonaldehyde in the erythrocytes and gastrocnemius of tumor-bearing transgenic mice were elevated as compared to the same tissue in control non-transgenic mice. Brain, liver, kidney, heart, and spleen tissues of the tumor-bearing mice exhibited decreased malonaldehyde levels. Similar results were obtained for formaldehyde and acetaldehyde.

Acetaldehyde↗
PubMed1994

Analysis of malondialdehyde in biological samples by capillary gas chromatography.

An analytical method to measure malondialdehyde (MDA) was developed. MDA was derivatized with N-methylhydrazine (NMH) to 1-methylpyrazole (1-MP). 1-MP was extracted and analyzed by capillary gas chromatography with nitrogen-phosphorus detection. Analyte concentration, pH, and matrix effects of 1-MP-spiked samples were investigated to determine optimal recovery conditions. Efficiencies for solid-phase extraction ranged from 95.6 +/- 0.9 to 81.6 +/- 3.5% compared to 75.0 +/- 6.4 to 67.5 +/- 9.6% for liquid-liquid extraction for 20 to 1 nmol/ml 1-MP-spiked samples, respectively. Solid-phase extraction of 1-MP was more effective than liquid-liquid extraction over a range of pH 2-8.5 and in various aqueous matrices. Addition of methanol to the matrix decreased the solid-phase extraction efficiency. Reaction yield at pH 2-8.5 showed full conversion of MDA to 1-MP following reaction with NMH. Recovery of bound MDA was investigated by incubating bovine serum albumin (BSA) spiked with MDA at 37 degrees C for 18 h and separating the free MDA and MDA-bound protein. The recovery of bound MDA from BSA increased by increasing the acidity and temperature. Specific applications of this method for biological samples are given for the analysis of endogenous MDA in the plasma and red blood cells of mice and the formation of MDA in ultraviolet-irradiated cells in culture.

Animals↗
PubMed1994

Inhibitory effect of 2"-O-glycosyl isovitexin and alpha-tocopherol on genotoxic glyoxal formation in a lipid peroxidation system.

The inhibitory effect of 2"-O-glycosyl isovitexin (2"-O-GIV), isolated from young barley leaves, on glyoxal formation from the oxidative degradation of three fatty acid ethyl esters was measured. Ethyl linoleate, ethyl linolenate and ethyl arachidonate were oxidized by Fenton's reagent. Glyoxal formed from these fatty acid esters was analysed by gas chromatography after it had been derivatized to quinoxaline with 1,2-phenylenediamine. The comparative study was performed using alpha-tocopherol. Generally, alpha-tocopherol exhibited a greater inhibitory effect at lower levels, whereas 2"-O-GIV showed a greater effect than alpha-tocopherol at higher levels. 2"-O-GIV was more effective than alpha-tocopherol towards fatty acid esters with high numbers of double bonds. 2"-O-GIV exhibited a dose-response effect but alpha-tocopherol did not. Maximum inhibition of 82% was obtained from oxidation of ethyl arachidonate at 8 mumol 2"-O-GIV, whereas maximum inhibition of 77% was observed from oxidation of ethyl arachidonate at 0.25 mumol alpha-tocopherol.

Arachidonic Acids↗
PubMed1994

Hepatic vascular response to anaphylaxis in isolated canine liver.

We determined the vascular response to anaphylaxis in isolated canine livers perfused with autologous blood at a constant pressure via the portal vein, with hepatic artery ligation to simplify the vascular system. We also studied the validity of the double occlusion pressure (Pdo) as a measure of the capillary pressure (Pc) in the isolated canine liver. Pdo was compared with Pc measured using the traditional isogravimetric method (Pc,i), and both parameters showed a strong correlation (Pdo = 0.34 + 0.90 Pc,i; r = 0.93; P < 0.01). This indicated that Pdo provided an accurate indication of Pc in the isolated liver. In livers with anaphylaxis induced by the intraportal injection of Ascaris suum antigen (5 mg; 1.0 +/- 0.03 mg/kg body wt), hepatic vascular resistance and Pc (assessed as Pdo) were increased transiently by 29-fold and 3.4 mmHg, respectively, along with a significant increase of liver weight. The ratio of presinusoidal to postsinusoidal vascular resistance decreased from 0.89 +/- 0.05 to 0.36 +/- 0.12, suggesting that hepatic venous constriction was predominant. In livers perfused in the antidromic direction from the hepatic vein to the portal vein, anaphylaxis caused marked presinusoidal vasoconstriction that was consistent with hepatic venoconstriction as well as a significant and sustained decrease of liver weight below the baseline. These results suggest that anaphylaxis produced hepatic weight gain because of an increase in sinusoidal pressure caused by hepatic venoconstriction. Such hepatic venoconstriction may play an important role in the development of portal hypertension and hepatic congestion associated with anaphylactic shock.

