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Biomedical subjects

S Fukudo

Publications and source records attributed to S Fukudo.

31 records · Page 2Linked to original sources
PubMed1997

Brain-gut induction of heat shock protein (HSP) 70 mRNA by psychophysiological stress in rats.

Restraint water-immersion stress-induced expression of heat shock protein (HSP)70 mRNA in the cerebral cortex and stomach of rats was evaluated by Northern blotting. Cerebral and gastric HSP70 mRNA significantly increased in the 6 h-stressed rats and the amount of mRNA measured as optical densities was highest in the 12 h-stressed rats. These data confirmed our previous observations and suggest that families of HSPs play a salient cytoprotective role in stress-vulnerable organs.

Animals↗
PubMed1995

Psychophysiological stress induces heat shock cognate protein (HSC) 70 mRNA in the cerebral cortex and stomach of rats.

Families of 70 kDa heat shock proteins have essential roles in cellular coping to noxious stimuli. However, their roles in psychophysiological stress have not been precisely clarified. We tested our hypothesis that heat shock cognate protein (HSC)70 messenger RNA would increase in stress-vulnerable organs under psychophysiological stress. In control rats, cerebral HSC70 mRNAs were constitutively expressed while gastric HSC70 mRNAs were scarcely identified. Restraint-water immersion stress significantly increased the level of cerebral HSC70 mRNAs for 6 h and 12 h. Stress for 6 h with recovery for 6 h induced more gastric HSC70 mRNA levels than that without recovery, while stress for 12 h expressed the highest gastric HSC70 mRNA levels. Hypothermia, induced by water immersion, excluded a possible role of hyperthermia in inducing HSC70 mRNA. Our results point to a crucial cytoprotective role for families of heat shock proteins in stress-vulnerable brain-gut link in mammals under psychophysiological stress.

Animals↗
PubMed1995

Personality deviation and gastric motility in patients with functional dyspepsia.

We studied gastric motor functions by scintigraphic gastric emptying analysis and surface electrogastrography (EGG), and personality trait deviation in patients with functional dyspepsia. Delayed gastric emptying was observed in 17/35 patients and reduced normal EGG activity in 22/35 functional dyspepsia patients. There was a highly significant negative correlation between the gastric retention rate (at 150 min) and the duration of normal EGG waves. Abnormally high T scores on the Minnesota Multiphasic Personality Inventory (MMPI) test (70 or above) were found in 14/21 patients. Hypochondriasis (Hs) and conversion hysteria (Hy) were the most common abnormal findings. Ninety percent of functional dyspepsia patients (19/21) had either gastric dysmotility and/or psychological deviation. Although there was no significant correlation between gastric dysmotility and deviation in personality traits in functional dyspepsia patients, these data suggest that brain-gut interactions may play an important role in the symptoms of functional dyspepsia.

Adolescent↗
PubMed1993

Case report: reversal of severe leukopenia by granulocyte colony-stimulating factor in anorexia nervosa.

Recent attempts to reduce weight by patients with anorexia nervosa have sometimes led to life-threatening hematologic complications. This report describes an instance in which a patient with anorexia nervosa and pancytopenia drastically improved with treatment that included administration of granulocyte colony-stimulating factor. The patient had lost 27 kg of body weight within 8 months. Even after admission, the blood cell count continued to decrease rapidly as follows: platelet, from 244 x 10(3)/microliters to 44 x 10(3)/microliters; erythrocyte, from 4.04 x 10(6)/microliters to 2.58 x 10(6)/microliters; and leukocyte, from 4.8 x 10(3)/microliters to 1.6 x 10(3)/microliters (granulocyte, 0.8 x 10(3)/microliters). Complications included pneumomediastinum, pneumothorax, purpura, petechiae, hepatomegaly, fever, gangrenous stomatitis, and somnolence. Bone marrow aspiration disclosed absence of fat cells, marrow hypoplasia, and infiltration of the mature lymphocytes. Intravenous hyperalimentation, blood transfusion, gamma-globulin, and antibiotics were administered, but leukopenia and fever remained. However, administration of recombinant human granulocyte colony-stimulating factor dramatically reversed the leukopenia and fever. With careful nutrition therapy, the patient's blood cell count and bone marrow normalized by the time of discharge. It was concluded that severe hematologic disorders may occur in patients with anorexia nervosa, and advanced treatment may be required to save the patient's life.

Adolescent↗
PubMed1993

Brain-gut response to stress and cholinergic stimulation in irritable bowel syndrome. A preliminary study.

