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Biomedical subjects

H Toda

Publications and source records attributed to H Toda.

At least 91 records · Page 5Linked to original sources

Influence of left ventricular filling profile during preceding control beats on pulse pressure during ventricular premature contractions.

We investigated whether the left ventricular filling profile, defined as the early to late diastolic left ventricular filling volume ratio, during the preceding control beats actually affects the pulse pressure during a ventricular premature contraction (PVC). Twenty patients underwent invasive electrophysiological study for sinus bradycardia. VPCs with various coupling intervals were induced by right ventricular electrical stimulation, and the mitral filling flow velocity by pulsed Doppler echocardiography, the femoral arterial pressure curve and the electrocardiogram were simultaneously recorded. The early to late diastolic velocity-time integral ratio (Ei/Ai ratio) of the mitral filling flow velocity during the control beats which preceded the VPC was measured as an index characterizing left ventricular filling profile. The coupling interval of each VPC and the extrasystolic beat pulse pressure were measured. The ratio of the extrasystolic beat pulse pressure to the control beat pulse pressure was expressed in % (% extrasystolic beat pulse pressure). The correlation between the coupling interval and the % extrasystolic beat pulse pressure was investigated. Coupling intervals of 0.80, 0.70, 0.60, 0.50, and 0.45 s were used. At a coupling interval of 0.80 or 0.45 s, the % extrasystolic beat pulse pressure showed no significant correlation with the Ei/Ai ratio. In contrast, the % extrasystolic beat pulse pressure with coupling intervals of 0.70, 0.60, and 0.50 s showed a significant positive correlation with the Ei/Ai ratio (r = 0.67, 0.74, and 0.66, P < 0.01, respectively). In addition to the prematurity and the site of origin of the VPCs, the left ventricular filling profile during the preceding control beats may significantly affect the height of the pulse pressure during extrasystoles with medium length coupling intervals.

Adolescent↗

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↗

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↗

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↗

Phasic venous return abnormality in chronic pulmonary diseases: pulsed Doppler echocardiography study.

Features of venous return in chronic pulmonary diseases and factors determining such features were studied by analysis of respiration-related variation in the superior vena cava flow on pulsed Doppler echocardiography. Subjects of this study were 85 patients with chronic pulmonary diseases; 54 healthy subjects served as normal controls. In the healthy subjects, the velocity of the S and D waves increased during inspiration (type I pattern), and the velocity of the A wave increased during expiration. In the patients with pulmonary diseases, the pattern of the superior vena cava flow was either type I or type II (disappearance of the D wave or disappearance of both the D and S waves). The incidence of the type II pattern was significantly higher in the patients showing a reduction of both FEV1.0% and % VC. The respiration-related variation in the superior vena cava flow pattern was found to be determined by the pressure fall between right atrium and subclavian vein. A type II pattern was attributed to the elevation of right atrial pressure caused by positive pleural pressure. The velocity of the A wave increased during expiration, showing a good correlation with pulmonary vascular resistance. Venous return in the presence of chronic pulmonary disease was found to be affected by the type of ventilatory disturbance and intensity of pulmonary vascular resistance.

Adult↗

Assessment of the gas exchange function of the middle ear using nitrous oxide. A preliminary study.

A method for assessing the gas exchange through the middle ear (ME) mucosa using nitrous oxide is introduced. Increases in the ME pressure was determined by a tympanogram or a micropressure sensor inserted into the mastoid cavity during ear surgery under general anesthesia using 67% nitrous oxide, 33% oxygen, and sevoflurane on 30 normal ears, 12 ears with otitis media with effusion (OME), and 3 postoperative ears with chronic adhesive otitis media or cholesteatoma. All the 30 normal ears except one showed varying pressure increase, and an inverse correlation was observed between pressure increase and area of mastoid on radiographs. Pressure increase was observed in 6 (50%) ears with OME, and this finding correlated well with the presence or absence of air space in the ME on computed tomography images examined preoperatively, on ears which had ear surgery, the presence or absence of pressure increase correlated with the degree of previous surgical intervention on the mastoid. The rationale and possibility of clinical application of this method is discussed.

