Biomedical subjects

M Fujishima

Publications and source records attributed to M Fujishima.

At least 73 records · Page 4Linked to original sources

PubMed2000

Natural history of ampullary adenoma in familial adenomatous polyposis: reconfirmation of benign nature during extended surveillance.

OBJECTIVE: Surgical or endoscopic papillectomy may be one of the therapeutic strategies for patients with familial adenomatous polyposis (FAP). To determine whether prophylactic papillectomy is necessary for FAP, we investigated the natural history of the ampullary adenoma in FAP. METHODS: Eighteen subjects with FAP were surveyed by duodenoscopy with biopsy for >10 yr. Endoscopic appearance, histological findings, and immunohistochemical stainings for Ki-67 of ampulla were compared between initial and final endoscopic examinations. RESULTS: The endoscopic grade in the ampulla remained unchanged in 16 subjects, whereas in two subjects an increase in the endoscopic grade was noted. In two subjects adenoma developed from an endoscopically and histologically normal ampulla. The histological grade of dysplasia increased in three of 12 subjects who initially had adenoma. The labeling index for Ki-67 was not different between initial and final examinations. CONCLUSIONS: These data suggest that most ampullary adenoma of patients with FAP is static and that aggressive endoscopic or surgical removal is unnecessary for the adenoma.

Adenoma↗

PubMed2000

Central effects of leptin on cardiovascular and neurohormonal responses in conscious rabbits.

We determined the cardiovascular and neurohormonal responses to intracerebroventricular injection of leptin in conscious rabbits. Intracerebroventricular injection of leptin elicited dose-related increases in mean arterial pressure and renal sympathetic nerve activity while producing no consistent, significant increases in heart rate. Peak values of mean arterial pressure and renal sympathetic nerve activity induced by intracerebroventricular injection of 50 microgram of leptin (+17.3 +/- 1.2 mmHg and +47.9 +/- 12.0%) were obtained at 10 and 20 min after injection, respectively. Plasma catecholamine concentrations significantly increased at 60 min after intracerebroventricular injection of leptin (control vs. 60 min; epinephrine: 33 +/- 12 vs. 97 +/- 27 pg/ml, P < 0.05; norepinephrine: 298 +/- 39 vs. 503 +/- 86 pg/ml, P < 0.05). Intracerebroventricular injection of leptin also caused significant increases in plasma vasopressin and glucose levels. However, pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion blocking agent, abolished these cardiovascular and neurohormonal responses. On the other hand, intravenous injection of the same dose of leptin (50 microgram) as used in the intracerebroventricular experiment failed to cause any cardiovascular and renal sympathetic nerve responses. These results suggest that intracerebroventricular leptin acts in the central nervous system and activates sympathoadrenal outflow, resulting in increases in arterial pressure and plasma glucose levels in conscious rabbits.

Animals↗

PubMed2000

Sympathetic control of arterial membrane potential by ATP-sensitive K(+)-channels.

Stimulation of perivascular nerve terminals leads to a release of various neurotransmitters such as norepinephrine, epinephrine, acetylcholine, nitric oxide, and calcitonin gene-related peptide (CGRP). Because some of these substances have been shown to cause smooth muscle hyperpolarization by direct or endothelium-dependent mechanisms, we hypothesized that the liberation of 1 or more of these transmitters may lead to neurogenic hyperpolarization in arterial muscle cells. The present study was designed to determine the presence or absence of neurogenic hyperpolarization and, if present, its underlying mechanisms in isolated rat mesenteric resistance arteries, through the use of conventional microelectrode techniques. The experiments were performed under the combined blockade of alpha-adrenoceptors and purinoceptors with phentolamine and suramin to eliminate depolarizing responses to nerve stimulation. Under these conditions, perivascular nerve stimulation (5 Hz, 30 seconds) evoked smooth muscle hyperpolarization (-3.3+/-0.3 mV, n=15), which was abolished by tetrodotoxin, indicating the neurogenic origin of the response. This neurogenic hyperpolarization was resistant to atropine, nitro-L-arginine, or CGRP8-37, a CGRP antagonist, but was abolished by guanethidine and beta-blocker propranolol. This hyperpolarization was also abolished by glibenclamide, an ATP-sensitive K(+) channel (K(ATP)) blocker, but was unaffected by apamin, a Ca(2+)-activated K(+) channel blocker. In separate experiments, exogenous norepinephrine caused glibenclamide-sensitive hyperpolarization in the presence of phentolamine. On the other hand, norepinephrine-induced depolarization in the absence of phentolamine was enhanced by propranolol. These findings suggest that neurally released catecholamines cause membrane hyperpolarization through the activation of K(ATP) by beta-adrenoceptors. Such hyperpolarization may play an important role in the control of arterial membrane potential by opposing alpha-adrenergic depolarization.

