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H J Silverman

Publications and source records attributed to H J Silverman.

28 records · Page 2Linked to original sources
PubMed1990

Effects of canine endotoxin shock on lymphocytic beta-adrenergic receptors.

To determine whether beta-adrenergic receptors on circulating lymphocytes are impaired during endotoxemia and the precise role of catecholamines in this process, we allocated 16 dogs to three groups: I) control-saline vehicle (n = 5), II) endotoxin--Escherichia coli endotoxin 1.0 mg/kg iv bolus (n = 6), and III) endotoxin + propranolol--E. coli endotoxin 1.0 mg/kg after pretreatment with propranolol, 1.5 mg/kg iv bolus followed by a continuous infusion, 30 micrograms/kg per min, (n = 5). Five hours after endotoxin injection, lymphocytic beta-adrenergic receptor number and sodium fluoride (NaF)-stimulated cyclic AMP accumulation were reduced by 41 +/- 6% and 25 +/- 7% of baseline values, respectively, which were significantly different from those observed in the control group (both P less than .01). Propranolol pretreatment prevented the endotoxin-induced reduction in lymphocytic beta-adrenergic receptor number (P less than .02 compared with the endotoxin group), but not the decrease in NaF-stimulated cyclic AMP accumulation (P less than .01 compared with the control group). Myocardial beta-adrenergic receptor number was reduced in the endotoxin group compared with that observed in the control group (P less than .06). These changes were associated with a decreased chronotropic response to isoproterenol in the endotoxin group compared with the control group (P less than .05). We conclude that decreased lymphocytic beta-adrenergic receptor number in endotoxin shock is caused by circulating catecholamines, whereas alterations distal to the receptors may be due to other mechanisms.

Animals↗
PubMed1989

Myocardial toxic effects during recombinant interleukin-2 therapy.

Arterial and pulmonary artery catheters were used to monitor the cardiopulmonary effects of recombinant interleukin-2 (rIL-2) given iv at a dose of 100,000 U/kg every 8 hours on days 1-5 to 10 patients with metastatic solid tumors. As anticipated, a severe capillary leak syndrome developed in all patients. Myocardial infarction (MI) occurred unexpectedly in three patients, as evidenced by a focal injury pattern on ECG and elevations of creatinine phosphokinase myocardial band fractions. All patients receiving rIL-2 exhibited major reductions in their left ventricular stroke work index (47 +/- 11 g.m/m2 to 29 +/- g.m/m2), an index of cardiac contractility. It remains uncertain whether the MIs were a byproduct of the capillary leak syndrome in patients with underlying coronary artery disease or whether rIL-2 directly or indirectly damages cardiac muscle.

Adult↗
PubMed1988

Effects of antihistamines on the cardiopulmonary changes due to canine anaphylaxis.

Histamine has long been considered to be an important chemical mediator in the pathogenesis of immediate hypersensitivity reactions. We evaluated the efficacy of antihistamines to determine the physiological role of histamine in canine anaphylaxis. Either a saline vehicle (control group), an H1 antihistamine (chlorpheniramine, 10 mg/kg), or this H1 antihistamine and an H2 antihistamine (cimetidine, 30 mg/kg) was administered to three separate groups of anesthetized dogs (n = 8). Cardiopulmonary responses and plasma histamine levels were measured after the separate intravenous injection of Ascaris suum antigen and histamine. Results were analyzed only from the animals demonstrating physiological responses or histamine release after antigen injection. In the control group, antigen produced a 43 +/- 15% (mean +/- SE) decrease in mean arterial blood pressure, a 34 +/- 13% fall in cardiac output, and a 19 +/- 9% decrease in lung compliance, whereas pulmonary vascular resistance increased 161 +/- 87% and airway resistance rose 114 +/- 66%. Similar physiological abnormalities were observed with histamine shock. However, peak plasma histamine levels were, in most cases, greater after histamine injection than after antigen injection. An H1 antihistamine alone or in combination with an H2 antihistamine did not alter the physiological changes associated with systemic anaphylaxis. In contrast, the combined use of H1 and H2 antihistamines prevented the cardiopulmonary responses associated with the intravenous administration of histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylaxis↗
PubMed1988

Effects of interleukin-2 on oxygen delivery and consumption in patients with advanced malignancy.