Acoustic Impedance Tests↗

[Predominantly ipsilateral smooth pursuit impairment associated with a lesion in the basal pons].

In contrast to the well-defined brainstem centers for saccades and eye reflexes, the brainstem centers mediating smooth pursuit eye movements are poorly understood. In monkeys, unilateral damage to the basal pons impairs horizontal smooth pursuit in the direction of the side of the lesion. The major source of afferents to the basal pons is the middle temporal area (MT). The dorsolateral pontine nucleus (DLPN) in the basal pons is considered to be the major gateway for smooth pursuit related signals to the contralateral flocculus. In humans, only one patient was found to have a unilateral lesion in the basal pons and selective impairment of smooth pursuit toward the side of the lesion. We report a 34-year-old man with a lesion in the basal pons identified by MRI. He had suffered from recurrent oral aphthosis, erythema nodosum and enterocolitis, and was hospitalized because of dysarthria. He was clinically diagnosed as neuro-Behçet disease. Saccades, smooth pursuit, vestibulo-ocular reflex (VOR), and VOR cancellation were measured. Ipsilateral smooth pursuit eye movements were predominantly impaired and interrupted by saccades, whereas VOR cancellation was impaired in both directions, in contrast with normal saccades and VOR. This observation of predominantly ipsilateral smooth pursuit impairment after a lesion in the human basal pons suggests that the concept of a middle temporal-ponto-floccular pathway for smooth pursuit, previously established in monkeys, can be extended to humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

A randomized, controlled trial of human lymphoblastoid interferon in patients with compensated type C cirrhosis.

OBJECTIVE: To determine the efficacy of human lymphoblastoid interferon (L-IFN) in the treatment of compensated type C cirrhosis, 30 patients were assigned randomly to three groups, consisting of 10 patients each, who were treated as follows. METHODS: The 1- and 3-megaunit (MU) groups received 1 or 3 MU of L-IFN, respectively, daily for 2 wk, and three times weekly for 24 wk thereafter. The control group received no treatment. All of the patients had positive C100-3 hepatitis C virus antibody (anti-HCV) titers. RESULTS: The serum alanine aminotransferase (ALT) levels decreased 26 wk after L-IFN treatment was began, in both treatment groups. In the 3-MU group, the ALT levels became normal [complete response (CR)] in 40%, improved to less than twice the upper limit of the normal value [partial response (PR)] in 10%, and remained unchanged [no change (NC)] in 50%. In the 1-MU group, a PR occurred in 30%. There was NC in 70%, and NC occurred in the control group. Twenty-four weeks after stopping L-IFN, the CR and NC rates in the 3-MU group were 10% and 90%, respectively, and NC was observed in all of the 1-MU and control patients. 2',5'-Oligoadenylate synthetase activities increased in both treatment groups (p < 0.05), but not in the control group. The anti-HCV titers decreased in the 3-MU group (p < 0.05), but not in the 1-MU and control groups. Higher doses of L-IFN were more effective. No serious side effects occurred. CONCLUSIONS: These findings suggest that IFN administration can be effective and safe in patients with compensated type C cirrhosis, and that it would be worthwhile to evaluate IFN therapy for cirrhotic patients further.

2',5'-Oligoadenylate Synthetase↗

[Slow-upward ocular bobbing in a patient with striatonigral degeneration].

We herein report a patient with the abnormal eye movement characterized by a conjugate slow-upward eye movement followed by a fast-downward movement to the primary position (slow-upward ocular bobbing). A 55-year-old man with a 12 years' history of striatonigral degeneration developed pneumonia and was admitted to our hospital. In addition to the parkinsonian features like akinesia and rigidity, examination revealed slow-upward ocular bobbing. There were no accompanying ocular abnormalities. This spontaneous eye movement was recognized throughout his stay in the hospital, irrespective of his consciousness level. Although other forms of ocular bobbing/dipping are usually associated with the loss of consciousness, all three reported patients with this slow-upward ocular bobbing were awake and responsive, therefore, suggesting a different kind of background pathophysiology in this unique eye sign.

Brain Diseases↗

Sweet potato beta-amylase. Primary structure and identification of the active-site glutamyl residue.

