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Biomedical subjects

S Fujinuma

Publications and source records attributed to S Fujinuma.

11 recordsLinked to original sources

[Nutritional therapy for ulcerative colitis].

Despite its supplementary role for a remedy of the Ulcerative Colitis, nutritional therapy performs the important role as well as medicine. In the active state, the aim of nutrition therapy is to reduce the activity of the disease. In the remission state, the aim is to keep the condition and to supply elements of nutrition which the disease causes these deficiency such as vitamins or minerals. Needless to say, it is required to consider a few points; patient's condition, lesion's digestion disorder and leakage, or side effects of caused by medicines. High calorie, low fat and rich protein is ideal for the nutrition therapy for this disease, however it is suggested to satisfy patient's mental health at the same time. Nutrition therapy for Ulcerative Colitis should be regarded as the long-term treatment that requires the co-operation and comprehension between patients and medical supporting staffs.

Colitis, Ulcerative↗

[Treatment of mild and moderate ulcerative colitis].

Selection of treatment for ulcerative colitis is based on the definition of clinical severity. In those medication is a main course. Mild and moderate cases are treated mainly with salicylazosulfapyridine or mesalazine. Patients with proctitis-type are added betamethazone suppositories and those with left-sided and total colitis-type predonisolone enema therapy simultaneously. If there is no response, they are given additional oral predonisolone. Even after remission, patients should be carefully observed. A good patient-physician relationship, continuation of maintenance therapy, and periodic follow-up examinations using colonoscopy or barium enema are essential to successful long-term management of this disease. Patients who have repeated relapsing should receive the stronger treatment, according to the endoscopic findings and clinical course in addition to the clinical severity.

Anti-Inflammatory Agents↗

[Left ventricular filling disturbances in cardiac amyloidosis: a study of atrial sound and diastolic inflow velocities].

Cardiac amyloidosis is characterized by left ventricular filling disturbances in a relatively early stage. To investigate such disturbances more precisely, we studied atrial sound and left ventricular inflow velocity patterns. Twelve cases diagnosed as cardiac amyloidosis according to the clinical criteria including rectal biopsies and serum amyloid proteins or at autopsy were reviewed and analyzed. Their mean age was 60.9 +/- 12.5 years. Twelve age-matched cases with hypertrophic cardiomyopathy (HCM) served as the controls. We measured the amplitude of atrial sound by low-frequency phonocardiograms and the ratio of the heights of the A wave of apexcardiograms (ACG) to the total amplitude of the ACG. The mitral inflow velocity patterns were recorded using pulsed Doppler echocardiography. The rapid filling wave (R), atrial filling wave (A) and the ratio of A to R (A/R) were measured. In the amyloidosis group, atrial sound moderately increased in 2 cases, it was faint in 9 and not manifest in the remaining one. The A wave in the amyloidosis group was significantly smaller than that in the HCM group (p < 0.001) (12.4 +/- 3.9 vs 22.4 +/- 5.6%). In the left ventricular inflow velocity patterns, the R in amyloidosis was smaller than that in HCM (41.7 +/- 16.0 vs 56.4 +/- 12.1 cm/sec) (p < 0.02). The A in amyloidosis was also smaller than that in HCM (40.5 +/- 13.4 vs 58.1 +/- 13.0 cm/sec) (p < 0.006). The A/R was 1.0 +/- 0.34 in amyloidosis and 1.1 +/- 0.32 in HCM (N.S.). Both A and R were significantly less in amyloidosis than those in HCM.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Global and regional abnormalities of left ventricular diastolic filling in hypertrophic cardiomyopathy.

Left ventricular diastolic filling was studied by left ventriculography in 17 patients with hypertrophic cardiomyopathy (HCM). In 8 patients this manifested as a spadelike shape (HCM-S type) on the left ventriculogram, and in 9 patients as a banana shape (HCM-B type). Seven patients were studied as controls. Left ventricular end-diastolic pressure was higher in HCM than in controls. In HCM, peak filling rate was decreased from 1.57 +/- 0.28 of the control to 1.28 +/- 0.20 (p less than 0.05), and the time to peak filling rate was prolonged from 27 +/- 6%DT of the control to 37 +/- 7%DT (p less than 0.01). Serial volume analysis in diastole showed filling fraction was also significantly decreased to 8.2 +/- 4.1 (p less than 0.001) at the 25% diastole time and 29.6 +/- 7.2 (p less than 0.01) at half time, compared with 19.8 +/- 6.3 and 32.8 +/- 5.8 for controls, respectively. In HCM-S type, the rate of distention of left ventricular radial axes at the apical area was lower at early and mid-diastole. In HCM-B type, the rate at the basal area was lower at early and mid-diastole. Results suggest that the left ventricular diastolic filling in HCM was impaired not uniformly but regionally in the hypertrophic area at early and mid-diastole.

Adult↗

[Pharmacological characterizations of the in vitro anaphylactic contraction of the guinea-pig esophageal muscularis mucosae].