Adenosine Triphosphate↗

PubMed2000

Renin-angiotensin system blockade improves endothelial dysfunction in hypertension.

Angiotensin-converting enzyme (ACE) inhibitor improves the impaired hyperpolarization and relaxation to acetylcholine (ACh) via endothelium-derived hyperpolarizing factor (EDHF) in arteries of spontaneously hypertensive rats (SHR). We tested whether the angiotensin type 1 (AT(1)) receptor antagonist also improves EDHF-mediated responses and whether the combined AT(1) receptor blockade and ACE inhibition exert any additional effects. SHR were treated with either AT(1) receptor antagonist TCV-116 (5 mg. kg(-1). d(-1)) (SHR-T), enalapril (40 mg. kg(-1). d(-1)) (SHR-E), or their combination (SHR-T&E) from 8 to 11 months of age. Age-matched, untreated SHR (SHR-C) and Wistar Kyoto (WKY) rats served as controls (n=8 to 12 in each group). Three treatments lowered blood pressure comparably. EDHF-mediated hyperpolarization to ACh in mesenteric arteries in the absence or presence of norepinephrine was significantly improved in all treated SHR. In addition, the hyperpolarization in the presence of norepinephrine was significantly greater in SHR-T&E than in SHR-E (ACh 10(-5) mol/L with norepinephrine: SHR-C -7; SHR-T -19; SHR-E -15; SHR-T&E -22; WKY -14 mV). EDHF-mediated relaxation, assessed in the presence of indomethacin and N:(G)-nitro-L-arginine, was markedly improved in all treated SHR. Hyperpolarization and relaxation to levcromakalim, a direct opener of ATP-sensitive K(+)-channel, were similar in all groups. These findings suggest that AT(1) receptor antagonists are as effective as ACE inhibitors in improving EDHF-mediated responses in SHR. The beneficial effects of the combined AT(1) receptor blockade and ACE inhibition appears to be for the most part similar to those of each intervention.

Acetylcholine↗

PubMed2000

Angiotensin-converting enzyme inhibitor prevents age-related endothelial dysfunction.

Vascular relaxation via endothelium-derived hyperpolarizing factor (EDHF) declines in association with aging and also with hypertension, and antihypertensive treatment improves the endothelial dysfunction connected with hypertension. We tested whether the angiotensin-converting enzyme inhibitor improves EDHF-mediated responses in normotensive rats, with special reference to the age-related process. Wistar-Kyoto rats (WKY) were treated with either 20 mg. kg(-1). d(-1) enalapril (WKY-E group) or a combination of 50 mg. kg(-1). d(-1) hydralazine and 7.5 mg. kg(-1). d(-1) hydrochlorothiazide (WKY-H group) from 9 to 12 months of age. Twelve-month-old WKY (WKY-O) and 3-month-old WKY (WKY-Y) served as controls (n=6 to 10 in each group). The 2 treatments lowered systolic blood pressure comparably. EDHF-mediated hyperpolarization to acetylcholine (ACh) in mesenteric arteries was significantly improved in WKY-E, but not in WKY-H, compared with WKY-O, and the hyperpolarization in WKY-E was comparable to that in WKY-Y (hyperpolarization to 10(-)(5) mol/L ACh in the presence of norepinephrine: WKY-O, -14+/-2 mV; WKY-E, -22+/-3 mV; WKY-H, -15+/-2 mV; and WKY-Y, -28+/-0 mV). EDHF-mediated relaxation, as assessed by relaxation to ACh in norepinephrine-precontracted rings in the presence of indomethacin and NO synthase inhibitor, was also significantly improved in WKY-E, but not in WKY-H, to a level comparable to that in WKY-Y (maximum relaxation: WKY-O, 45+/-6%; WKY-E, 63+/-8%; WKY-H, 43+/-4%; and WKY-Y, 72+/-4%). Hyperpolarization and relaxation to levcromakalim, an ATP-sensitive K(+) channel opener, were similar in all groups. These findings suggest that the angiotensin-converting enzyme inhibitor prevents the age-related decline in EDHF-mediated hyperpolarization and relaxation in normotensive rats, presumably through an inhibition of the renin-angiotensin system.