Anaphylaxis↗
PubMed1994

Role of hypogastric nerve activity in opossum internal anal sphincter function: influence of surgical and chemical denervation.

The exact role of the hypogastric nerve (HGN) in the regulation of basal internal anal sphincter pressures (IASP) and rectoanal reflex (RAR)-induced internal anal sphincter (IAS) relaxation is not known. The studies were performed to investigate the effect of electrical stimulation of HGN (HGNS) on IASP and RAR-induced fall in IASP, simultaneously record the HGN activity (HGNA) and IASP in response to different volumes of rectal balloon distension (RBD) to mimic RAR and determine the neural pathway involved in RBD-induced changes in HGNA. The recording of multifiber unit efferent HGNA was carried out after ipsilateral deafferentation in animals. HGNS produced a frequency-dependent rise in IASP and suppression of RBD-induced fall in IASP. Hexamethonium markedly attenuated the basal HGNA by 86% without causing a significant change in the basal IASP. Five cc of RBD caused a fall in IASP of 70.8 +/- 4.8% without any significant change in HGNA. Further increases in the RBD volume caused a volume-dependent increase in the basal HGNA and a biphasic systemic arterial pressure response (an initial fall followed by an elevation). These responses were suppressed by sympathectomy or sacral denervation. Sympathectomy plus sacral denervation caused complete obliteration of these responses. The data suggest that in the basal state, HGN may not play a significant role in the resting IASP and RAR-induced IAS relaxation. However, there was a significant sympathoexcitation in response to higher volumes of RBD (supramaximal stimulus for RAR). Hypogastric and sacral nerves may participate in the afferent pathways for the RBD-induced sympathoexcitation.

Anal Canal↗
PubMed1993

Renal vascular and sympathetic nerve responses to hypotension induced by platelet-activating factor in anesthetized dogs.

This experiment was designed to determine renal sympathetic and renal vascular responses to platelet-activating factor (PAF)-induced hypotension in anesthetized dogs with and without systemic baroreceptor denervation. The left kidney was perfused at a constant flow, and renal perfusion pressure and efferent left renal sympathetic nerve activity were measured simultaneously. Intrarenal injection of PAF (1.25-5.0 x 10(-2) micrograms/kg, n = 6) produced a dose-dependent increase in renal perfusion pressure without any change in systemic blood pressure. An intravenous injection of PAF (10 micrograms/kg) to intact animals (n = 7) caused an initial increase in renal nerve activity (157 +/- 14%) followed by a gradual reduction below baseline (72 +/- 7%) with concomitant systemic hypotension (from 116 +/- 7 to 46 +/- 6 mmHg). Renal perfusion pressure increased significantly from 84 +/- 2 to 161 +/- 33 mmHg concomitant with an increase in renal nerve activity at 1 min and was maintained at this elevated level throughout the experiment. Similar responses of renal nerve activity and renal perfusion pressure were found in animals with complete systemic baroreceptor denervation (n = 7). These results suggest that renal vascular response during PAF-induced hypotension may presumably be mediated by a direct vasoconstrictor effect of PAF on the renal vasculature and that baroreceptor reflex is not involved in either renal sympathetic or renal vascular changes.

Animals↗
PubMed1993

PAF increases capillary pressure but not vascular permeability in isolated blood-perfused canine lungs.

