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Biomedical subjects

H Kai

Publications and source records attributed to H Kai.

At least 91 records · Page 5Linked to original sources
PubMed1994

Effects of continuous intravenous infusion of isosorbide dinitrate on development of tolerance to vasodilating action in human epicardial coronary arteries.

This study was performed to determine the effects of long-term intravenous infusion on the coronary vasodilating actions of continuous intravenous and bolus intracoronary administration of isosorbide dinitrate (ISDN). With quantitative coronary angiography, the coronary diameter and the vasodilating response to intracoronary ISDN (1 mg) at angiographically normal segments were studied before and after intravenous administration of ISDN, 10 to 60 micrograms/min for 1 hour, 2 days, or 5 days. The vasodilating effects of intravenous ISDN were 72% +/- 13%, 65% +/- 21%, and 6% +/- 11% of the response to intracoronary ISDN in the baseline study in each group. Irrespective of the duration of intravenous infusion, subsequent intracoronary ISDN dilated coronary arteries to extent similar to that observed in each baseline study. In conclusion, significant coronary vasodilating effects of intravenous ISDN were observed after a 2-day infusion, whereas tolerance to the vasodilating effects apparently developed within 5 days of infusion. The vasodilating response to bolus intracoronary ISDN was preserved even when the vasodilating effects of intravenous ISDN were no longer present.

Angina Pectoris↗
PubMed1994

Right-to-left shunt across atrial septal defect related to tricuspid regurgitation: assessment by transesophageal Doppler echocardiography.

The purpose of this study was to assess the factors involved in the development of the right-to-left (R-L) shunt in patients with atrial septal defect (ASD), especially the role of tricuspid regurgitation (TR). Thirty-one consecutive patients with ASD underwent transesophageal Doppler echocardiography to determine the size of ASD, the shunt flow, and the TR flow, and they were compared with hemodynamics examined by cardiac catheterization. Sixteen patients with the R-L shunt were older (53 +/- 11 vs 34 +/- 9 years; p < 0.001) and had higher pulmonary arterial pressure (36 +/- 17 vs 25 +/- 5 mmHg; p < 0.05) and a greater Qp/Qs (3.6 +/- 1.2 vs 2.4 +/- 0.9 L/min; p < 0.01) as compared with 15 patients with the pure left-to-right shunt. In six of 21 patients with TR, the regurgitant flow oriented toward ASD and blew into the left atrium through the defect. Besides the deviation of TR flow, the prevalences of the maximum diameter of ASD > 2.5 cm and the maximal TR flow area > 4 cm2 were significantly higher in the six patients as compared with patients with TR not related to the R-L shunt (p < 0.05 and p < 0.05), despite the pulmonary arterial pressure being similar in the two groups. Reversal of pressure gradient between the left and right atrium was not observed during the cardiac cycle in all patients. In conclusion, TR is a determinant of the R-L shunt in patients with ASD even in the absence of the reversal of pressure gradient between the left and right atrium.

Adolescent↗
PubMed1994

Effect of L-arginine on acetylcholine-induced endothelium-dependent vasodilation differs between the coronary and forearm vasculatures in humans.

OBJECTIVES: The goal of this study was to determine whether the effect of L-arginine on endothelium-dependent vasodilation evoked with acetylcholine differs between the coronary and forearm vasculatures in humans. BACKGROUND: Administration of L-arginine, a substrate in the production of endothelium-derived nitric oxide, may stimulate the release of nitric oxide. METHODS: Seven patients with normal coronary angiograms and seven with mild coronary artery disease and hypertension underwent coronary arteriography and an intracoronary Doppler catheter technique, and the diameter of the large epicardial coronary artery and coronary blood flow were measured. Forearm blood flow was measured by use of a strain gauge plethysmograph. RESULTS: Before L-arginine administration, acetylcholine (1 to 30 micrograms/min) increased coronary blood flow with modest vasoconstriction of a large coronary artery. Acetylcholine (4 to 24 micrograms/min) also increased forearm blood flow. The acetylcholine-induced increases in coronary and forearm blood flow were significantly less in patients with coronary artery disease than in control patients. Intracoronary infusion of L-arginine at 50 mg/min did not alter responses of the large coronary artery diameter or coronary blood flow to acetylcholine in either group. In contrast, L-arginine at 10 mg/min significantly (p < 0.01) augmented the forearm blood flow response to acetylcholine (4 to 24 micrograms/min) to a similar extent in the two groups. CONCLUSIONS: The effect of L-arginine on acetylcholine-induced vasodilation differs between the coronary and forearm vasculatures in humans. It is suggested that impaired acetylcholine-induced coronary and forearm vasodilation in patients with coronary artery disease and hypertension may not be related to a limited availability of L-arginine.