Acetylcholine↗

PubMed2000

Ovariectomy exacerbates and estrogen replacement attenuates photothrombotic focal ischemic brain injury in rats.

BACKGROUND AND PURPOSE: We previously reported the infarct volumes in female spontaneously hypertensive rats (SHR) to be significantly smaller than those in male SHR. The purpose of the present study was to determine whether estrogen is responsible for the sex difference in ischemic vulnerability in SHR. METHODS: In experiment 1, 1 week (short-term) or 4 weeks (long-term) after the ovariectomy (OVX), female SHR (5 months old) were randomly subjected to photothrombotic occlusion of the middle cerebral artery, and the infarct volumes were determined. In experiment 2, the rats were randomly assigned to 3 groups (ie, the sham-ovariectomized, ovariectomized, and estrogen replacement groups). In the replacement group, estradiol valerate (200 microgram/kg) was subcutaneously injected once a week after the OVX. Four weeks after the OVX or sham-OVX, all rats were subjected to middle cerebral artery occlusion. Changes in regional cerebral blood flow were determined by laser-Doppler flowmetry. RESULTS: In experiment 1, the infarct volume produced 1 week after the OVX was not different from that of the sham-ovariectomized group. In contrast, the infarct volume produced 4 weeks after the OVX was significantly larger than that of the sham-ovariectomized group (82.4+/-11.6 versus 54.5+/-16.0 mm(3), P=0.0058). In experiment 2, estradiol replacement after the OVX was observed to attenuate the infarct volume compared with the ovariectomized group (55.6+/-18.8 versus 78.5+/-21.0 mm(3), P=0.0321). The degrees of regional cerebral blood flow reduction did not differ among the sham-ovariectomized, ovariectomized, and estrogen replacement groups. CONCLUSIONS: Chronic estrogen depletion was thus found to increase the infarct size, which was attenuated by estradiol replacement. These findings indicate that estrogen contributes to the sex difference in ischemic vulnerability and that endogenous estrogen also has a neuroprotective effect against ischemic brain damage.

Animals↗

PubMed2000

Role of phosphatidylinositol 3-kinase in acetylcholine-induced dilatation of rat basilar artery.

BACKGROUND AND PURPOSE: We tested the hypothesis that activation of phosphatidylinositol (PI) 3-kinase is involved in dilator responses of the basilar artery to acetylcholine in vivo. METHODS: Responses of the basilar artery were measured by the cranial window technique in anesthetized rats. To examine the role of PI 3-kinase in acetylcholine-induced calcium signaling, we measured intracellular free calcium concentration ([Ca(2+)](i)) of cultured rat basilar arterial endothelial cells using a fluorescent calcium indicator, indo 1. RESULTS: -Topical application of acetylcholine (10(-6), 10(-5.5), and 10(-5) mol/L) increased the diameter of the basilar artery by 8+/-1%, 14+/-2%, and 24+/-3%, respectively. An inhibitor of PI 3-kinase, wortmannin (10(-8) mol/L), did not change the baseline diameter of the artery. In the presence of wortmannin, acetylcholine (10(-6), 10(-5.5), and 10(-5) mol/L) dilated the artery only by 3+/-2%, 6+/-2%, and 12+/-2%, respectively. Thus, wortmannin attenuated acetylcholine-induced dilatation of the basilar artery (P<0.05 versus control). Wortmannin had no effect on dilatation of the artery in response to a nitric oxide donor, sodium nitroprusside. LY294002, another inhibitor of PI 3-kinase, also inhibited dilator response of the basilar artery to acetylcholine. Acetylcholine produced an increase in [Ca(2+)](i) of the endothelial cells. Genistein, an inhibitor of tyrosine kinase, markedly attenuated acetylcholine-induced calcium influx to the cells; however, wortmannin had no effect on acetylcholine-induced calcium changes. CONCLUSIONS: These results suggest that acetylcholine-induced dilatation of the basilar artery is mediated, at least in part, by activation of PI 3-kinase in vivo. Acetylcholine-induced [Ca(2+)](i) changes of the endothelial cells may not be mediated by activation of the kinase. PI 3-kinase as well as [Ca(2+)](i) may play an important role in the acetylcholine-induced nitric oxide production of the basilar arterial endothelial cells.