Characteristics of the antigen-induced contraction of the isolated esophageal muscularis mucosae of actively sensitized guinea-pigs to ovalbumin (OA) were examined in vitro, and they were compared with those of compound 48/80- or polymyxin B-induced contraction. OA, above 0.01 microgram/ml, produced a sustained contraction of the sensitized esophageal muscularis mucosae, the amplitude of which was about 80-100% of the maximum contraction induced by carbachol (10 microM), while compound 48/80 and polymyxin B (10-300 micrograms/ml) produced less potent contractions of the non-sensitized esophageal muscularis mucosae. Contractions to OA or compound 48/80, but not to polymyxin B, were diminished by their repetitive applications. The contractile responses to OA, compound 48/80 and polymyxin B depended on the external calcium concentrations, and were abolished in the calcium-free medium. Pretreatment with tetrodotoxin (0.3 microM), atropine (0.3 microM), diphenhydramine (30 microM) or DSCG (300 microM) did not modify any of these contractions, whereas BW755C (100 microM) and quercetin (10 microM) significantly inhibited them. Indomethacin (10 microM) largely prevented only the polymyxin B-induced contraction, while FPL55712 (10 microM) inhibited both contractions to OA and compound 48/80. These findings indicate that the OA-induced anaphylactic contraction of the esophageal muscularis mucosae taken from the OA-sensitized guinea-pig may be an indirect action via the stimulation of releases of some mast cell-derived spasmogens. The spasmogens may involve the lipoxygenase products of arachidonic acid in part, but not histamine, acetylcholine or the cyclooxygenase products.

Anaphylaxis↗

Contractile responses of the guinea-pig esophageal muscularis mucosae in vitro to arachidonic acid and its metabolites.

The responsiveness of the guinea-pig esophageal muscularis mucosae to arachidonic acid (AA) and its cyclooxygenase and lipoxygenase metabolites was examined in vitro. AA (0.1-30 microM) produced a concentration-dependent contraction of the muscularis mucosae (mean EC50 +/- S.E.M. = 5.1 +/- 1.0 microM). The contractions in response to low concentrations of AA (0.1-3 microM) were prevented by pretreatment of the tissue with indomethacin (1-10 microM), while those in response to high concentrations (10-100 micron) were prevented by BW755C (10-100 microM). The contractile response to AA was antagonized by polyphloretin phosphate (PPP, 1-10 micrograms/ml) and by FPL 55712 (1-10 microM). All cyclooxygenase and lipoxygenase metabolites of AA tested also produced a sustained contraction of the muscularis mucosae with the following order of sensitivity; leukotriene (LT) D4 greater than LTC4 greater than prostaglandin (PG) E2 greater than PGF2 alpha greater than PGI2 greater than thromboxane B2. The responses to LTC4 and LTD4 were antagonized by FPL 55712 (0.1-1 microM), while those to PGE2 and PGF2 alpha were antagonized by PPP (3-100 micrograms/ml). The present results indicate that exogenously applied AA contracts the isolated muscularis mucosae of the guinea-pig esophagus by an indirect action via its metabolism to both PGs and LTs. The putative PG and LT receptors located in this tissue are probably similar to those in the ileal longitudinal muscle, but differ from those in the airway smooth muscle.

Animals↗

Pharmacological characterization of the histamine receptor in the isolated muscularis mucosae of the guinea-pig oesophagus.

To characterize the histamine receptors in the muscularis mucosae, the isotonic responsiveness of the isolated muscularis mucosae of the guinea-pig oesophagus to histamine receptor agonists and antagonists was examined in vitro. Histamine (0.1-100 microM) produced a concentration-dependent contraction of the muscularis mucosae (EC50 = 1.6 +/- 0.2 microM). The contractions were rapid in onset, sustained, reversible by washing and the preparation did not show tachyphylaxis. 2-Methylhistamine (2-MH), 2-pyridylethylamine (PEA) and 4-methylhistamine (4-MH) produced similar sustained contractions of the muscularis mucosae. The order of sensitivity was histamine greater than 2-MH greater than PEA greater than 4-MH. Impromidine (10-300 microM) and dimaprit (10-300 microM) caused no response in this tissue. The contractile responses to histamine, 2-MH, and PEA were competitively antagonized by diphenhydramine, and the pA2 values were almost the same (approximately 8.1). Cimetidine (100 microM) could not modify the contractile response to these agonists. The contractile response to histamine was slightly inhibited by tetrodotoxin (0.3 microM), atropine (1 microM), indomethacin (0.1-3 microM) or aspirin (30-300 microM), and the EC50 value was increased about 2-6 times by these drugs. When the preparation was incubated in Tyrode solution containing various calcium concentrations (0, 0.45, 0.9 and 1.8 mM), the concentration-response curve to histamine was shifted to the right and downward; the effect was inversely dependent on the calcium concentration, and in a calcium-free medium the response to histamine was abolished. Verapamil (1-10 microM) partially inhibited the contractile response to histamine. 7 The present results indicate that the contraction of the guinea-pig oesophageal muscularis mucosae to histamine is mediated mainly by a direct action on the smooth muscle and partly by indirect actions via the stimulation of either endogenous prostaglandin biosynthesis or intramural cholinergic nerves. The histamine receptors responsible for contractions of this tissue are probably mainly of the H,- subtype with H2-receptors having a negligible role.

Animals↗