Mycobacterium avium was recovered from 21 birds and 10 pigs. Bird isolates carried IS901 and a few copies of IS1245 and appeared highly related by pulsed-field gel electrophoresis. Pig isolates showed features previously described in human isolates: a lack of IS901, a high copy number of IS1245, and marked polymorphism by pulsed-field gel electrophoresis. Mycobacterium avium represents an important pathogen in both humans (5, 7, 12, 19, 25) and animals (8, 16). For humans, water has been identified as a definitive source of infection (24). However, the observed genetic diversity of M. avium strains recovered from AIDS patients (1) and the occurrence of M. avium in animals and various environmental samples suggest the existence of additional reservoirs (17). The purpose of this study was to characterize M. avium strains recovered from animal sources within a defined geographical area-the German-speaking part of Switzerland-by using a number of genotype markers, namely, the presence of insertion elements IS900 (9), IS901 (15), and the novel element IS1245 (10), and by evaluating strain relatedness by pulsed-field gel electrophoresis (PFGE). Materials investigated (n ϭ 398) included mandibular and mesenteric lymph nodes from 120 slaughtered pigs collected from two different abattoirs; 103 samples from 25 chickens and 15 eggs from eight different flocks; organs (n ϭ 21) from seven additional birds, including five exotic birds, in which acid-fast bacilli had been detected (Institute for Veterinary Bacteriology, University of Berne); and environmental samples, such as those from soil (n ϭ 8), pig and chicken litter (n ϭ 9), pondwater (n ϭ 1), and chicken feed (n ϭ 1). Samples were homogenized, decontaminated with sodium dodecyl sulfate-sodium hydroxide, and neutralized, and the sediments were resuspended in phosphate-buffered saline (20). One BACTEC 12B vial supplemented with Panta Plus (Becton Dickinson Diagnostic Instrument Systems, Sparks, Md.), one pyruvate-containing Löwenstein-Jensen slant, and one slant of Herrold's medium were inoculated. Slants were incubated at 37ЊC for 12 weeks and inspected for growth weekly. BACTEC 12B vials were processed for 12 weeks with the BACTEC-460 TB apparatus (Johnston Laboratories Inc., Sparks, Md.) according to the manufacturer's recommendations. For identification, mycobacterial isolates underwent PCR-restriction enzyme analysis of the gene coding for the 65-kDa heat shock protein of mycobacteria (21) and conventional biochemical tests (13).

To study the effect of chronic exposure to elevated plasma catecholamines on surface beta 2-adrenoceptor density, we measured these receptors in the lymphocytes of 9 patients with pheochromocytoma as well as in 27 healthy control subjects. Binding experiments were performed on intact lymphocytes using the hydrophilic ligand [3H]-CGP12177. Lymphocyte beta 2-adrenergic response was also measured in three patients. beta 2-adrenoceptor density (p < 0.01), and isoproterenol-stimulated increase in cAMP were reduced in patients with pheochromocytoma. Both parameters normalized (p < 0.05) when patients were reevaluated 4 weeks after tumor removal, coinciding with normalization of plasma epinephrine (r = -0.95, p < 0.01) and to log of plasma norepinephrine (r = -0.58, p < 0.05) in patients. We conclude that chronic catecholamine excess induces a decrease of lymphocyte beta 2-adrenoceptor surface number and response that is reversible upon normalization of plasma catecholamine levels. This regulation is mainly dependent on plasma levels of the hormone epinephrine, but norepinephrine may also play a regulatory role at supraphysiological levels.

No abstract

The effect of different antihypertensive drugs on the increased surface beta 2-adrenoceptor density in essential hypertension was evaluated to elucidate whether the possible effect of the treatment on these receptors was secondary to blood pressure decreases or a specific effect of the drugs. Thirty-nine untreated essential hypertensive patients and 28 normotensive control subjects were studied in basal conditions. Hypertensive patients were randomly assigned to three treatment groups: bisoprolol (10 mg/day, n = 15), enalapril (20 mg/day, n = 12), and verapamil SR (240 mg/day, n = 12), and were studied before and after 1 month of treatment. Plasma catecholamines were determined by a radioenzymatic assay. Surface beta 2-adrenoceptors were measured in intact lymphocytes by radioligand binding assay using the hydrophilic ligand [3H]-CGP12177. beta 2-adrenoceptor density was increased in hypertensive patients (P < .01). After treatment, mean blood pressure decreased similarly in the three groups, while plasma catecholamines showed no significant changes in any group. beta 2-adrenoceptor number decreased only in bisoprolol-treated patients (P < .05). Mean blood pressure decreases correlated with beta 2-adrenoceptor decrements only in bisoprolol-treated patients (r = 0.65, P < .05). beta 2-adrenoceptor density correlated with plasma epinephrine levels in the control group (r = -0.50, P < .01), but not in hypertensive patients before treatment. This correlation was also observed in hypertensive patients treated with bisoprolol (r = -0.52, P < .05), but not in those treated with verapamil or enalapril. Our results suggest that bisoprolol treatment reduces the increased surface beta 2-adrenoceptor density and restores its regulation by epinephrine in essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract