[Modification of the smoking-induced hemodynamic effect by nifedipine].

Effects of nifedipine, a Ca(++)-channel blocker, on smoking-induced hemodynamic changes were studied in 35 habitual male smokers. They were divided into three groups: 20 healthy persons (G1), 11 patients with essential hypertension (G2) who were under nifedipine treatment, and 4 patients (G3) with essential hypertension but who were receiving no medication. After abstaining from smoking for more than 12 hours, they smoked, within 10 minutes, two filtered cigarettes each containing 2 mg of nicotine. Hemodynamic parameters were measured and blood samples were taken before and 5, 10, and 30 minutes after beginning to smoke. In each group, smoking produced significant increases in blood pressure, heart rate and cardiac output. Plasma adrenaline increased significantly in 3 groups, and tended to be highest in G2. Plasma noradrenaline was the highest in G2 predominantly, but did not change after smoking. These results indicate that a smoking-induced hyperdynamic state including vasoconstriction due to catecholamine release might not depend on the calcium channel which is blocked by nifedipine, and the reflex activation of the sympathetic nerve system would develop in the presence of nifedipine.

[Acute hemodynamic effect of cigarette smoking and its relationship with nicotine content].

We studied the acute effects of cigarette smoking on the cardiovascular system, especially regarding nicotine-related hemodynamic effects using cigarettes with low and high nicotine contents. 40 healthy men who were habitual smokers were divided into two groups: 20 subjects smoked cigarettes of low nicotine content [0.4 mg/cigarette; group 1 (G1)] and another 20 tested cigarettes containing high nicotine [2 mg/cigarette; group 2 (G2)]. All of the subjects were requested to abstain from cigarette smoking for at least 12 hours prior to study, and to rest in the supine position for 30 minutes just prior to the test. They smoked two consecutive cigarettes for 10 minutes, inhaling every 30 seconds by drawing on the cigarette for two seconds, and holding the smoke for three seconds before exhaling. Blood pressure (BP), heart rate (HR) and cardiac output (CO) were measured and blood samples were taken before, and 5, 10 and 30 minutes after the start of smoking. Smoking with a high nicotine content (G2) produced a significant increase in both systolic and diastolic BP (124 +/- 14/78 +/- 8----138 +/- 21/90 +/- 10 mm Hg), but no significant changes in BP were observed in the low nicotine group. HR and CO increased predominantly in both groups (HR: G1; 62 +/- 7----66 +/- 7, G2; 64 +/- 7----76 +/- 9/min, CO: G1; 4.85 +/- 1.36----5.31 +/- 1.37, G2; 4.95 +/- 1.58----5.63 +/- 2.01 l/min), but the present increases were significantly less in G1 than in G2.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum secretory component level in myeloma patients with disorders of the secretory surface.

Secretory component (SC) in myeloma serum was measured by a double antibody radioimmunoassay. It was elevated in patients with IgA myeloma and the highest level was observed in a patient with macroglobulinemia. The presence of disorders of secretory surface in myeloma patients slightly but not significantly elevated the serum SC concentration. A significant correlation between serum SC and IgG is demonstrated, but not between serum SC and IgA. Over the whole patient groups, serum SC is significantly related to serum IgM but not when patients with macroglobulinemia are excluded from the calculation. Serum SC is present as SC-IgM in macroglobulinemia and SC-IgM and SC-IgA in IgA myeloma.

A radioimmunoassay for quantitation of secretory component.

Secretory component (SC) isolated from human colostrum was radioiodinated with chloramin-T method and it was subjected to a radioimmunoassay for quantitation of SC. A monospecific rabbit anti-sera against human SC which could react with free SC as well as immunoglobulin bound SC was used for the assay. The present method can measure as low as 300 ng/ml of SC. The level (mean +/- 2 S.D.) of serum SC in healthy subjects was determined to be 31.3 +/- 7.2 micrograms/ml. Studies with Sephadex G-200 gel filtration demonstrated that SC in the normal sera existed mostly as a form of SC-IgA. In contrast, free SC was never detected in them.

Studies on circulating immune complexes of the liver diseases. 5. Anti-DNA antibodies and C1q binding activity.

Anti-dsDNA and anti-ssDNA antibodies, rheumatoid factors, HBsAg and C1q binding activity were determined in sera of patients with various liver diseases. Anti-dsDNA were only slightly increased in chronic aggressive hepatitis, activity severe and liver cirrhosis. A moderate elevation of anti-dsDNA was detected in possible lupoid hepatitis and it was highly increased in lupoid hepatitis as well as systemic lupus erythematosus. Non-specific elevation of anti-ssDNA titers were observed in all of the liver disease groups. In patients with increased anti-dsDNA titers, C1q binding activity and titers for rheumatoid factor and HBsAg tended to increase. According to reactivity of their sera to DNA, patients with liver disease could be divided in 4 groups: 1. high responders to dsDNA (lupoid hepatitis), 2. moderate responders to dsDNA (possible lupoid hepatitis or lupoid-like liver disease), 3. low responders (only positive for ssDNA), and 4. non-responders.

