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Biomedical subjects

I Abe

Publications and source records attributed to I Abe.

At least 109 records · Page 6Linked to original sources

Adsorbability of 1,1,1,2-Tetrafluoromethane (HFC134a) onto Plasma-Treated Activated Carbon in CF4 and CCl4

The adsorbability of 1,1,1,2-tetrafluoroethane (HFC134a), which has been the CFC12 replacement, onto tetrafluoromethane and tetrachloromethane plasma-treated activated carbon (FT-ACs and CT-ACs) was investigated. It is proved that the fluorine and the chlorine, which were produced by plasma treatment, were introduced into the pores having radii greater 7.5 A and with less than 7.5 A by plasma treatment, respectively. The adsorption site of HFC134a onto activated carbon may change with the quantities of fluorine or chlorine on the surface of the activated carbon. The amount of HFC134a adsorbed per unit specific surface area of FT-ACs and CT-ACs slightly increased a little compared to the untreated activated carbon (U-AC). The amount of fluoride ion eluted before the adsorption of HFC134a from the FT-ACs increased with the increasing plasma treatment time. That after the adsorption of HFC134a from only the activated carbon with the shortest plasma treatment time decreased. The amount of chloride ion eluted before the adsorption of HFC134a from the CT-ACs increased after 15 min of plasma treatment, but decreased with 30 min of plasma treatment. The chloride ion amount from the CT-ACs decreased after the adsorption of HCF134a. These results could be explained by the Langmuir constants a and Ws, which represent the adsorption equilibrium constant and the saturated amount of HFC134a adsorbed, respectively. The ratio of fluorine and chlorine species, the adsorption type, the layer interstitial type, and the covalent type, is different based on the plasma treatment time. It is concluded that the amount of HFC134a adsorbed onto the FT-ACs and CT-ACs did not depend upon the change of pore structure by the fluorine and chlorine.

Journal Article↗

Effects of CP-060S on membrane channels in vascular smooth muscle cells from guinea pig.

The newly developed cardioprotective drug, CP-060S, (-)-(S)-2-[3,5-bis(1,1-dimethylethyl)-4-hydroxyphenyl]-3-[3-[N-methyl-N- [2-(3,4-methylenedioxyphenoxy) ethyl] amino] propyl]-1,3-thiazolidin-4-one hydrogen fumarate, is reported to possess a vasodilating action. Our objective was to examine the effects of CP-060S on the membrane channels in mesenteric arterial cells from guinea pigs, using whole-cell patch-clamp techniques. CP-060S inhibited the Ca2+ channel current in a concentration-dependent manner (ED50 = 1.7 microM at a holding potential of -80 mV and a stimulation frequency of 0.1 Hz). The inhibition was potentiated by a more depolarized holding potential and a higher stimulation frequency. These effects of CP-060S resembled those of diltiazem and gallopamil more than to those of nifedipine; the inhibition was more frequency dependent and less holding-potential dependent than with nifedipine. Higher concentrations of CP-060S also inhibited the delayed K+ channel currents (ED50 = 18 microM). The present observations suggest that CP-060S exhibits the profile of a Ca2+ channel antagonist, similar to that of diltiazem and gallopamil.

Animals↗

Stretch-activated whole-cell currents in smooth muscle cells from mesenteric resistance artery of guinea-pig.

1. Stretch-activated (SA) channels were studied in smooth muscle cells isolated from mesenteric resistance arteries using the whole-cell patch-clamp method. Membrane stretch was achieved by cell inflation after application of positive pressure through a patch electrode. 2. In the voltage-clamp configuration, cell inflation increased and cell deflation decreased the membrane conductance. Conductance of the evoked current depended on the increase in cross-sectional area of the cell. The current-voltage relationship was linear between -80 and 0 mV, while further hyperpolarization showed a slight inward rectification. 3. The reversal potential of the SA current depended on the extracellular Na+ concentration, suggesting that the inward SA current was carried predominantly by Na+. The SA current was also carried by other cations, suggesting that the channel responsible for this current is a non-selective cation channel. The permeability sequence of cations as assessed by reversal potential was as follows: K+ > or = CS+ > or = Na+ > Li+. The channel was also permeable to Ca2+. 4. Extracellular Ca2+ and Gd3+ inhibited the SA current carried by monovalent cations in a concentration-dependent manner with IC50 (concentration giving 50% of maximal inhibition) values of 0.9 mM and 14 microM, respectively. 5. In the current-clamp configuration, membrane stretch depolarized the cell, and 100 microM Gd3+ inhibited the stretch-induced depolarization. 6. The results suggest that SA cation channels exist in arterial smooth muscle cells. Activation of the channels may modify membrane potential and intracellular ionic environment, and promote stretch-mediated cell responses.