We determined the effects of platelet-activating factor (PAF) on pulmonary vascular resistance, lung weight, and microvascular permeability in isolated canine lungs perfused at constant pressure with autologous blood. PAF caused a dose-dependent increase in total pulmonary vascular resistance (Rt) and pulmonary capillary pressure assessed as double-occlusion pressure. PAF (33 micrograms; n = 7) caused a 10-fold increase in Rt and a decrease in precapillary-to-postcapillary vascular resistance ratio from 0.97 +/- 0.10 to 0.38 +/- 0.03, suggesting predominant pulmonary venoconstriction. Shortly after PAF, lung weight decreased transiently and then increased, reaching a plateau above baseline (112.5 +/- 1.6%) at 30 min. In lungs perfused in the antidromic direction from the pulmonary vein to the artery (n = 5), PAF (33 micrograms) produced marked precapillary vasoconstriction, consistent with pulmonary venoconstriction, and a remarkable and sustained decrease in lung weight below baseline by 30 min. Vascular permeability, measured 30 min after PAF using the capillary filtration coefficient and isogravimetric capillary pressure, did not change significantly from baseline. Thus we conclude that PAF produces lung weight gain by means of an increase in capillary pressure predominantly due to pulmonary venoconstriction without significant changes in vascular permeability in isolated blood-perfused canine lungs.

Animals↗
PubMed1993

Role of sympathetic nervous system in hypotension induced by platelet-activating factor in anesthetized dogs.

This experiment was designed to investigate whether platelet-activating factor (PAF)-induced hypotension in anesthetized dogs produces changes in sympathetic activity in the heart, kidney, liver, and adrenal gland in intact animals (n = 5) and in animals with complete systemic baroreceptor denervation (n = 5). Following intravenous injection of PAF (10 micrograms/kg) in animals with intact baroreceptors, systemic blood pressure fell significantly. However, sympathetic nerve activity in the kidney, liver, and adrenal gland revealed a biphasic pattern: an initial increase (within 30 sec) followed by a progressive reduction below the preinjection level. In contrast to these nerve responses to PAF, only cardiac nerve activity showed an initial and significant increase, and it remained elevated above the preinjection level until the end of the experiment (10 min). In animals with complete systemic baroreceptor denervation, these sympathetic responses to PAF did not differ significantly from the responses in the intact animals. These results indicate that intravenous injection of PAF produces differential control of sympathetic nerve activity in different organs. The contribution of systemic baroreceptors to reflex compensations is minor in PAF-induced hypotension.

Adrenal Glands↗
PubMed1993

Relative contribution of renal nerve and adrenal gland to renal vascular tone during prolonged canine hemorrhagic hypotension.

This study was designed to determine roles of renal sympathetic nerve activity (RNA) and adrenal catecholamines in the changes of renal vascular resistance during prolonged hemorrhagic shock in anesthetized dogs. In animals with intact baroreceptors, hemorrhagic hypotension (40 mm Hg) caused RNA to increase significantly within 1 min after bleeding, followed by a return to baseline within 10 min. Thereafter, a secondary increase in RNA occurred that was followed by a gradual decline towards the baseline level. The renal perfusion pressure (RPP) showed a progressive and significant increase until the end of the experiment. The initial increase in RNA was abolished by complete denervation of the systemic baroreceptors. The initial increase in RPP, which was observed within 10 min after bleeding in animals with intact baroreceptors, was attenuated by the denervation. In animals with bilateral adrenalectomy, RPP still showed an initial increase, but the progressive increase throughout the entire experimental period did not occur. In animals with baroreceptor denervation and bilateral adrenalectomy, RPP did not show any significant changes during the experiment. These results indicate that the initial renal vasoconstrictive response to hemorrhage is regulated by a reflex sympathetic mechanism. In contrast, a late renal vasoconstriction during hemorrhagic hypotension is predominantly evoked by humoral substances such as adrenal catecholamines.

Adrenal Glands↗
PubMed1993

Differential control of sympathetic outflow to kidney, heart, adrenal gland, and liver during systemic hypotension induced by cardiac tamponade in anesthetized dogs.