Acetylcholine↗

PubMed2000

Incidence and risk factors for subtypes of cerebral infarction in a general population: the Hisayama study.

BACKGROUND AND PURPOSE: We estimated the incidence of first-ever cerebral infarction in regard to its subtypes and analyzed their risk factors separately in a community-based prospective cohort study in Japan. METHODS: Stroke-free subjects (n=1621) aged >/=40 years were followed up for 32 years from 1961. During this period, 298 cerebral infarctions occurred and were divided into 167 lacunar, 62 atherothrombotic, 56 cardioembolic, and 13 undetermined subtypes of infarction on the basis of clinical information including brain imaging and autopsy findings. RESULTS: The age-adjusted incidence of lacunar infarction (3.8 per 1000 person-years for men and 2.0 for women) was higher than that of atherothrombotic infarction (1.2, 0. 7) and cardioembolic infarction (1.3, 0.5) in both sexes. Time-dependent Cox's proportional hazard analysis revealed systolic blood pressure as well as age to be independent risk factors for all subtypes of cerebral infarction except for cardioembolic infarction in men. Additionally, ST depression on ECG, glucose intolerance, and smoking in men and left ventricular hypertrophy on ECG and body mass index in women remained significant risk factors for lacunar infarction. ST depression was also significantly related to events of atherothrombotic infarction in women. The risk of atrial fibrillation for cardioembolic infarction was outstandingly high in both sexes, and left ventricular hypertrophy and lower total cholesterol were additional risk factors for cardioembolic infarction in women. CONCLUSIONS: In this Japanese population, lacunar infarction was the most common subtype of cerebral infarction and had a greater variety of risk factors, including not only hypertension but also ECG abnormalities, diabetes, obesity, and smoking, than did atherothrombotic infarction or cardioembolic infarction.

Adult↗

PubMed2000

Isolated dissection of the celiac artery--a case report.

Isolated arterial dissection, which occurs with the absence of aortic dissection, has been reported in carotid and renal arteries but rarely in visceral arteries. A case of isolated celiac artery dissection is reported here. A healthy 58-year-old man experienced sudden upper abdominal pain, which continued for several days. A body computed tomogram (CT) showed a multiple low-density wedge-shaped area in the spleen, which was diagnosed as splenic infarction, and an aneurysm with thrombus in the celiac artery. A selective angiogram showed dilatation of the celiac artery with wall irregularity, and proximal occlusion of the hepatic artery. The distal hepatic artery was fed by collateral arteries from the superior mesenteric artery. Splenic infarction was probably due to the embolism from the thrombus in the dissected celiac artery. The absence of other vascular lesions and causes or risks for the arterial dissection would suggest the occurrence of spontaneous dissection. The dissection of visceral arteries should be considered in diagnosing acute abdominal pain.

Abdominal Pain↗

PubMed2000

Crohn's disease of aphthous type: serial changes in intestinal lesions.

In Crohn's disease (CD), aphthous lesions are regarded as possible precursors of typical intestinal involvement. To determine the natural course of intestinal lesions in CD of aphthous type, the clinical course of 10 patients was retrospectively investigated during a period ranging from 6 to 16 years after diagnosis. The criterion for inclusion was confirmed aphthous lesions within the gastrointestinal tract with histologically verified epithelioid granuloma. The degrees of aphthous lesions in the small intestine and the colon were graded by small bowel radiography, barium enema examination and colonoscopy. Five patients developed typical CD during a period ranging from 0.8-3.3 years. The site of involvement was the ileum in three patients, the colon in one patient and both the ileum and the colon in one patient. Typical small intestinal CD occurred in four of seven patients with marked aphthous lesions of the small intestine, whereas colonic CD occurred in two of eight patients with such aphthous lesions of the colon. These findings suggest that CD of aphthous type is not necessarily a precursor of clinically overt disease. This may especially be the case for colonic aphthous lesions.