Animals↗

Human BAC library: construction and rapid screening.

We have constructed a human genomic bacterial artificial chromosome (BAC) library using high molecular weight DNA from a pre-pro-B cell line, FLEB14-14, with a normal male diploid karyotype. This BAC library consists of 96,000 clones with an average DNA insert size of 110 kb, covering the human genome approximately 3 times. The library can be screened by three different methods. (1) Probe hybridization to 31 high-density replica (HDR) filters: each filter contains 3072 BAC clones which were gridded in a 6 x 6 pattern. (2) Probe hybridization to two Southern blot filters to which 31 HindIII digests of the pooled 3072 BAC clones were loaded. This identifies a particular HDR filter for which further probe hybridization is performed to identify a particular clone(s). (3) Two-step polymerase chain reaction (PCR). First, PCR is applied to DNA samples prepared from ten superpools of 9600 BAC clones each to identify a particular superpool and the second PCR is applied to 40 unique DNA samples prepared from the four-dimensionally assigned BAC clones of the particular superpool. We present typical examples of the library screening using these three methods. The two-step PCR screening is particularly powerful since it allows us to isolate a desired BAC clone(s) within a day or so. The theoretical consideration of the advantage of this method is presented. Furthermore, we have adapted Vectorette method to our BAC library for the isolation of terminal sequences of the BAC DNA insert to facilitate contig formation by BAC walking.

B-Lymphocytes↗

Cardiovascular effects of nitric oxide in the rostral ventrolateral medulla of rats.

To investigate the cardiovascular role of nitric oxide (NO) in the rostral ventrolateral medulla (RVLM), NOC 18, an NO donor, was microinjected into the RVLM of rats. NOC 18 significantly decreased mean arterial pressure (MAP). Pre-treatment with an NO trapper, carboxy-PTIO, abolished the NOC 18-induced decrease in MAP. Microinjection of L-NAME, an NO synthase inhibitor, increased MAP. L-Arginine reduced MAP and inhibited the pressor response induced by L-NAME. Results suggest that NO acts on the RVLM neurons and plays an important role in cardiovascular regulation.

Animals↗

Pressor and sympathetic responses to excitatory amino acids are not augmented in the ventrolateral medulla of Dahl salt-sensitive rats.

We assessed the pressor and sympathetic responses to microinjection of excitatory amino acids (EAA) into the rostral ventrolateral medulla (RVLM) to see whether the response would be augmented in salt-induced hypertension. Seven-week-old Dahl-Iwai salt-sensitive rats were fed either a high- (8%, n = 10) or a low- (0.3%, n = 12) salt diet for 3 weeks. Then, L-glutamate (2 nmol), N-methyl-D-aspartate (NMDA; ionotropic EAA receptor agonist, 20 pmol) or (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD; metabotropic EAA receptor agonist, 1 nmol] was microinjected into the RVLM of urethane-anesthetized, artifically ventilated rats. The rats fed a high-salt diet showed a significantly (P < 0.001) higher mean arterial pressure (123 +/- 3 mmHg) than those fed a low-salt diet (99 +/- 2 mmHg). We found similar increases in mean arterial pressure and splanchnic sympathetic nerve activity elicited by microinjection of L-glutamate into the RVLM in the high- (33 +/- 2 mmHg and 52 +/- 10%) and low- (35 +/- 3 mmHg and 46 +/- 8%) salt groups. Similarly, pressor and sympathoexcitatory responses to either NMDA or (1S,3R)-ACPD did not differ between the groups. Microinjections of the lower doses of L-glutamate, NMDA and (1S,3R)-ACPD also showed comparable pressor responses between the groups. These results indicate that salt-induced hypertension in Dahl salt-sensitive rats is not associated with enhanced responsiveness of the RVLM to EAA. This is in contrast with our previous findings that pressor and sympathetic responses to EAA are enhanced in spontaneously hypertensive rats.

Analysis of Variance↗

Localization of 16 exons to a 450-kb region involved in the autoimmune polyglandular disease type I (APECED) on human chromosome 21q22.3.