To investigate the influence of the brain-gut interactions on the pathophysiology of irritable bowel syndrome (IBS), we compared such patients (n = 10) with healthy control subjects (n = 11) by measuring the pressure of the colon and small intestine simultaneously with analysis of power spectrum of the electroencephalography (EEG) under mental stress and administration of neostigmine. Stress slightly increased the colonic motility index, reduced the percentage of alpha power, and increased the percentage of beta and theta power of the EEG in the patients with IBS more than in the controls (p < 0.05). The patients with IBS had a longer phase II (p < 0.01) and shorter phase I (p < 0.02) of fasting duodenal motor activity than the controls. Neostigmine (10 micrograms/kg) caused a significant difference in the colonic motility index (p < 0.01) and power spectra of EEG (p < 0.05) in the patients with IBS compared to the controls. Significant positive correlation was detected between colonic motility and power spectral change induced by stress (r = 0.46, p < 0.05) or neostigmine (r = 0.51, p < 0.01). These results suggest that patients with IBS have exaggerated responsivity of the gut and the brain to mental stress and cholinergic stimulation. Moreover, there is a possibility that these exaggerated responses are related.

Abdominal Pain↗
PubMed1993

Impact of stress on serum gastrin in Zollinger-Ellison syndrome.

We report an impressive case with Zollinger-Ellison syndrome (ZES), in which stress-induced sympathetic discharge influenced serum gastrin. Our patient was a 35-yr-old female who complained of frequent and massive vomiting (more than 4000 ml of gastric juice) which was aggravated especially by psychosocial stress. Basal hypergastrinemia (1900 pg/ml) was found after the admission. The most striking finding was that laboratory stress dramatically increased serum gastrin (from 1900 to 5400 pg/ml) and plasma noradrenaline (from 180 to 1130 pg/ml). Mental arithmetic stress further enhanced hypergastrinemia (5800 pg/ml) with a concomitant increase in plasma noradrenaline (1240 pg/ml). Neostigmine (10 micrograms/kg im) also increased serum gastrin up to 6100 pg/ml but propranolol (40 micrograms/kg i.v.) reduced these elevations (noradrenaline: 990 pg/ml, gastrin: 5000 pg/ml). In this case, the effect of stress on serum gastrin mimicked the effect of catecholamine infusion in ZES. These findings suggest that psychological stress induces serum gastrin secretion via beta-adrenoceptor with exacerbation of symptoms in some cases with ZES.

Adult↗
PubMed1992

Accentuated vagal antagonism of beta-adrenergic effects on ventricular repolarization. Evidence of weaker antagonism in hostile type A men.

BACKGROUND: Prior research has suggested a weaker parasympathetic antagonism of sympathetic effects on the heart in type A (coronary-prone) men. To confirm this phenomenon and extend our understanding of it, we investigated the effects of prior muscarinic blockade on the electrocardiogram T wave and other cardiovascular and neuroendocrine responses to isoproterenol in type A and type B (non-coronary-prone) men. METHODS AND RESULTS: Responses to two 5-minute intravenous isoproterenol infusions (0.01 micrograms/kg/min and 0.02 micrograms/kg/min) were evaluated in six type A and six type B men after pretreatment with either dextrose placebo or atropine (1.2 mg). Atropine significantly potentiated T wave attenuation in the recovery period after isoproterenol infusion (0.30 +/- 0.07 mV) compared with placebo (0.54 +/- 0.09 mV, p less than 0.001). Atropine also potentiated the heart rate increase to isoproterenol (39 +/- 3 beats per minute versus 20 +/- 2 beats per minute after placebo). Atropine enhanced decreases in systolic, diastolic, and mean arterial pressures as well as pulse pressure to isoproterenol. Atropine enhancement of many of these responses was increased among subjects with high scores on various hostility/anger scales. Isoproterenol alone produced greater T wave attenuation in type A than in type B men. However, atropine enhancement of T wave attenuation and blood pressure falls by isoproterenol was present only in type B men. CONCLUSIONS: These findings indicate that there is accentuated parasympathetic antagonism of T wave attenuation and blood pressure responses induced by beta-adrenergic stimulation. Relative weakness of this antagonism of sympathetic effects on the heart in hostile type A individuals may contribute to their higher coronary disease risk.

Adult↗
PubMed1992

[Brain-gut interactions in irritable bowel syndrome: physiological and psychological aspect].