Adolescent↗

PubMed2000

Left ventricular mass predicted by a single reading of ambulatory blood pressure in essential hypertension.

The spectral power of heart rate variability has been shown to be negatively correlated with left ventricular mass (LVM), suggesting the contribution of left ventricular hypertrophy to autonomic dysfunction in essential hypertension. However, a simultaneous assessment of autonomic function and ambulatory blood pressure in relation to LVM has not been carried out. The objective of the present study was to elucidate the synergistic effects of ambulatory blood pressure and autonomic nerve activity on the heart. We enrolled 25 ambulant patients with untreated essential hypertension (9 men and 16 women; mean age 50.6 +/- 2.0 years). The ambulatory blood pressure and heart rate variability were simultaneously monitored every 30 min for 24 h. The spectral power of high-frequency (HF: 0.15 to 0.4 Hz) and low-frequency (LF: 0.05 to 0.15 Hz) bands were measured, and the ratio of LF to HF (LF/HF) was calculated. LF/HF and HF were used as indexes of sympathetic and parasympathetic activities, respectively. LVM was determined by echocardiography. Both the average daytime and nighttime systolic ambulatory blood pressures significantly correlated with the LVM index (r= 0.644, p< 0.001; and r= 0.428, p< 0.05; respectively), although there was no such correlation with the clinic blood pressures. In contrast, a single reading of ambulatory systolic blood pressure measured when LF/HF reached a maximum value was significantly correlated with the LVM index independently of age and sex (partial r= 0.484, p< 0.05). These results suggest that the ambulatory systolic blood pressure during increases in the activity of the sympathetic nervous system is able to infer LVM in essential hypertension.

Blood Pressure↗

PubMed2000

Central infusion of L-arginine or superoxide dismutase does not alter arterial pressure in SHR.

Cardiovascular responses to L-arginine and nitric oxide (NO) are augmented in the rostral ventrolateral medulla (RVLM) of spontaneously hypertensive rats (SHR), and the intravenous injection of superoxide dismutase (SOD) mimetic decreases the arterial pressure in these rats. In the present study, we examined whether the chronic central infusion of L-arginine or an SOD mimetic would reduce the blood pressure of SHR and alter responses to an NOS inhibitor or an NO donor in the RVLM. For this purpose, we administered L-arginine (SHR-Arg: 13.2 micromol/day, n=6), a stable membrane-permeable SOD mimetic, 4-hydroxy-2, 2,6,6-tetramethyl piperidine-1-oxyl (tempol) (SHR-Temp: 13.2 micromol/day, n=6), or vehicle (SHR-C: n=6) into the lateral ventricle of 12-week-old SHR for 2 weeks. When the rats reached 14 weeks of age, N(G)-nitro-L-arginine methyl ester (L-NAME: 10 nmol/50 nl) or NOC 18 (NO donor: 10 nmol/50 nl) was microinjected into the unilateral RVLM. Blood pressure did not decrease in any of the treatment groups (SHR-Arg: 209+/-4 mmHg, SHR-Temp: 210+/-6 mmHg, SHR-C: 197+/-6 mmHg). The microinjection of L-NAME into the RVLM induced a significant increase in the mean arterial pressure (MAP) (SHR-Arg: 10-4 mmHg, SHR-Temp: 12+/-4 mmHg, SHR-C: 11+/-3 mmHg), and the increases in MAP did not differ among the groups. The micro-injection of NOC 18 reduced MAP (SHR-Arg: -12+/-2 mmHg, SHR-Temp: -15+/-3 mmHg, SHR-C: -13+/-3 mmHg), and the depressor responses were comparable among groups. These results do not support the hypothesis that chronic L-arginine deficiency or the enhanced degeneration of NO by superoxide radicals in the central nervous system contributes to the maintenance of arterial pressure in SHR.

Animals↗

PubMed2000

Cardiovascular responses to glutamate and angiotensin II in ventrolateral medulla of hypertension induced by chronic inhibition of nitric oxide.