Acetylcholine↗
PubMed1994

Tardive dyskinesia affected by occlusal treatment--a case report.

The following is a case report of occlusal treatment for involuntary mandibular movement occurring in a 79-year old woman. This was diagnosed as sulpiride-induced tardive dyskinesia. The patient had been treated with sulpiride to improve gastrointestinal symptoms for five years until the onset of involuntary mandibular movement. The involuntary movement worsened even after discontinuation of the drug for 10 weeks. The dyskinesia improved in the course of treatment with an occlusal splint placed over her upper denture. After wearing the new denture with increased occlusal vertical dimension, the dyskinesia disappeared almost completely. Sirognathographic observation showed that previous denture wear evoked remarkable involuntary movement of the mandible once again. It is uncertain whether such improvement may result from discontinuation of the drug or from the occlusal treatment. However, it appears that occlusal factors played an important role in orofacial manifestation of tardive dyskinesia (TD) in this case.

Aged↗
PubMed1994

Effects of intracoronary infusion of atrial natriuretic peptide on pacing-induced myocardial ischemia in patients with effort angina pectoris.

BACKGROUND: Atrial natriuretic peptide (ANP) has been shown to dilate the coronary artery. The aim of this study was to determine whether, in patients with effort angina pectoris, intracoronary infusion of ANP attenuates pacing-induced myocardial ischemia either by dilating the stenotic lesion in a large coronary artery or by dilating collateral vessels. METHODS: We studied six patients who had total or subtotal occlusion in one coronary artery and well-developed, angiographically visible collateral vessels (group A) and five patients who had a significant stenosis in a large coronary artery with no visible collateral vessels (group B). Their heart rate was increased by atrial pacing both before and after intracoronary infusion of ANP (0.03 microgram/kg/min for 15 min) into the donor artery of collateral vessels in group A or into the stenotic artery in group B. RESULTS: Before ANP infusion, all patients of both groups developed an ischemic ST-segment depression (> or = 0.1 mV) and angina-like chest pain from pacing tachycardia. After ANP infusion, significant ST-segment depression was induced by rapid pacing in only one out of six patients of group A, whereas it was noted in all patients of group B (P < 0.01). After ANP infusion, chest pain developed in one out of six patients in group A, whereas it appeared in four out of five patients in group B (P < 0.05). ANP significantly dilated the angiographically normal segment of the epicardial coronary artery, but it did not significantly change the severity of the stenotic lesion in either group. ANP did not change the basal arterial pressure or heart rate, nor did it change their response to pacing tachycardia. CONCLUSION: Infusing ANP into the donor artery of collateral vessels, but not into the artery with culprit stenotic lesion, attenuated pacing-induced myocardial ischemia. Therefore, the beneficial effects of ANP in reducing pacing-induced myocardial ischemia may result from the increase in myocardial perfusion to the ischemic area caused by dilating the collateral vessels.

Aged↗
PubMed1994

Involvement of protein kinase C in mucus secretion by hamster tracheal epithelial cells in culture.

Abnormal regulation of airway mucus secretion may underlie many pulmonary diseases. The exact evidence for the involvement of intracellular signaling mechanisms in mucus secretion has not been fully elucidated to date. The purpose of this study is to clarify the involvement of protein kinase C in the secretion of high-molecular-weight glycoconjugates (HMWG) by hamster tracheal epithelial cells in culture, which elute in the void volume on Sepharose CL-4B column chromatography. HMWG were secreted by the cells cultured on the thick collagen gel, but not on the plastic plate. Two known activators of protein kinase C, 4 beta-phorbol 12 alpha-myristate 13-acetate (PMA) and 1-oleoyl-2-acetyl-sn-glycerol (OAG), stimulated HMWG secretion. In contrast, 4 alpha-phorbol 12,13-didecanoate, a biologically inactive phorbol, did not influence HMWG secretion. D-Sphingosine, an inhibitor of protein kinase C, suppressed the maximal PMA- (10(-8) M) and OAG- (200 microM) stimulated HMWG secretion. PMA induced protein kinase C translocation from cytosol to membrane. These data indicate that protein kinase C is involved in HMWG secretion in hamster tracheal epithelial cells in culture.