We evaluated the effects of fluid challenges on oxygen delivery (DO2) and oxygen consumption (VO2) in nine patients receiving immunotherapy with interleukin-2. Fluid resuscitation produced an increase in DO2 from 15.7 +/- 3.1 to 17.4 +/- 3.5 ml/min/kg (mean +/- SD, p less than 0.001), which was associated with a corresponding increase in VO2, from 2.8 +/- 0.7 to 3.1 +/- 0.6 ml/min/kg (p less than 0.01). These results suggest that oxygen consumption may be dependent on oxygen delivery in patients on IL-2 therapy. The presence of oxygen supply dependency may contribute to the multiple organ failure observed with IL-2 administration.

Adult↗
PubMed1988

Factors associated with fatal hemoptysis in cancer patients.

We reviewed the clinical outcome of 58 patients with hemoptysis associated with either a hematologic or solid malignancy. Pulmonary hemorrhage causing death (fatal hemoptysis) occurred in 36 percent of these patients. Fatal hemoptysis occurred in six of eight patients with a hematologic malignancy and a fungal pneumonia. Examination of pathologic specimens from five of these patients revealed fungal invasion of blood vessels. An inflammatory response was absent in three, suggesting that granulocytes are not required for fungal-induced tissue destruction. In patients with a bronchogenic tumor, fatal hemoptysis occurred in six of seven patients with a necrotic squamous cell carcinoma. In contrast, hemoptysis was fatal in only two of ten patients with metastatic lung disease. We conclude that hemoptysis in cancer patients with a fungal pneumonia is an ominous sign that may warrant aggressive interventions to prevent a fatal complication.

Aged↗
PubMed1986

Prevention of canine anaphylaxis with isoproterenol.

Sympathomimetic agents are used to reverse the cardiovascular and respiratory abnormalities that are associated with anaphylactic shock. In addition, in vitro studies have demonstrated that beta-adrenergic stimulation modulates IgE-mediated release of chemical mediators. To separately evaluate the ability of isoproterenol, a beta-adrenergic agonist, to prevent mediator release and anaphylactic shock, as well as to reverse the cardiopulmonary manifestations of systemic anaphylaxis, we administered a continuous infusion of isoproterenol before and during canine anaphylactic shock. An intravenous injection of Ascaris suum antigen was used to produce shock, which was characterized by a 50 +/- 15% (mean +/- SEM) decrease in mean arterial blood pressure, a 30 +/- 8% decrease in cardiac output, and a 122 +/- 95% increase in total pulmonary resistance. These changes were associated with significant increases in plasma histamine concentrations from 1.1 +/- 0.1 to 158.4 +/- 137 ng/ml. Administration of a continuous infusion of isoproterenol during anaphylactic shock did not significantly improve any of these physiologic abnormalities. However, when isoproterenol was administered prior to the injection of antigen, these physiologic changes were prevented and histamine release was inhibited in a significant proportion of animals. In contrast, beta-adrenergic stimulation did not prevent nonimmunologic shock and mediator release induced with compound 48/80. We conclude that the administration of a beta-adrenergic agonist prevented the cardiopulmonary manifestations of anaphylactic shock by inhibiting mediator release and that the physiologic effects of isoproterenol administered during systemic anaphylaxis were minimal.

Airway Resistance↗
PubMed1984

Hemodynamic changes in human anaphylaxis.

Human anaphylactic reactions are usually unexpected and catastrophic. Therefore, opportunities to record the physiologic changes that occur are uncommon. A patient is described who experienced an anaphylactic reaction to a penicillin drug while being monitored in an intensive care unit for ischemic heart disease. Hemodynamic monitoring indicated that the decrease in cardiac output was most likely due to a decrease in venous return. In addition, this patient's previous reactions to other penicillins demonstrated that variations in the clinical manifestations of systemic anaphylaxis can occur within the same person.

Aged↗