It has been suggested that nitric oxide (NO) influences the actions of L-glutamate and angiotensin II in the brain. In the present study, we examined whether cardiovascular responses to L-glutamate and angiotensin II would be altered in the rostral ventrolateral medulla (RVLM) of rats treated with an NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). Wistar rats were treated with either L-NAME (100 mg/kg/day, n=9) or vehicle (n=8) for 4 weeks. L-glutamate (2 nmol/50 nl) or angiotensin 11 (100 pmol) was then microinjected into unilateral RVLM of anesthetized rats. Upon completion of the experiments, angiotensin-converting enzyme (ACE) activity of the brain stem was measured. The systolic blood pressure after 4 weeks of the treatment was significantly higher in the L-NAME group (203+/-8 mmHg) than in the control group (142+/-3 mmHg, p< 0.01). The pressor response to L-glutamate microinjected into the RVLM was significantly greater in the L-NAME group (31+/-2 mmHg) than in the control group (24+/-1 mmHg, p< 0.01). Similarly, angiotensin II showed a greater pressor response in the L-NAME group. ACE activity of the brain stem did not differ between the groups. In conclusion, NO may have an inhibitory influence on the actions of L-glutamate and angiotensin II in the RVLM.

Angiotensin II↗

PubMed2000

Effects of monosodium glutamate-induced obesity in spontaneously hypertensive rats vs. Wistar Kyoto rats: serum leptin and blood flow to brown adipose tissue.

We compared the effects of hypothalamic obesity induced by neonatal monosodium glutamate (MSG) treatment between spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Newborn WKY and SHR were injected intraperitoneally with 4 mg/kg body weight of MSG daily for 5 days. At 6 months of age, the obesity of SHR was more advanced than that of WKY, but at 14 months of age the severity of obesity was similar between the two strains. Hypertriglyceridemia was enhanced in MSG-treated SHR as compared with MSG-treated WKY. Systolic blood pressure measured by the tail-cuff method was consistently lower in MSG-treated SHR than in control SHR, whereas blood pressure was not affected by neonatal MSG treatment in WKY. Food restriction reduced body weight more in control SHR than in control WKY, with the former also showing enhanced ketogenesis. Neonatal MSG treatment abolished the accelerated reduction of body weight in SHR. Serum leptin concentration was markedly increased in MSG-treated obese rats, though no differences were seen between WKY and SHR in the control or MSG-treated groups. Serum leptin was closely correlated with both Lee obese index and mesenteric fat weight over the strain. Blood flow in interscapular brown adipose tissue (BAT) measured by Laser Doppler flowmetry was significantly increased in response to beta3-adrenoceptor agonist BRL26830A in both the control and MSG-treated rats. However, the response of blood flow was not affected by MSG treatment or strain difference. The present study demonstrated some strain differences in response to neonatal MSG treatment between WKY and SHR. These differences could not be explained by the difference in serum leptin level or beta3-adrenergic reactivity in BAT.

Adipose Tissue, Brown↗

PubMed2000

Voltage-dependent Ca2+ channels in resistance arteries from Dahl salt-sensitive rats.

To determine whether chronic salt-loading would alter voltage-dependent Ca2+ channels in resistance arteries of Dahl salt-sensitive rats, whole-cell voltage-clamp experiments were performed on single cells that were isolated from small mesenteric arteries. Dahl salt-sensitive rats were fed either an 8% NaCl diet (high-NaCl group) or a 0.3% NaCl diet (low-NaCl group) from the age of 6 or 7 weeks. After 4 to 5 weeks, systolic blood pressure was significantly higher in the high-NaCl group than in the low-NaCl group. In the high-NaCl group, the threshold potential for Ca2+ channel current was more negative and the current amplitude that was normalized by cell capacitance was higher at negative command potentials (-40 mV to -20 mV), as compared with the low-NaCl group. When the current was separated into fast transient current and slow sustained (L-type) current, the alteration in the high-NaCl group was attributable to the change in L-type current. The steady-state inactivation curve was not different between the high-NaCl and low-NaCl groups. In conclusion, L-type Ca2+ channels in resistance arteries of Dahl salt-sensitive rats became more available for opening near the resting potential after dietary salt-loading.