Animals↗
PubMed1994

Reduction in serum cholesterol with pravastatin improves endothelium-dependent coronary vasomotion in patients with hypercholesterolemia.

BACKGROUND: This study aimed to determine if cholesterol-lowering therapy improves endothelium-dependent coronary vasomotion in patients with hypercholesterolemia. METHODS AND RESULTS: Nine patients with hypercholesterolemia were studied before and after cholesterol-lowering therapy with pravastatin (an inhibitor of HMG-CoA reductase) for 6 +/- 3 months, which lowered serum cholesterol from 272 +/- 8 to 187 +/- 16 mg/dL (P < .01). Control patients with serum cholesterol of 218 +/- 23 mg/dL also were studied twice in a similar interval (8 +/- 2 months) with no cholesterol-lowering drugs. Acetylcholine (the endothelium-dependent vasodilator) and papaverine and nitrate (endothelium-independent vasodilators) were infused into the study coronary artery. Changes in the diameter of the epicardial coronary artery and coronary blood flow were assessed by quantitative coronary arteriography and an intracoronary Doppler catheter. In patients with hypercholesterolemia, acetylcholine-induced vasoconstriction of the epicardial artery was less (P < .05) and the acetylcholine-induced increases in coronary blood flow were greater (P < .001) after than before pravastatin. In control patients, responses of the epicardial coronary artery and coronary blood flow to acetylcholine did not change over the follow-up period. The vasomotor responses to papaverine or nitrate were similar between the two groups, and no interval changes in their responses were noted in either group. CONCLUSIONS: These results suggest that cholesterol-lowering therapy with pravastatin may improve endothelium-dependent coronary vasomotion, which may possibly contribute to the improvement of myocardial perfusion as well as the regression of coronary atherosclerosis.

Adult↗
PubMed1994

Agonist-induced phosphorylation of the vascular type 1 angiotensin II receptor.

Agonist-induced receptor phosphorylation plays a role in transmembrane signal transduction systems. Although the cDNA for the rat vascular type 1 angiotensin II receptor (AT1AR) encodes a G protein-coupled receptor with several potential phosphorylation sites for serine/threonine and tyrosine kinases, little is known about the phosphorylation of this receptor. The aim of this study was to determine the effects of angiotensin II (Ang II) on phosphorylation of the AT1AR in rat aortic vascular smooth muscle cells. Using [32P]orthophosphate-labeled cells, immunoprecipitates with anti-AT1AR antibody revealed a labeled band of molecular weight 52 kD, corresponding to the Ang II receptor. Ang II induced a rapid and significant increase in phosphorylation of the Ang II receptor, with a peak at 20 minutes. Phosphoamino acid analysis showed that the major phosphoamino acid is serine, in both the basal and Ang II-stimulated states. Constitutive and agonist-stimulated tyrosine phosphorylation is also observed to a lesser extent. Immunoblotting of anti-phosphotyrosine immunoprecipitates with anti-AT1AR antibody showed that Ang II caused a delayed tyrosine phosphorylation of the receptor with a peak at 20 minutes in a dose-dependent manner. Forskolin increased total phosphorylation of AT1AR but had no effect on tyrosine phosphorylation. Neither phorbol 12-myristate-13-acetate nor ionomycin altered receptor phosphorylation. These findings suggest that Ang II induces the phosphorylation of its own G protein-coupled receptor through both serine and tyrosine kinases and raise the possibility that phosphorylation of the AT1AR is an important regulator of receptor function.

Angiotensin II↗
PubMed1994

[Effects of a novel orally-active antiallergic drug, quinotolast (FK021), on airway clearance].