The complete amino acid sequence of a subunit of sweet potato beta-amylase, a homotetramer, was established by sequence analysis of peptides obtained by digestions with Achromobacter protease I and Staphylococcus aureus V8 protease and by cyanogen bromide cleavage of the S-carboxymethylated subunit. The subunit of the enzyme is a single polypeptide consisting of 498 amino acid residues. It showed 50-60% identity in the amino acid sequence with those of beta-amylases from soybean and barley, while it about 25% with those of three bacterial beta-amylases deduced from the cDNA sequences. Sweet potato beta-amylase was completely inactivated with 2,3-epoxypropyl alpha-D-[U-14C]glucopyranoside. Sequence analysis of the inactivated enzyme revealed that Glu187 was specifically esterified by the affinity labeling with the above reagent, proposing that Glu187 is a potent candidate involved directly in the catalysis with this plant beta-amylase.

Amino Acid Sequence↗

Therapeutic efficacy of granulocyte colony stimulating factor against rat cecal ligation and puncture model.

To identify the therapeutic efficacy of granulocyte colony stimulating factor (G-CSF) in severe sepsis, we examined its effect on the mortality and pathological changes in vital organs using the rat lethal sepsis model. Rats were given 15 micrograms of recombinant human (rh)G-CSF after the onset of peritonitis brought about by cecal ligation and puncture. The mortality rate after 72 h was significantly decreased by administration of 15 micrograms of rhG-CSF (p < 0.001). In addition, the administration of rhG-CSF induced an improvement in liver and renal functions. It also produced marked pathological improvement in the lungs. These results strongly indicated that administration of rhG-CSF, even after the onset of sepsis, was effective in decreasing the mortality from peritonitis-induced multiple organ failure, and this finding was clearly useful in the clinical treatment of such sepsis-induced critical illness.

Animals↗

Comparison of the direct effects of sevoflurane, isoflurane and halothane on isolated canine coronary arteries.

We have demonstrated previously, using dog epicardial arteries of different sizes, that isoflurane, like adenosine, is preferentially a small coronary artery dilator, whereas halothane, like nitroglycerin, is a large artery dilator. The present study was designed to compare the direct effects of sevoflurane with those of isoflurane and halothane. Proximal large coronary arteries with an outer diameter (o.d.) of 2.5-3.2 mm and distal small arteries of 0.6-0.9 mm o.d. were isolated from dogs and then cut into vascular rings. They were precontracted with KCl (20 mM), and their relaxant responses to anaesthetics were compared relative to the maximal responses induced by papaverine. Sevoflurane, halothane and isoflurane (1-3 human MAC) induced dose-dependent relaxation of these arteries. The relaxant response to sevoflurane did not differ between large and small arteries. However, the relaxant response of the large arteries to halothane (1.5-2.3%) was greater than that of small arteries (P < 0.01) and the response of small arteries to isoflurane (3.5%) was greater than that of large arteries (P < 0.05). In large arteries, the potency of the relaxant effect at equivalent human MAC could be ranked as halothane > or = sevoflurane > isoflurane, and, in small epicardial arteries as isoflurane > sevoflurane >> halothane. We conclude that, unlike isoflurane, sevoflurane is not a preferential dilator of small coronary arteries.

Anesthetics↗

Detection of reperfusion 30 and 60 minutes after coronary recanalization by a rapid new assay of creatine kinase isoforms in acute myocardial infarction.

We measured creatine kinase (CK) isoforms by a new immunoinhibition method to evaluate their usefulness in detecting early coronary reperfusion. Blood samples were collected at 15-minute intervals from 50 patients with acute myocardial infarction. CK isoforms were determined by a 10-minute immunoinhibition method with an autoanalyzer. Values for inhibited isoforms (MM3, MM2/2, and MB2/2) were divided by those of noninhibited isoforms (MM1, MM2/2, MB1, MB2/2, and BB) to calculate the isoform ratio. In the reperfused group the increase in the isoform ratio was 2.69 +/- 1.80 (SD) 30 minutes after reperfusion and 2.41 +/- 2.01 at 60 minutes, which was significantly higher than the corresponding values in the nonreperfused group (0.17 +/- 0.16 and 0.32 +/- 0.26, respectively). When an increase of 0.70 or more in the isoform ratio was used as the criterion for reperfusion, the sensitivity and specificity were 92% and 100% at 30 minutes and 100% and 100% at 60 minutes after recanalization, respectively. We conclude that the isoform ratio obtained by the new 10-minute assay of CK isoforms is useful for the noninvasive detection of reperfusion 30 and 60 minutes after recanalization in acute myocardial infarction.