As a step toward identifying the pathogenic genes for autoimmune polyglandular disease type I (APECED) and other disorders mapped to the PFKL locus on chromosome 21q22.3, we have constructed a cosmid/BAC (bacterial artificial chromosome) contig of 450 kb covering markers D21S1460-D21S25-PFKL-D21S154 and performed exon trapping. We isolated 22 distinct exons including 6 exons derived from two known genes (PFKL and EHOC-1). Among 16 novel exons, 2 exons matched with human expressed sequence tags (EST) and 7 exons showed homology at predicted amino acid sequence level with proteins from other species. These 16 exons were mapped back to the cosmid contigs, 12 of which were confirmed for their expression by polymerase chain reaction (PCR) screening of human cDNA libraries of various tissues. These exon sequences and a transcript map will aid for isolation of corresponding genes which will be identified as candidate genes involved in the pathogenesis of disorders mapped to the 21q22.3 region.

Amino Acid Sequence↗

Synthesis and inhibition studies of sulfur-substituted squalene oxide analogues as mechanism-based inhibitors of 2,3-oxidosqualene-lanosterol cyclase.

The synthesis and biological evaluation of three new sulfur-substituted oxidosqualene (OS) analogues (1-3) are presented. In these analogues, C-11, C-15, or C-18 in the OS skeleton was replaced by sulfur. The sulfur position in the OS skeleton was chosen to disrupt one or more key processes involved in cyclization: (a) the folding of the B-ring into a boat conformation, (b) the anti-Markovnikov cyclization leading to the C-ring, or (c) the formation of the D-ring during the lanosterol biosynthesis. Enzyme inhibition kinetics using homogeneous mammalian oxidosqualene cyclases (OSC) were also examined for the previously reported S-19 analogue 4. The four analogues were potent inhibitors of mammalian OSCs (IC50 = 0.05-2.3 microM for pig and rat liver OSC) and fungal cell-free Candida albicans OSC (submicromolar IC50 values). In particular, the S-18 analogue 3 showed the most potent inhibition toward the rat liver enzyme (IC50 = 50 nM) and showed potent, selective inhibition against the fungal enzyme (IC50 = 0.22 nM, 10-fold more potent than the S-19 analogue 4). Thus, 3 is the most potent OSC inhibitor known to date. The Ki values ranged from 0.5 to 4.5 microM for pig OSC, with 3 and 4 showing about 10-fold higher potency for rat liver OSC. Interestingly, the S-18 analogue 3 showed time-dependent irreversible inhibition with homogeneous pig liver OSC (kinact = 0.06 min-1) but not with rat OSC.

Animals↗

Percutaneous transluminal angioplasty attenuates day-night difference in ambulatory blood pressure in renovascular hypertension.

To evaluate whether the circadian rhythm of blood pressure (BP) was altered in renovascular hypertension (RVH), ambulatory BP was monitored using a noninvasive recorder in nine patients with RVH attributable to fibromuscular dysplasia before and after percutaneous transluminal angioplasty (PCTA). The circadian rhythm of BP was assessed by the day-night difference in BP and by the single cosinor method. The day-night difference in BP before PCTA was significantly greater than in age- and sex-matched normotensive subjects (n = 9, P < .01) and patients with essential hypertension (n = 9, P < .05). PCTA decreased significantly the 24-h BP as well as plasma renin activity (P < .01). In the chronogram, the BP reduction after PCTA was evident especially during the day. Accordingly, the day-night difference in BP decreased significantly after PCTA (P < .01). In the cosinor analysis, the mesor and the percent amplitude of BP decreased significantly after PCTA (P < .01). In summary, circadian rhythm of BP was preserved or rather exaggerated in RVH. The stimulated renin angiotensin system in RVH possibly contributes to the altered circadian rhythm of BP primarily by elevating the daytime BP.

Adolescent↗

Ambulatory blood pressure monitoring in patients with essential hypertension treated with a new calcium antagonist, cilnidipine.