This study was designed to determine if cardiac tamponade-induced hypotension produces differential control in efferent sympathetic nerve activity to the kidney (RNA), heart (CNA), adrenal gland (AdNA), and liver (HNA) in pentobarbital-anesthetized dogs and to define whether systemic baroreceptors modify this response. We recorded RNA, CNA, AdNA, and HNA simultaneously during a 10 min period of sustained hypotension of 50 mm Hg, which was produced by intrapericardial saline infusion at 20 ml/min. When blood pressure reached 50 mm Hg, sympathetic nerve activity to all four organs increased significantly. Following this, RNA decreased significantly below the control (72 +/- 12%) at the end of experiment, while CNA, AdNA, and HNA remained elevated above control values throughout the experiment. Renal sympathoinhibition was reversed by cervical vagotomy, whereas this had no effect on CNA, AdNA, and HNA responses to hypotension. Additionally, the combined denervation of vagal, carotid sinus, and aortic nerves did not show any significant change in any variables. Thus these results indicate that hypotension due to cardiac tamponade in dogs produces an initial equivocal sympathoexcitation to the kidney, heart, adrenal gland, and liver followed by vagal afferent-mediated sympathoinhibition to the kidney but sustained excitation to the other three organs.

Adrenal Glands↗
PubMed1992

Analysis of reactive carbonyls in the expired air of transgenic mice.

Methods for the determination of trace levels of volatile carbonyl compounds in air expired from mice were developed and validated. Tumor bearing transgenic mice or nontransgenic control mice were placed into a glass chamber through which air was passed continuously at 90 ml/min for 1 h. The effluent gas stream was bubbled into an aqueous cysteamine solution or an aqueous methylhydrazine solution. Formaldehyde, acetaldehyde, and acetone in expired air were derivatized to thiazolidine with cysteamine and malonaldehyde was derivatized to 1-methyl-2-pyrazole with methylhydrazine. The derivatized compounds were analyzed by capillary gas chromatography with flame photometric or nitrogen-phosphorous-specific detection. The lowest level quantitated was 4 micrograms/ml thiazolidine, equivalent to 1.35 micrograms/ml formaldehyde. Formaldehyde was recovered at a level of 1356 +/- 234 nmol/kg0.75 (mean +/- SD) from mice with tumors and 898 +/- 97 nmol/kg0.75 from mice without tumors, suggesting that tumor bearing transgenic mice expired significantly more formaldehyde than did tumor free controls. Amounts of expired acetaldehyde and acetone were not different among mice. Malonaldehyde was not detected in either group of mice.

Acetaldehyde↗
PubMed1992

Formation of formaldehyde and malonaldehyde by photooxidation of squalene.

Formaldehyde and malonaldehyde were identified upon exposure of squalene to ultraviolet (UV) irradiation at 300 nm. Formaldehyde was derivatized by reaction with cysteamine to form thiazolidine; malonaldehyde was derivatized by reaction with N-methylhydrazine to produce N-methylpyrazole. The derivatives were subsequently analyzed with a gas chromatograph equipped with a fused silica capillary column and a nitrogen/phosphorus detector. The levels of formaldehyde and malonaldehyde produced increased with irradiation time. The amount of formaldehyde produced reached a maximum of 3.40 nmol/mg squalene after 7 hr irradiation; the maximum amount of malonaldehyde generated, 0.92 nmol/mg, was found after 5 hr of irradiation. Prior to this study, formaldehyde had not been reported as a photoproduct of squalene. Acetaldehyde and acetone were also detected in the irradiated squalene, which may be formed via a 6-methyl-5-hepten-2-one intermediate. 6-Methyl-5-hepten-2-one can also undergo breakdown to form malonaldehyde.

Formaldehyde↗
PubMed1992

Acute effect of hypobaria and hypoxia on renal nerve activity in anaesthetized rabbits.

To determine the acute effect of reduced barometric pressure and hypoxia on renal nerve activity, urethane-anaesthetized and mechanically ventilated rabbits were randomly exposed to the following four separate conditions in a decompression chamber: hypoxic hypobaria (n = 7), hypoxic normobaria (n = 5), normoxic hypobaria (n = 8) and slow normoxic hypobaria (n = 7). A combination of rapid decompression and simultaneous adjustment of inspired PO2 was used to simulate an altitude of 6600 m, and renal nerve activity and haemodynamics, such as systemic blood pressure and heart rate, were measured. During both hypoxic hypobaria and hypoxic normobaria, there were significant and similar increases in renal nerve activity at 6600 m (54 +/- 7% and 61 +/- 13% from each baseline, respectively). However, there were no changes in renal nerve activity during normoxic hypobaria or slow normoxic hypobaria with decompression rates of 1000 or 400 m min-1, respectively. From these results, we conclude that a reduction in barometric pressure without hypoxia does not affect renal nerve activity in anaesthetized rabbits.

Anesthesia↗