Animals↗

PubMed2000

Multilocular pyogenic hepatic abscess complicating ascaris lumbricoides infestation.

A 74-year-old man was admitted to our hospital with frequent right flank pain. The multiple multilocular hepatic abscesses were revealed by computed tomography. Radiographs following a barium meal showed a linear filling defect in the ileum consistent with ascariasis. One day after treatment with pyrantel pamoate, an Ascaris was passed in the stool. The pyogenic hepatic abscesses gradually healed with both antibiotics and continuous drainage. After 2 months, he was discharged. In this case, the pyogenic hepatic abscesses were thus considered to have been caused by an inflammation which spread through the portal vein.

Aged↗

PubMed2000

Deep white matter lesions on MRI, and not silent brain infarcts are related to headache and dizziness of non-specific cause in non-stroke Japanese subjects.

OBJECTIVE: Silent or asymptomatic cerebrovascular disease is believed to be an important risk factor for symptomatic stroke and vascular dementia. Although non-specific complaints such as mild to moderate headache and/or dizziness may also be caused by silent stroke, which remains a topic of controversy. METHODS: To investigate the relationship between silent brain infarcts and non-specific complaints, we assessed findings on magnetic resonance images using a common protocol in the following three groups of subjects; Group 1:78 subjects with non-specific complaints, Group 2:47 subjects with vascular risk factors, and Group 3:75 normal subjects without any subjective complaints or vascular risk factors. In addition to silent stroke, deep white matter lesions on MRI were also evaluated. All subjects were recruited from 12 institutes of the study group located at various parts of Japan. RESULTS: Silent brain infarcts were demonstrated in 44%, 43%, and 20% of subjects in Groups 1, 2, and 3, respectively. In Group 1, the average number of infarcts per individual who had silent brain infarction was 1.8, which was significantly fewer than 3.8 in Group 2 or 3.5 in Group 3 (p<0.0167). White matter lesions were found in 68%, 49%, and 11% in Groups 1, 2, and 3, respectively, indicating that non-specific complaints are more closely related to deep white matter lesions than to silent infarct lesions. Such white matter lesions were found more frequently in subjects with depressive state than in non-depressed subjects (67% vs. 39%, p=0.0155). CONCLUSION: The present results suggest that deep white matter lesions, rather than silent brain infarcts, appear to be important in producing headache and/or dizziness of non-specific cause and also to be related to the depressive state.

Aged↗

PubMed2000

Natriuretic effect of barnidipine, a long-acting dihydropyridine calcium channel blocker, in patients with essential hypertension.

OBJECTIVE: To evaluate the effect of barnidipine hydrochloride, a long-acting dihydropyridine calcium channel blocker on urinary sodium excretion in patients with essential hypertension. PATIENTS: Twelve patients (2 males, 10 females) with mild to moderate essential hypertension. METHODS: A single-blinded study. After the control (placebo) period, 10 to 15 mg barnidipine hydrochloride was administered for 7 days, followed by a post-treatment (placebo) period. Daily changes in blood pressure, urinary volume, and urinary electrolyte excretions were evaluated. Plasma levels of atrial natriuretic peptide (ANP) and aldosterone were also determined in each period. Daily sodium intake was kept at 120 mEq. RESULTS: Blood pressure decreased from 161 +/- 4/92 +/- 2 mmHg to 146 +/- 4/85 +/- 2 mmHg (p<0.05) after 7-day-treatment with barnidipine. Barnidipine significantly increased urinary sodium excretion; the change was evident on the first day of administration (control period 41 +/- 3 mEq/day, and first day 59 +/- 3 mEq/day, p < 0.05). Drug discontinuation transiently decreased sodium excretion to 35 +/- 3 mEq/day. Cumulative sodium balance after 7-day-treatment reached 47 +/- 19 mEq. Urine volume, potassium excretion, and creatinine excretion did not change during the treatment period. The plasma levels of ANP tended to increase, but those of aldosterone did not change with barnidipine. CONCLUSION: Barnidipine administration for a week decreased the blood pressure and made the sodium balance negative by increasing the urinary sodium excretion in patients with essential hypertension. The natriuretic effect of this drug could contribute at least in part to its antihypertensive effect.

Adult↗