Antigen-specific desensitization of patients allergic to penicillin

Three penicillin-allergic patients with life-endangering infections requiring β-lactam antibiotic therapy were desensitized by means of increasing oral then parenteral doses and were treated with full doses of β-lactam agents. Malignant otitis externa caused by Pseudomonas aeruginosa, osteomyelitis caused by Staphylococcus aureus, and bacterial endocarditis caused by an enterococcus were treated with carbenicillin, nafcillin, and benzylpenicillin G, respectively. No acute allergic reactions occurred during desensitization or within 1 wk of the onset of therapy. Immediate wheal and flare skin-test reactions to β-lactam determinants diminished or became negative after the desensitization procedure in each patient. Wheal and flare responses provoked by histamine, compound 48/80, and environmental antigens were not affected by the desensitization procedure or continued β-lactam drug therapy. Mild urticaria appeared after 15 days of penicillin therapy in one patient and after 23 days of carbenicillin therapy in another patient. Skin-test reactions to penicillin reagents had reverted to positive at the time of the urticarial reactions. One patient developed a severe immune hemolytic anemia after 10 days of therapy with nafcillin. The results of this study indicate that acute clinical desensitization of these three penicillin-allergic patients was associated with antigen-specific desensitization of tissue mast cells.     

Activation of μ-opiate receptors as a factor of regulation of heart resistance to ischemia-reperfusion and oxidative stress

Intravenous injection of the selective μ-opiate receptor agonist DAMGO (0.1 mg/kg, 15 min before isolation of the heart) improved resistance of isolated perfused rat heart to ischemia (45 min) and reperfusion (60 min) damages.In vivo administration of DAMGO prevented reperfusion-induced damages to cardiomyocytes and decreased the content of conjugated dienes in the myocardium during ischemia-reperfusionin vitro. Furthermore, stimulation of μ-opiate receptors promoted recovery of myocardial contractility during reoxygenation, but had no effect on heart resistance to free radical-induced damages during perfusion of isolated heart with a solution containing Fe²⁺ and ascorbic acid. Translated fromByulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 130, No. 8, pp. 163–167, August, 2000     

Mechanism of action of baclofen on myocardial and vascular contractility

Department of Anatomy and Physiology of Man and Animals, A. I. Gertsen Leningrad Pedagogic Institute. Department of Pharmacology, Academician I. P. Pavlov First Leningrad Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR A. V. Val'dman.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 106, No. 10, pp. 436–438, October, 1988.     

Action of burn serum on electrical and contractile activity of the homoiothermic myocardium

In experiments on isolated rabbit papillary muscles the action of burn serum (BS) obtained 1 h after thermal injury to rabbits was studied. During stimulation varying in frequency between 0.1 and 2 Hz isometric contractions and action potentials (AP) of myocardial cells were recorded. BS (diluted 1:1 in Tyrode solution) inhibited the contractile activity of the papillary muscles, increased the duration of AP, and reduced the duration of the contractile response. Inotropic effects on the rhythm of contractions remained unchanged: An increase in the frequency of stimulation to 2 Hz led to an increase in the amplitude of contractions. Inhibition of the contractile response increased progressively with an increase in the duration of perfusion of the preparations with BS. Addition of 6.4 mM Ca⁺⁺ to the solution of BS caused only a temporary increase in contractions, and rinsing the preparations with Tyrode solution did not result in complete recovery of the orginal contractions. It is concluded that humoral factors play an important role in the disturbance of the contractile properties of heart muscle during burn shock.Laboratory of Biophysical Research, A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR M. I. Kuzin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 8, pp. 157–159, August, 1979.     

Postextrasystolic potentiation does not distinguish ischaemic from stunned myocardium

Myocardial function is impaired by ischaemia, and it remains depressed during reperfusion following short periods of ischaemia (stunned myocardium). We tested whether ischaemic and reperfusion dysfunction, in particular the time course of its recovery, can be distinguished by postextrasystolic potentiation (PESP). In eight open-chest dogs, posterior systolic wall thickening (sonomicrometry) was reduced by graded occlusion of the left circumflex coronary artery (LCX) from 17.4±6.8% (SD) during control conditions to 10.7±1.3% (mild ischaemic dysfunction), 7.2±2.3% (moderate ischaemic dysfunction), 3.6±1.4% (severe ischaemic dysfunction), and -4.4±3.6% (complete coronary occlusion). Extrasystoles with constant prematurity and a fully compensated postextrasystolic interval were induced after at least 4 min steady-state ischaemia. After each ischaemic period full recovery of posterior systolic wall thickening was assured. During 8 h of reperfusion following a 15-min LCX occlusion, extrasystoles were induced when posterior systolic wall thickening was comparable to one degree of the preceding ischaemic dysfunction. The increases in posterior systolic wall thickening induced by PESP were 10.5±5.8% during control conditions, during ischaemia they were 11.5±3.5% (mild dysfunction), 12.3±4.6% (moderate dysfunction), 12.6±4.1% (severe dysfunction) and 10.4±4.4% (complete coronary occlusion), and during reperfusion they were 12.8±8.2% (severe dysfunction), 13.0±9.7% (moderate dysfunction) and 10.7±2.2% (mild dysfunction). These increments in systolic wall thickening as well as those in ejection thickening were not significantly different. PESP can thus not distinguish between ischaemic and reperfusion dysfunction nor between different degrees of myocardial dysfunction.This study was supported by the Deutsche Forschungsge-meinschaft (He 1320/3-2). cand. med. S. Schäfer was involved in some of these experiments and presented part of the data at the 56th Annual Meeting of the Deutsche Gesellschaft für Herz- und Kreislaufforschung in Mannheim (Z Kardiol 79 [Suppl 1]: 24,1990). Part of the data were also presented at the 11th Congress of the European Society of Cardiology in Nice (Eur Heart J 10 [Suppl]: 242, 1989) and at the 73rd Annual Meeting of the Federation of American Societies for Experimental Biology in New Orleans (FASEB J 3: A841, 1989)     

Monoclonal antibodies cross-reacting with fibroblasts of myocardial interstitial connective tissue and with group a streptococcal cell wall protein antigens

N. F. Gamaleya Research Institute of Epidemiology and Microbiology. Institute of Rheumatology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR, P. A. Vershilova.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 108, No. 7, pp. 74–76, July, 1989.     

Adrenalin-induced pacemaker activity in the isolated atrial myocardium of mitral stenosis patients and its inhibition by ethmozine and ethacizine

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