Studies on circulating immune complexes of the liver disease. 3. Conditions for Clq binding assay and low molecular weight Clq reactants.

Assay conditions for Clq binding activity (ClqBA) of aggregated human gamma globulin and pathologic sera were studied. The Clq component of complement was isolated by precipitation method and effectively radioiodinated using lactoperoxidase without loss of binding activity. The assay method was reproducible and the binding activity of normal sera was 5.0 +/- 2.4% (mean +/- S.D.). Amount of 125I-Clq, in the range of 50--1000 ng per assay tube, did not influence the binding activity. Competitive inhibition of intrinsic Clq was very limited. Sample sera for the determination can be stored at --20 degrees C and freezing-throwing of the sera did not increase ClqBA. In normal sera, the existence of solubilizer of Clq-reactant-complex or inhibitor of Clq-reactant binding working at 37 degrees C is suggested. For the low molecular weight reactants in pathologic sera reacting with Clq at 4 degrees C, following substances are proposed: 1. abnormal IgG, 2. hapten-IgG complexes or 3. anionic substances.

Studies on circulating immune complexes of the liver disease. 4. Clq binding activity.

Serum Clq binding activity (ClqBA) is increased in diabetes mellitus with liver injury, carcinoma of gastrointestinal tract with metastatic liver and chronic liver disease (CLD). Significant elevations of ClqBA level are observed in the order of liver cirrhosis, chronic aggressive hepatitis and chronic persistent hepatitis. In CLD there are significant correlations between ClqBA and gamma-globulin, rheumatoid factor, anti-DNA-antibody, CH50, C3, C4, C3-activator and HBsAg.

Studies on secretory component in digestive disease. III. Levels of serum secretory component in digestive disease.

The levels of serum secretory component (SC) were measured in 147 patients with digestive disease. Decreased levels were found patients with acute hepatitis, HBs-antigen associated chronic hepatitis, HBs-antigen associated liver cirrhosis and hepatoma. Normal levels were observed in patients with diabetes mellitus, gastric cancer and colonic carcinoma. Elevated levels were found in patients with cholecystitis, obstructive jaundice and acute pancreatitis. The serum SC level in almost all disease groups showed no correlation with immunoglobulin levels.

Studies on secretory component in digestive disease. IV. Levels of serum secretory component in liver disease.

The levels of serum secretory component (SC), immunoglobulins, rheumatoid factor, HBs-antigen and HBs-antibody were determined in patients with liver disease, especially chronic liver disease. In chronic liver disease, decreases in serum SC were accompanied by increases in the titer of rheumatoid factor. Patients with chronic liver disease and HBs-antigen or HBs-antibody had decreased levels of serum SC compared to seronegative patients. There was no correlation between the levels of serum SC and immunoglobulin in patients with chronic liver disease.

Studies on circulating soluble immune complexes of the liver disease. 2. Serum inhibitory activity of polyclonal rheumatoid factor binding to IgG-sepharose.

Circulating immune complexes were tested in the liver disease by measuring polyclonal rheumatoid factor (pRF) inhibition activity. The test is based on the inhibition of 125I-pRF binding to IgG-p-azobenzamidoethyl Sepharose 6B. Normal levels of the test were less than 23%. The inhibition activity in sera with liver disease was found to correlate with severity of the disease, as defined by histological criteria. There were correlations of the activity with serum gamma-globulin concentration, seropositivities for rheumatoid factor and hepatitis B antigen.

Studies on circulating soluble immune complexes of the liver disease. 1. Inhibition assay of polyclonal rheumatoid factor binding to IgG-sepharose.

Polyclonal rheumatoid factor (pRF) was isolated from sera seropositive for RF and it was radioiodinated with lactoperoxidase method. Using the 125I-pRF and IgG-p-azobenzamidoethyl Sepharose 6B, a competitive inhibition radioassay for detecting immune complexes is described. The assay can be performed in 90 min utilizing 10 microliter of serum with good reproducibility and endogenous RF in test serum did not interfere the reaction. The test can detect complexes nearly to 8s and as low as 0.1 microgram/ml of aggregated human IgG. Decomplementation by heating test sera is unnecessary. The assay was performed at 4 degrees C but less inhibition activity was obtained when it was carried out at 24 degrees C.