Infusion-related adverse events (IRAEs) such as nausea, vomiting, fever, chills, and thrombophlebitis that are associated with amphotericin B therapy often lead clinicians to prescribe a number of adjunctive pretreatment medications in an attempt to reduce the incidence and severity of these events. The purpose of this study was to determine the incidence of IRAEs during the first week of systemic amphotericin B therapy and to identify pretreatment regimens that are effective in preventing these IRAEs. Three hundred ninety-seven adult inpatients receiving amphotericin B therapy were prospectively monitored, and data regarding IRAEs and pretreatment regimens were collected. Of these patients, 282 (71%) developed at least one IRAE during the first 7 days of therapy. The IRAEs most commonly reported were fever (51% of patients) and chills (28%), followed by nausea (18%), headache (9%), and thrombophlebitis (5%). The most common regimens included diphenhydramine, a corticosteroid, acetaminophen, and heparin, administered alone or in combination with these or other drugs. Overall, common pretreatment regimens were similar in efficacy to no pretreatment in the prevention of IRAEs. Thus empirical premedication for IRAEs associated with amphotericin B cannot be routinely advocated; instead, patients should be treated when symptoms first arise and then premedicated for subsequent amphotericin B infusions.
The purpose of this study was to determine whether cardiac hypertrophy in response to hemodynamic overloading is a primary result of the increased load or is instead a secondary result of such other factors as concurrent sympathetic activation. To make this distinction, four experiments were done; the major experimental result, cardiac hypertrophy, was assessed in terms of ventricular mass and cardiocyte cross-sectional area. In the first experiment, the cat right ventricle was loaded differentially by pressure overloading the ventricle, while unloading a constituent papillary muscle; this model was used to ask whether any endogenous or exogenous substance caused uniform hypertrophy, or whether locally appropriate load responses caused ventricular hypertrophy with papillary muscle atrophy. The latter result obtained, both when each aspect of differential loading was simultaneous and when a previously hypertrophied papillary muscle was unloaded in a pressure overloaded right ventricle. In the second experiment, epicardial denervation and then pressure overloading was used to assess the role of local neurogenic catecholamines in the genesis of hypertrophy. The degree of hypertrophy caused by these procedures was the same as that caused by pressure overloading alone. In the third and fourth experiments, fi-adrenoceptor or a-adrenoceptor blockade was produced before and maintained during pressure overloading. The hypertrophic response did not differ in either case from that caused by pressure overloading without adrenoceptor blockade. These experiments demonstrate the following: first, cardiac hypertrophy is a local response to increased load, so that any factor serving as a mediator of this response must be either locally generated or selectively active only in those cardiocytes in which stress and/or strain are increased; second, catecholamines are not that mediator, in that adrenergic activation is neither necessary for nor importantly modifies the cardiac hypertrophic response to an increased hemodynamic load.
Antibiotic prescribing information was prospectively collected on 1822 hospitalized patients treated for suspected or documented bacterial pneumonia. Antibacterial therapy with a single antibiotic was employed in more than 50 percent of the patients, with cefazolin, cefuroxime, ampicillin, and ceftriaxone sodium representing the most commonly employed agents. Combination therapy using two antibiotics was employed in approximately 30 percent of patients with the aminoglycosides, particularly gentamicin, used extensively. A satisfactory outcome was achieved in approximately 80 percent of patients with a community- or institutional-acquired pneumonia; only 66 percent of nosocomial pneumonias had a satisfactory outcome. An important observation was the apparently common practice of switching patients to an oral antibiotic regimen after an average of seven days of antibiotics and subsequently discharging the patient. No difference was observed in the patterns of clinical response or duration of therapy for culture-positive versus culture-negative patients. The results of this surveillance program can serve as a basis for comparison of institution-specific drug utilization evaluation programs.
assessed and controlled; second, to define the effects of this intervention on myocardial energetics in terms of any changes dependent on or independent ofalterations ofthese determinants of MVO2; third, to define any change in myocardial sensitivity to catecholamine action after the withdrawal of long-term (3-adrenoceptor blockade; fourth, to determine whether chronic f3-adrenoceptor blockade alters the number, affinity, or biochemical activity of this autonomic receptor. MethodsFour separate series ofexperiments, each employing paired sets ofcontrol and chronically ,8-blocked cats, comprise the data base for this study. In the first series, mechanical and metabolic behavior of myocardium isolated from these two sets of cats was measured. In the second series, the specific relationship of any differences found between these two sets of animals to changes in the activity of the cardiac fl-adrenoceptor was examined. In the third series, the effect ofchronic fl-adrenoceptor blockade on fl-adrenoceptor number, affinity, and affinity state was assayed. In the fourth series, the effect of chronic fl-adrenoceptor blockade on the major immediate U-mediated biochemical response, cyclic AMP generation, was determined. Experimental animalsThe animals used were 1.7-3.6-kg adult cats of random sex. The cats in the control groups received normal saline (I cm3/kg i.p.) twice daily for 14 d prior to study. The chronically fl-blocked cats were prepared and characterized as follows. First, their baseline responsiveness to (3-adre-
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