Tachyphylaxis. V. Tyramine in isolated organs.
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We describe 2 patients with refractory inflammatory myositis who had an initial favorable response to intravenous immunoglobulin (IVIG) therapy. In contrast to all other reported cases, our patients reached a nadir in creatine phosphokinase (CPK) levels at 6 and 14 weeks after initiation of therapy, respectively, then experienced a relentless rise in CPK levels as well as a return of muscle weakness while still receiving IVIG. While IVIG may benefit some patients with refractory myositis, future studies must address the sustained efficacy of this agent.
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Fourteen patients with moderate bronchial asthma were selected for the study. Asthmatics were treated with intravenous salbutamol for one week. Peripheral blood lymphocyte beta-2-adrenergic receptor density and affinity were determined before and after the treatment. To investigate an effect of corticosteroids on beta-2-agonist induced desensitization of beta-2-receptors, beta-2-receptor density and affinity following prednisone administration have been determined in lymphocytes in 7 asthmatics. Patients have been given prednisone in the dose of 20 mg daily for 1 wk after salbutamol discontinuation. Spontaneous recovery of beta-2-adrenergic receptor density in the lymphocytes was estimated in further 7 asthmatics, not given corticosteroids following salbutamol therapy. Our data showed that down-regulation of beta-2-adrenergic receptors improves spontaneously and to significantly higher degree after corticosteroid therapy.
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The cardiocirculatory actions on the oral vasodilator prazosin were evaluated by cardiac catheterization, forearm plethysmography, echocardiography, treadmill exercise and symptoms in patients with advanced long-standing congestive heart failure. The administration of oral prazosin (2 to 7 mg) reduced forearm venous tone and forearm vascular resistance. Concomitantly, mean systemic arterial pressure and left ventricular filling pressure decreased, and the cardiac index increased. These effects of a single dose of prazosin on left ventricular function were rapid in onset, maximal at 1 hour and sustained for the entire 6-hour period of observation. After two weeks of outpatient therapy with 2 to 7 mg of prazosin four times daily, echographic end-diastolic dimension decreased, whereas the duration of treadmill exercise increased. Symptoms (dyspnea, fatigue, angina) were diminished throughout the course of prazosin therapy, and there was an improvement in the New York Heart Association functional class from 3.7 to 2.2. Thus, prazosin possesses sustained nitroprusside-like balanced dilator actions of the systemic arterial and venous beds, which are effectively translated into the beneficial hemodynamic effects of augmenting cardiac output and relieving excessive left ventricular end-diastolic pressure. The delayed vasodilator tolerance that occurs in 30 percent of the patients is prevented by the prior use of aldosterone antagonists and is easily treated when present. Subacute hemodynamic suppression of beneficial prazosin vasodilator actions is transient and does not preclude successful sustained prazosin therapy of severe heart failure.
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