CARDIOVASCULAR AND PULMONARY RESPONSES TO PICHINDE VIRUS-INFECTION INSTRAIN-13 GUINEA-PIGS

In fatal human Lassa fever, severe hypotension, circulatory shock, and pulmonary edema develop as terminal events. We examined cardiovascula r and respiratory functions in strain 13 guinea pigs infected with Pic hinde virus, an animal model for studying human Lassa fever. Cardiovas cular functions were studied in anesthetized and conscious guinea pigs , whereas pulmonary functions were measured only on animals under anes thesia. In anesthetized animals, cardiovascular disturbances were seve re 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 a rterial blood pressure and heart rate. Although left ventricular systo lic pressure decreased significantly, the left ventricular +dp/dtmax a nd -dp/dtmax decreased only slightly on PID 12. Similar depressed card iovascular 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 postul ate that a global cardiovascular dysfunction with the involvement of r ight and left sides of the heart may be the main cause of irreversible circulatory deterioration and death during Pichinde virus infection i n strain 13 guinea pigs.