Cilnidipine (FRC-8653), a new dihydropyridine calcium antagonist, was given to 14 hospitalized patients with essential hypertension, and 24-hour ambulatory blood pressure (BP) monitoring was performed. Once-daily administration of cilnidipine (5-20 mg) for 1-3 weeks decreased the 24-hour average BP significantly from 149 +/- 4/88 +/- 2 mmHg to 141 +/- 3/82 +/- 2 mmHg without any change in the pulse rate. The decrease in ambulatory BP by cilnidipine was evident during the daytime (156 +/- 4/93 +/- 2 mmHg to 143 +/- 5/84 +/- 2 mmHg, p < 0.01 for systolic BP and p < 0.01 for diastolic BP), while it was mild during nighttime (141 +/- 4/80 +/- 2 mmHg to 133 +/- 4/76 +/- 3 mmHg, p < 0.05 for systolic and ns for diastolic BP). The decrease in the ambulatory BP over the whole day and during the nighttime was significantly correlated with the basal ambulatory BP levels. When the subjects were divided into the high ambulatory BP (n = 7) and low ambulatory BP (n = 7) groups, the BP reduction by cilnidipine was evident throughout 24 hours in the high ambulatory BP group, while it was mild and significant only during daytime in the low ambulatory BP group. In summary, once-daily cilnidipine exerts a sufficient and prolonged reduction of BP without an increase in the pulse rate in patients with hypertension. The potency of cilnidipine to decrease ambulatory BP may depend on the basal ambulatory BP level. Cilnidipine is thus a useful antihypertensive drug that may not cause an excessive decrease in BP or a reflex tachycardia.

Adult↗

Role of eicosanoids in alteration of membrane electrical properties in isolated mesenteric arteries of salt-loaded, Dahl salt-sensitive rats.

1. The role of eicosanoids in altered membrane electrical properties of Dahl salt-sensitive (DS) rats was investigated, by use of conventional microelectrodes technique, in isolated superior mesenteric arteries of DS rats and Dahl salt-resistant (DR) rats fed either a high or low salt diet. 2. The membrane was significantly depolarized in salt-loaded DS rats compared with the other three groups. In addition, the arteries of salt-loaded DS rats exhibited spontaneous electrical activity. 3. Spontaneous electrical activity in salt-loaded DS rats was inhibited by the following: indomethacin, a cyclo-oxygenase inhibitor; ONO-3708, a prostaglandin H2/thromboxane A2 receptor antagonist; OKY-046, a thromboxane A2 synthase inhibitor; nicardipine, a Ca(2+)-channel antagonist and by Ca(2+)-free solution. In addition, spontaneous electrical activity was enhanced by a thromboxane A2 analogue and by prostaglandin H2. Spontaneous electrical activity was unaffected by phentolamine, atropine and tetrodotoxin. 4. Membrane potential in arteries of salt-loaded DS rats was not affected by either indomethacin or ONO-3708. 5. Spontaneous contraction, sensitive to indomethacin, was present, and contractile sensitivity to high potassium solution was enhanced in arteries of salt-loaded DS rats. 6. These findings suggest that eicosanoid action, together with membrane depolarization, may lead to the activation of voltage-dependent Ca(2+)-channels, thereby causing spontaneous electrical activity in mesenteric arteries of salt-loaded DS rats. In addition, tension data suggest that these changes in membrane properties are related to enhanced contractile activities in salt-loaded DS rats. Mechanisms of depolarization remain to be determined.

Animals↗

Enhancement by exogenous and locally generated angiotensin II of purinergic neurotransmission via angiotensin type 1 receptor in the guinea-pig isolated mesenteric artery.

1. Angiotensin II is known to enhance sympathetic neurotransmission in the vasculature by increasing the release of noradrenaline, but little is known about the effect on the co-released transmitter, adenosine 5'-triphosphate (ATP). In the present study we have examined the effect of angiotensin II on the excitatory junction potential (e.j.p.) elicited by repetitive field stimulation in the guinea-pig isolated mesenteric artery, to establish the angiotensin II receptor subtype involved in modulating the release of ATP and the role of the endothelium in converting angiotensin I to angiotensin II. 2. Suramin (300 microM), a P2 purinoceptor antagonist, abolished both the e.j.p.s and depolarizing response to alpha,beta-methylene-ATP, a stable analogue of ATP, without affecting the resting membrane potential and noradrenaline-induced depolarization. 3. Angiotensin II (0.1 microM) affected neither the resting membrane potential nor the amplitude of the first e.j.p., but increased the amplitudes of the subsequent e.j.p.s. This enhancing effect of angiotensin II was abolished by CV-11974 (0.1 microM), an angiotensin II type 1 (AT1) receptor antagonist, but unaffected by PD 123319 (1 microM), an angiotensin II type 2 (AT2) receptor antagonist, or CGP 42112A (1 microM), AT2 receptor ligand. 4. Angiotensin I (0.1 microM) exerted a similar effect on e.j.p.s to that of angiotensin II. CV-11974 (0.1 microM) or temocaprilat (10 microM), an angiotensin converting enzyme (ACE) inhibitor, abolished the effect of angiotensin I. Removal of the endothelium did not alter the action of angiotensin I. 5. The results of the present study indicate that the release of ATP from sympathetic nerves innervating the guinea-pig isolated mesenteric artery, as determined from the magnitude of the e.j.p., can be enhanced by angiotensin II via activation of prejunctional AT1 receptors. Qualitatively similar effects were observed with angiotensin I, which appears to be converted into angiotensin II by a subendothelial process.

