Cardiovascular and pulmonary responses to Pichinde virus infection in strain 13 guinea pigs.

In fatal human Lassa fever, severe hypotension, circulatory shock, and pulmonary edema develop as terminal events. We examined cardiovascular and respiratory functions in strain 13 guinea pigs infected with Pichinde virus, an animal model for studying human Lassa fever. Cardiovascular functions were studied in anesthetized and conscious guinea pigs, whereas pulmonary functions were measured only on animals under anesthesia. In anesthetized animals, cardiovascular disturbances were severe and progressive from postinoculation day (PID) 10. Cardiac output, measured by thermodilution, decreased 28 to 53% below baseline values from PID 10 to 12 and was accompanied by a gradual reduction of mean arterial blood pressure and heart rate. Although left ventricular systolic pressure decreased significantly, the left ventricular +dp/dtmax and -dp/dtmax decreased only slightly on PID 12. Similar depressed cardiovascular responses were observed in conscious animals infected with Pichinde virus. Changes included decreased cardiac output, heart rate, cardiac work, cardiac power, and stroke volume, as well as increased total peripheral resistance and prolonged mean transit time. We postulate that a global cardiovascular dysfunction with the involvement of right and left sides of the heart may be the main cause of irreversible circulatory deterioration and death during Pichinde virus infection in strain 13 guinea pigs.