Recent advances in the investigation of brain-gut interaction in irritable bowel syndrome (IBS) were reviewed. Brain is suggested to play an important role in the pathophysiology of IBS on the basis of the following evidence. (1) Stress often induces major symptoms of IBS patients (Drossman et al., 1982), simultaneously with colonic hypermotility (Fukudo et al., 1987) or dysmotility of the small intestine (Kumar et al., 1985). (2) IBS patients rarely express symptoms or small intestinal dysmotility during sleep (Kellow et al., 1990). (3) IBS patients complain of more pain with balloon distension of the colon or rectum than normal controls; visceral perception is enhanced in IBS (Whitehead et al., 1990). (4) IBS patients often show psychoneurotic symptoms and extra-colonic somatic symptoms (Young et al., 1976). (5) There are some animal (Williams et al, 1987) or human (Dinan et al, 1990) experiments which indicate the possible involvement of brain peptide or brain monoamine in IBS. (6) Dysrhythmia or increased beta power in electroencephalogram is observed more often in IBS patients than in the normal controls (Fukudo et al, 1991) in addition to abnormal REM sleep in IBS patients (Kumar et al., 1992). These observations support our hypothesis that not only the gut but also the brain show dysfunction and exaggerated responsivity to the stimuli in IBS. Further research on brain-gut interaction in IBS is warranted.

Adrenocorticotropic Hormone↗
PubMed1989

Impact of stress on alcoholic liver injury; a histopathological study.

Certain behaviors can have an influence on the cause and progression of liver disorders. To clarify the relation between histopathological change of the liver and psychosocial stress, behavioral traits, and psychological state, patients with fatty liver (n = 14) were compared with patients with chronic hepatitis (n = 16). Both groups were alcohol-induced without other causes and consumed the same dose of alcohol. By morphometric methods, fat deposit ratio (FDR) and degree of liver damage (DLD) which reflects lobular fibrosis, inflammatory cell infiltration, and necrosis were evaluated. Life Change Unit scores from the Social Readjustment Rating Scale were significantly higher in chronic hepatitis than in fatty liver (p less than 0.001). DLD was significantly correlated with Life Change Unit (r = 0.59, p less than 0.01). It is suggested that psychosocial stress is one of the aggravating factors of fibrosis and inflammatory change of the liver which is previously damaged by alcohol in man just like the rat liver following stress.

Adult↗
PubMed1989

Muscarinic stimulation and antagonism and glucoregulation in nondiabetic and obese hyperglycemic mice.

Plasma glucose and insulin responses to a muscarinic agonist (bethanechol chloride) and a muscarinic antagonist (atropine) were evaluated in obese C57BL/6J ob/ob mice and in lean C57BL/6J + /? mice. In lean +/? mice, plasma glucose decreased in response to 1 and 2 micrograms/g bethanechol chloride, whereas insulin increased significantly. In ob/ob mice, insulin increased remarkably in response to bethanechol administration (saline, 632 +/- 80 microU/ml; 2 micrograms/g bethanechol chloride, 1794 +/- 97 microU/ml; n = 10), but surprisingly, plasma glucose also rose significantly (saline, 230 +/- 14 mg/dl; 2 micrograms/g bethanechol chloride, 363 +/- 18 mg/dl, n = 10). This exaggerated hyperglycemia in ob/ob mice was not associated with significant changes in plasma glucagon. Furthermore, administration of propranolol hydrochloride did not diminish bethanechol chloride-induced hyperglycemia in ob/ob mice. Administration of atropine (2.5, 5, and 10 mg/kg body wt) induced a significant decrease in plasma insulin without changes in plasma glucose in ob/ob mice, whereas neither plasma insulin nor plasma glucose changed in lean mice. Finally, conversion of [14C]alanine to glucose was increased in ob/ob mice after bethanechol chloride administration, indicating that muscarinic stimulation increases gluconeogenesis in an animal model of type II (non-insulin-dependent) diabetes.

Animals↗
PubMed1987

Colonic motility, autonomic function, and gastrointestinal hormones under psychological stress on irritable bowel syndrome.

Effects of an artificial mental stress on colonic motility, autonomic nervous system, and gastrointestinal hormones were examined in patients with irritable bowel syndrome (IBS). The subjects were 20 patients with typical IBS and 12 controls. A transducer was inserted to the sigmoid colon from the anus for measuring colonic intraluminal pressure, and mirror drawing test was loaded as psychological stress. At the same time, coefficient of variation of R-R interval on ECG (CV-RR) was measured and the levels of plasma catecholamines, gastrin, glucagon, and motilin were assessed. Colonic motility showed a significant increase in the IBS patients during the stress compared with that in controls (p less than 0.01). Motilin also increased significantly in the IBS patients after the stress (p less than 0.01). CV-RR and motilin revealed positive relationship with colonic motility alteration in the IBS patients although no significant change was detected in controls. These phenomena are thought to be due to autonomic nervous dysfunction and/or gastrointestinal hormonal derrangments induced by psychological stress. It is suggested that organ specificity of the alimentary tract for the stress exists in this disease.

Adolescent↗