Adenosine Triphosphate↗

Association between hyperinsulinemia and intima-media thickness of the carotid artery in normotensive men.

OBJECTIVES: To determine whether hyperinsulinemia is associated with early atherosclerosis in normotensive men of a work site population. DESIGN AND METHODS: Six hundred and seventeen subjects were screened from 8678 male transport workers for the further examination of cardiovascular disease and diabetes. Subjects aged less than 40 years, those with hypertension or diabetes, or both, and those being administered medications for hyperlipidemia were excluded. Finally, 164 normotensive, nondiabetic subjects were enrolled. The intima-media thickness (IMT) was measured by B-mode ultrasonography with a 7.5 MHz probe. Electrocardiography, a 75 g oral glucose-tolerance test (OGTT) and blood chemistry measurements were also performed. The sum of insulin values (sigmaIRI) and the ratio of the sum of insulin values to blood glucose levels (sigmaIRI/sigmaBG) in the 75 g OGTT were used as markers of hyperinsulinemia. RESULTS: The mean age of the subjects was 52 +/- 5 years (mean +/- SD). In a univariate analysis, IMT was associated with age, systolic blood pressure, body mass index, sigmaIRI, and sigmaIRI/sigmaBG. Multivariate analysis showed that age, total cholesterol, and sigmaIRI (or sigmaIRI/sigmaBG) were independent risk factors for IMT. CONCLUSIONS: These results suggest that, in addition to age and total cholesterol, hyperinsulinemia as assessed by an OGTT is associated with early atherosclerosis in normotensive, nondiabetic men of a work site population.

Arteriosclerosis↗

Intima-media thickness of the carotid artery in hypertensive subjects and hypertrophic cardiomyopathy patients.

While hypertension is known to cause left ventricular and vascular hypertrophy, the relationship between alterations of vascular and cardiac structures in patients with hypertrophic cardiomyopathy has not been fully clarified. We measured intima-media thickness of carotid arteries by ultrasonography in patients with hypertrophic cardiomyopathy (n = 16), normotensive subjects (n = 358), and hypertensive subjects (n = 386) in a cohort of 7940 male employees of a bus company. Our object was to determine whether vascular alteration occurs in hypertrophic cardiomyopathy similarly as in hypertension. Hypertrophic cardiomyopathy (wall thickness > or = 15 mm; asymmetrical hypertrophy without hypertension) was screened with family history and electrocardiography followed by echocardiography. The intima-media thickness in patients with hypertrophic cardiomyopathy (mean, 0.61 mm) did not differ from that of normotensive subjects (0.60 mm) but was significantly less than that of hypertensive subjects with left ventricular hypertrophy (wall thickness > or = 14 mm; n = 22; 0.73 mm). In a scatterplot of intima-media thickness versus interventricular septal thickness, these two parameters were significantly correlated in normotensives and hypertensives. The patients with hypertrophic cardiomyopathy distributed outside the 95% confidence range of the normotensive and hypertensive subjects. In summary, the increase in intima-media thickness of the carotid artery paralleled left ventricular hypertrophy in normotensive and hypertensive subjects. Patients with hypertrophic cardiomyopathy had a normal intima-media thickness regardless of the hypertrophied left ventricle. Thus, information on intima-media thickness may be useful in differentiating hypertensive left ventricular hypertrophy from hypertrophic cardiomyopathy.

Cardiomyopathy, Hypertrophic↗

Aortoiliac occlusion associated with the lupus anticoagulant. Report of two cases.

Aortoiliac occlusion due to atherosclerosis is known to occur in elderly people. Two unique cases are documented here in which aortoiliac occlusion was observed in young men. These patients had no identifiable risk factors for developing atherosclerotic thrombosis except for the lupus anticoagulant, an immunoglobulin associated with thromboembolic episodes. Although previously the lupus anticoagulant has been reported to cause thrombosis only in relatively small-sized arteries or veins, it may also be associated with aortoiliac atheromatous occlusion in young men.

