Possible Involvement of Endogenous β-Endorphin in the Pathophysiological Mechanisms of Pichinde Virus-Infected Guinea Pigs 1

Abstract

Previously, we demonstrated that naloxone, an opiate antagonist, prolonged survival of strain 13 guinea pigs infected with Pichinde virus. Thus, endogenous opiates may be involved in the pathogenesis of this viral disease. To determine whether endogenous opiate levels were affected by Pichinde viral infection, β-endorphin concentrations in plasma and cerebrospinal fluid (CSF) of normal and infected strain 13 guinea pigs were measured by radioimmunoassay. Cerebrospinal fluid β-endorphin concentrations were 78.0 ± 13.2 pg/ml on postinoculation day (PID) 7, 59.0 ± 5.6 pg/ml on PID 12, and 58.8 ± 5.4 pg/ml on PID 14. These values were significantly higher than baseline levels of CSF β-endorphin: 30.8 ± 1.9 pg/ml. Plasma β-endorphin concentrations of infected animals increased significantly to 202.1 ± 17.9 pg/ml on PID 7 and to 154.2 ± 21.4 pg/ml on PID 12 from a mean baseline value of 84.2 ± 13.1 pg/ml. After a primer intravenous injection of β-endorphin (10, 15, or 30 μg/kg), followed by constant infusion of β-endorphin (15, 45, or 90 μg/kg-hr) to control noninfected guinea pigs, heart rate (except with the lowest dose) and mean blood pressure decreased markedly. Under these experimental conditions, concentrations of plasma and CSF β-endorphin increased simultaneously with different magnitude. Because both Pichinde viral infection and β-endorphin administration produced a similar trend of cardiovascular disturbances, leading to hypotension and bradycardia, increased concentrations of plasma and CSF β-endorphin may play a partial role in the pathophysiological mechanisms of Pichinde virus infection.