PULMONARY HYPERTENSION(P-HTN) FOLLOWING BOLUS INFUSIONS OF PNEUMOCOCCUS(PNEU), OTHER GRAM+(GM+) BACTERIA, AND ZYMOSAN

Abstract

Group B Strep(GBS) infusions cause acute P-HTN in several animal models. This response includes increased pulmonary artery pressure (Ppa), and resistance (PVR), and decreased pulmonary flow; systemic flows are often decreased. We infused a bolus of PNEU in 2, <2-wk-old, acutely-operated, anesthetized lambs and found that P-HTN occurred. We then studied this effect in 2 unanesthetized, chronically-instrumented piglets, <1 mo. old. Infused bacteria were heat-killed, washed and resuspended in buffer. The pigs received 1 item/day at 3-4.5 × 10⁹ particles/dose. Qualitatively similar severe P-HTN resulted from bolus infusions of all PNEU strains tested (P1, P14, and P23) also from Group E, Group G, and a nontypeable Group B Strep, Staph aureus, and zymosan. Agitation, cyanosis, systemic hypotension, bradycardia and seizures also occurred. Latex particles, similar size as bacteria, had no effect at this dose. A mild, transient rise in Ppa and PVR was noted after a double dose, suggesting that a quantity of particles alone doesn't produce the same P-HTN. Indomethacin blocked the P-HTN caused by PNEU. We conclude that P-HTN is a nonspecific host response that can be elicited by a variety of GM+ bacteria. Agent(s) that may trigger the response are not unique to GBS or endotoxin. Cyclooxygenase pathway products appear to mediate this P-HTN which may be clinically important in shock occurring with GM+ infections.

Log in or create a free account to read this content

Gain free access to this article, as well as selected content from this journal and more on nature.com

Access through your institution

or

Sign in or create an account

Continue with Google

Continue with ORCiD