Adult↗

Ambulatory blood pressure monitoring in diagnosing a pheochromocytoma of the urinary bladder. A case report.

A patient is presented in whom the preoperative diagnosis of an intravesical pheochromocytoma was facilitated by noninvasive ambulatory blood pressure monitoring. A fifty-two-year-old Japanese man suffered headache and palpitation after micturition. Cystoscopy revealed an intravesical tumor. To investigate whether his symptoms were associated with an elevation of blood pressure, the authors monitored his ambulatory blood pressure automatically for twenty-four hours. The patient was also instructed to activate the recording manually upon the onset of symptoms. As a result, elevations of blood pressure were apparent following micturition. The twenty-four-hour urinary excretion of norepinephrine was elevated on the day of the blood pressure monitoring. Pheochromocytoma was suspected and was confirmed by histopathologic studies following the operation. Thus, ambulatory blood pressure monitoring may be useful in detecting the transient hypertension induced by micturition, which can provide preoperative evidence of pheochromocytoma of the urinary bladder.

Blood Pressure Monitoring, Ambulatory↗

Adsorption of inhalational anesthetics and hydrochlorofluorocarbons on activated carbons as a biological model.

Chlorofluorocarbon (CFC) replacements have recently been used for their lower stability and because they have carbon-hydrogen bonds, which means that their atmospheric lifetime is expected to be much shorter than those of CFCs. The adsorption properties of 1,1,2-trichloro-1,2,2-trifluoroethane (CFC113) and its replacement compounds, 1,1-dichloro-2,2,2-trifluoroethane (HCFC123), 1,1-dichloro-1-fluoroethane (HCFC141b), and 1,1-dichloro-1,2,2,3,3-pentafluoropropane (HCFC255ca) on four kinds of activated carbons were investigated. The amount of CFC and HCFCs adsorbed on the activated carbon was concluded to depend upon the number of chloride and carbon atoms in their molecules. The adsorption isotherms of inhalational anesthetics (halothane, chloroform, enflurane, isoflurane, and methoxyflurane) on the activated carbon were measured to evaluate the action mechanism of inhalational anesthesia. The adsorption isotherms of CFC, HCFC, and the inhalational anesthetics were fitted to the Freundlich equation. The Freundlich constant N was well correlated with the minimum alveolar concentration (MAC) of the inhalational anesthetic: 1 MAC means that 50% of the patients will not move during a surgical operation. The adsorption mechanism of inhalational anesthetics on the surface of the activated carbon is concluded to be similar to the adsorption mechanism on a nerve cell. The anesthesia of CFC replacements can be estimated by the Freundlich constant N of the adsorption isotherms.

Adsorption↗

Ultrasonographic assessment of regional differences in atherosclerotic lesions in patients with hypertension, diabetes mellitus, or both.

We evaluated risk factors involved in regional differences in atherosclerotic lesions in patients with hypertension, diabetes mellitus, or both. Using ultrasonography, we examined the brachial, common carotid, and common femoral arteries in 65 hospitalized Japanese patients (15 controls, 18 patients with hypertension, 16 with diabetes mellitus, and 16 with both hypertension and diabetes mellitus). They ranged in age from 39 to 81 yr, mean 60.3 yr. The thickness of the intima-media complex of the far wall was measured, and the severity of atherosclerotic plaques was graded according to maximal lumen stenosis. The intima-media thickness in the carotid and femoral arteries was significantly greater in the hypertensive patients and the hypertensive patients with diabetes than in the controls. Severity of plaque was greater in the hypertensive patients with diabetes than in the controls. Plaque grades were higher in the carotid and femoral arteries than in the brachial artery. Multiple regression analysis revealed that age and mean blood pressure were strongly associated with the intima-media thickness in all three arteries. In the femoral artery, cigarette smoking and hyperglycemia also significantly correlated with the intima-media thickness. Plaque grades increased with age in the carotid and brachial arteries, while in the femoral artery the grade increased with cigarette smoking and serum cholesterol concentration. These findings suggest that the extent of atherosclerosis and its underlying risk factors differ among arterial sites. In addition, risk factors may partly differ according to the stage of atherosclerosis. To prevent or reverse atherosclerosis, the above differences should be taken into account.

Adult↗