Angioplasty, Balloon, Coronary↗

Extrastriate cortical neurons correlated with ocular convergence in the cat.

Responses of neurons in the lateral suprasylvian area to visual stimulation in association with ocular convergence were studied in eight alert cats trained to track a visual target moving in depth. Activities of 18 (3%) of 659 cells were related to ocular convergence. These 18 neurons were divided into two groups: activities of seven neurons (40%) correlated with peak velocities of convergence eye movement at both fast and slow target speeds (group I), while those of five neurons (30%) correlated with them only at faster target speed (group II). Activities of six other neurons correlated with peak velocity of ocular convergence at faster target speed but were not tested at slower speed. Activities of four group-I neurons (60%) did not or only weakly correlate with lens accommodation, while those of four group-II neurons (80%) correlated with peak velocity or amplitude of lens accommodation. It can therefore be concluded that the four group-I neurons are primarily related to ocular convergence. Other cells were either convergence-related, lens accommodation-related or both. It is suggested that these different types of neurons contribute in combination to optimal control of convergence eye movement.

Accommodation, Ocular↗

Influence of left ventricular filling profile during preceding control beats on the occurrence of pulse deficit caused by ventricular premature contractions.

This study was designed to investigate whether the left ventricular filling profile during preceding control beats significantly affects the pulse deficit caused by ventricular premature contractions (VPCs). The study group consisted of 18 patients (10 men, eight women, 15-85 years old) who underwent electrophysiological catheterization because of sinus bradycardia. Using a temporary pacing lead inserted in the right ventricular apex, isolated VPCs with various coupling intervals were produced by electrical stimulation of the right ventricle. During the production of the VPCs, the mitral filling flow velocity using pulsed wave Doppler echocardiography, the femoral arterial pressure curve and the electrocardiogram were simultaneously recorded. The right ventricle was stimulated 800, 750, 700, 650, 600, 550, 500, 450 and 400 ms after the triggered control beat QRS complex. Pulse pressures during VPCs gradually decreased in relation to the shortening of the extrasystolic beat coupling interval. The longest coupling interval for each subject, which caused complete abolition of the pressure pulse during the VPC, was defined as the pulse deficit coupling interval. The early to late diastolic velocity-time integral ratio (Ei/Ai ratio) of the mitral filling flow velocity during the control beats which precede the VPC was obtained as an index expressing the left ventricular filling profile. The Ei/Ai ratio of the mitral filling flow velocity ranged from 0.7 to 4.5 (1.8 +/- 1.0). The pulse deficit coupling interval ranged from 440 to 640 ms (510 +/- 60 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The complete amino acid sequence of subunit d of rat liver mitochondrial H(+)-ATP synthase.

Subunit d of H(+)-ATP synthase from rat liver mitochondria was isolated from the purified enzyme by reverse-phase high performance liquid chromatography. The partial amino acid sequence of the subunit was determined by automated Edman degradation of the peptide fragments. The nucleotide sequence of subunit d of rat liver H(+)-ATP synthase was determined from a recombinant cDNA clone isolated by screening a rat hepatoma cell line H4TG cDNA library with a probe DNA. The sequence was composed of 581 nucleotides including a coding region for the import precursor of subunit d and noncoding regions on the 5'- and 3'- sides. The possible precursor of subunit d and its mature polypeptide deduced from the open reading frame consisted of 161 and 160 amino acid residues with molecular weights of 18,763 and 18,631, respectively. Subunit d is a hydrophilic protein with an isoelectric point of 6.19. The sequence of the rat subunit d is highly homologous with that of subunit d of bovine heart and slightly similar to that of the subunit d of the yeast mitochondria. However, it had no homology with the sequence of any of the subunits of bacterial or chloroplast H(+)-ATP synthase.

Amino Acid Sequence↗