The effects of a novel antiallergic drug, quinotolast (FK021, sodium 5-(4-oxo-1-phenoxy-4H-quinolizine-3-carboxamido) tetrazolate monohydrate), on airway clearance was studied in comparison with those of tranilast (an orally-active antiallergic drug). FK021 (10 mg/kg, p.o.) did not influence the rabbit airway secretion, whereas tranilast (100 mg/kg, p.o.) caused a slight suppression. Neither FK021 (10(-10)-10(-5) g/ml) nor tranilast (10(-6), 10(-4) g/ml) had any effect on pulmonary surfactant secretion in rat type II pneumocytes. FK021 (10 mg/kg, p.o.) caused a significant increase in the mucociliary transport rate in quails, whereas tranilast (320 mg/kg, p.o.) had no effect. Antitussive effects were examined in normal guinea pigs and guinea pigs made bronchitic by an exposure to SO2. FK021 (10 mg/kg, p.o.) and tranilast (320 mg/kg, p.o.) significantly depressed the cough reflex induced by citric acid in normal animals. FK021 (32 mg/kg, p.o.), but not tranilast (320 mg/kg, p.o.), showed antitussive effects on citric acid-induced cough in bronchitic animals. These results suggest that FK021 may have favorable effects on expectoration and cough reflex observed in the patients with chronic obstructive pulmonary diseases such as asthma.

Administration, Oral↗
PubMed1994

A chromogenic test to determine the procoagulant phospholipids in platelet-rich plasma and whole blood.

We have developed a chromogenic assay to measure the phospholipid-related procoagulant activity (PPA) in whole blood, or platelet-rich plasma. The test is based upon thrombin formation from prothrombin by prothrombinase and is designed in such a way that procoagulant lipids are rate limiting for the prothrombinase activity. In the chromogenic test PPA concentrations equivalent to 0-10 nM phospholipid vesicles containing 75% phosphatidyl choline (PC) and 25% phosphatidyl serine (PS) can be measured. The thrombin, which develops during the test, is measured with a chromogenic substrate. By the action of thrombin on this chromogenic substrate p-nitroaniline is liberated, which causes an increase in absorbance. Thrombin formed in the assay mixture activates the present platelets. This causes a linear increase of the velocity of thrombin generation during the test, i.e. a parabolic increase of product formation. For that reason the thrombin generation in time is characterized by two parameters, the basal PPA (PPA-B) of the original mixture and the increase in PPA due to platelet activation (PPA-A). To determine these figures the absorbency-data were fitted to parabolas. In most cases the contribution of PPA-A to the total amount of formed thrombin becomes considerable already after 30 s. Preliminary tests show that PPA-B activity in whole blood or platelet-rich plasma of patients with a thrombotic disorder is significantly higher than the activity of a control group of the same age.

Artifacts↗
PubMed1994

The effect of subcutaneous injection of unfractionated and low molecular weight heparin on thrombin generation in platelet rich plasma--a study in human volunteers.

We administered a dose of unfractionated heparin (UFH) and two doses of a low molecular weight heparin (LMWH) to healthy volunteers by SC injection. The doses given were: a) UFH, 5000 IU, which represents 8.7 mg of > 5,400 MW active heparin (ACLM) and no < 5,400 active heparin (BCLM), b) enoxaparin 40 mg (3.4 mg ACLM, 2.2 mg BCLM) and c) enoxaparin 1 mg/kg body weight (on the mean 75 mg, containing 6.4 mg ACLM and 4.1 mg BCLM). We determined the effect on thrombin generation in platelet rich plasma (PRP) between 1 and 8 h after injection. UFH administration caused only a 5-8% inhibition of the thrombin potential (i.e. the area under the thrombin generation curve). Significantly higher inhibition of the thrombin potential was seen after administration of both doses of enoxaparin. To wit 9-26% at the low dose and 29-46% at the high dose. UFH injection caused a prolongation of the lag-time before the thrombin burst. Only with the high dose of enoxaparin the lag-times were significantly more prolonged with enoxaparin than with UFH. Excess amounts of platelet factor 4 (PF4) were able to neutralize completely the anti-thrombin activity in normal plasma spiked with enoxaparin as well as in plasma samples obtained after SC enoxaparin injection. With a large excess of PF4 the anti-factor Xa activity could be inhibited to a maximum of 50%. This indicates that ACLM (above critical length material, MW > 5400) is neutralized completely by PF4 whereas BCLM (below critical length material, MW < 5400) is not.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Multiple cDNA sequences of bovine tracheal lysozyme.

The principal role of lysozyme is to prevent bacterial invasion at body surfaces. We are interested in how lysozyme is regulated at the surface of the respiratory tract, where the serous gland cell is regarded as the primary cellular source of this enzyme. Since the cow genome contains at least 10 lysozyme-like genes, our objective was to determine which of them are expressed in the cow tracheal gland serous cell. By screening tracheal cDNA libraries with a probe constructed from the cDNA encoding stomach lysozyme 2, we obtained 3 lysozyme cDNAs: 5a (1023 base pairs (bp)), 7a (1060 bp), and 14d (1249 bp). cDNA 7a corresponds to a previously reported gene (showing sequence identity to the stomach 2 lysozyme gene), whereas cDNAs 5a and 14d correspond to lysozyme genes not previously reported. Northern blot analysis of cow tracheal RNA showed lysozyme mRNAs of three distinct lengths. Based on hybridization with probes specific for each cDNA, we determined that the longest transcript corresponded to cDNA 5a, the shortest to 7a, and the intermediate-length transcript to 14d. Cultured cow tracheal gland serous cell RNA, reverse transcribed and amplified by the polymerase chain reaction with primers common to all three cDNAs, yielded a product that hybridized to oligonucleotide probes specific for all three cDNAs but most strongly to that for 5a. These results indicate that multiple lysozyme mRNAs are expressed in the cow trachea and that the lysozyme encoded by cDNA 5a is the major form expressed in the tracheal gland serous cell. This serous cell lysozyme is predicted to differ importantly in structure from both 7a and 14d lysozymes, with an arginine:lysine ratio almost 10-fold higher. The sequence differences may underlie functional differences, including variable resistance to proteolysis and variable affinity for large polyanions (e.g. mucins) found in the respiratory tract lumen.

Amino Acid Sequence↗
PubMed1993

The significance of posterior open bite after anterior repositioning splint therapy for anteriorly displaced disk of the temporomandibular joint.

Spontaneous posterior open bite was observed in 15 patients after the application of anterior repositioning splints in the treatment of anteriorly displaced disk. Recapture of the disk after treatment was clinically diagnosed in five patients. Arthrography performed on 10 patients with open bite revealed a completely recaptured disk in four patients, an anteriorly displaced disk without reduction in four patients, and an anteriorly displaced disk with reduction in two patients. This suggests that recapture of the disk in the correct position at mouth closing should be a major cause of the posterior open bite in patients who have a relatively short duration of locking and successful mandibular manipulation. Although the cause of posterior open bite with the persistently displaced disk is still unclear, an increase in the posterosuperior joint space by the posterior open bite appears to eventually produce favorable effects to joints with anteriorly displaced disks.

Adolescent↗
PubMed1993

Differences in the mode of cough augmentation by four angiotensin-converting enzyme inhibitors in guinea-pigs.

The effects of four angiotensin-converting enzyme (ACE) inhibitors, captopril, enalapril, quinapril and alacepril, on the cough responses caused by citric acid and capsaicin inhalation were studied in normal and bronchitic guinea-pigs. After an oral dose of 10 mg kg-1, none of the ACE inhibitors had an effect on the citric acid-induced coughing response in normal guinea-pigs. Enalapril 10 mg kg-1 significantly increased the number of coughs caused by capsaicin inhalation. In bronchitic guinea-pigs, 10 mg kg-1 captopril and enalapril significantly increased the number of capsaicin-induced coughs. When administered daily for 8 days, captopril was the only ACE inhibitor which significantly increased the number of coughs due to citric acid inhalation. The present results indicate that the ACE inhibitors had different modes of cough augmentation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Effects of age on endothelium-dependent vasodilation of resistance coronary artery by acetylcholine in humans.

BACKGROUND: It has been suggested that endothelium-related vasomotion is important in the control of coronary circulation. Our goal was to determine if endothelium-dependent dilation of the coronary vasculature was altered with aging in 18 patients with atypical chest pain (age, 23-70 years) who had angiographically normal coronary arteries and no coronary risk factors. METHODS AND RESULTS: We infused an endothelium-dependent vasodilator acetylcholine (1, 3, 10, and 30 micrograms/min) and an endothelium-independent vasodilator papaverine (10 mg) into the left coronary artery. The large coronary diameter was assessed by arteriography, and the increase in coronary blood flow was measured using the intracoronary Doppler catheter technique. Acetylcholine increased coronary blood flow in a dose-dependent manner with no changes in arterial pressure and heart rate. The maximum increase in coronary blood flow evoked by acetylcholine varied widely among patients (increase in coronary blood flow ranged from 200% to 560%) and was correlated significantly with aging (r = -.86, P < .001), whereas the peak coronary blood flow response to papaverine was affected slightly by aging (r = -.44, P = .07). The percent increase in blood flow response to acetylcholine to the response to papaverine correlated with aging (r = -.87, P < .001). The slope of the coronary blood flow response to acetylcholine also correlated significantly with aging. The large epicardial coronary artery response to the low doses of acetylcholine (< or = 10 micrograms/min) correlated inversely with aging. CONCLUSIONS: The results of this study suggest that endothelium-dependent dilation of coronary arteries evoked by acetylcholine may be decreased with aging in humans.

Acetylcholine↗
PubMed1993

Impaired coronary blood flow response to acetylcholine in patients with coronary risk factors and proximal atherosclerotic lesions.

We examined whether coronary risk factors and atherosclerotic lesions in the study artery were associated with impaired endothelium-dependent dilation of coronary resistance arteries. Acetylcholine (ACH) at graded doses (1, 3, 10 and 30 micrograms/min) and papaverine (10 mg) were selectively infused into the left anterior descending coronary artery of 28 patients, in whom the study artery was angiographically normal (n = 16) or with mild stenosis < or = 40% (n = 12). Coronary blood flow (CBF) was estimated from the product of mean CBF velocity measured by an intracoronary Doppler catheter and the arterial cross-sectional area of the study artery determined by quantitative arteriography. ACH increased CBF in a dose-dependent manner. However, the maximum CBF response to ACH varied widely among patients (from 50% to 660%). By multivariate analysis, the presence of atherosclerotic lesions in the study artery was an independent predictor for impaired CBF response to ACH (P < 0.01). Hypertension (P < 0.001), hypercholesterolemia (r = -0.52, P < 0.005), age > or = 50 yr (P < 0.01) and total number of coronary risk factors (r = -0.62, P < 0.001) were associated with the impaired increase in CBF with ACH by univariate analysis. The percent increase in CBF evoked with papaverine did not correlate with these risk factors. The results suggest that mild atherosclerotic lesions in the study artery and coronary risk factors are accompanied by impaired endothelium-dependent dilation of coronary resistance arteries evoked with ACH. Endothelial dysfunction of coronary resistance arteries may result in altered regulation of myocardial perfusion in patients with mild coronary atherosclerosis and coronary risk factors.

Acetylcholine↗
PubMed1993

[Method for evaluating pulmonary clearance in mice and its pharmacological applications].

The purpose of this study was to develop a method for evaluating pulmonary clearance in mice that inhaled aerosolized 99mTc-labeled human serum albumin (33mTc-HSA). Mice were ventilated with an aerosol of 99mTc-HSA for 10 min with an ultrasonic nebulizer in an acrylic chamber. Pulmonary clearance was estimated from lung retention ratio at various times after inhalation of 99mTc-HSA. Lung retention ratios in mice were 72.4 +/- 3.3% at 1 hr, 60.1 +/- 2.3% at 3 hr and 34.8 +/- 2.0% at 24 hr after inhalation of 99mTc-HSA, similar to the previous results obtained in humans by cinescintigraphy. The data were analyzed on the basis of two-compartment model. Mabuterol, a beta 2-adrenoceptor agonist, stimulated the pulmonary clearance. In contrast, metyrapone, an adrenal 11-beta steroid hydroxylase inhibitor, suppressed the clearance with a decreased corticosterone content in plasma. These findings suggest that the developed method is useful for evaluating the pharmacological effects on pulmonary clearance.

Adrenergic beta-Agonists↗