Prostanoid production and pulmonary hypertension after fat embolism are not modified by methylprednisolone

Abstract

Biliateral cemented arthroplasty (BCA) in anaesthetized mongrel dogs produces paniculate fat and marrow embolism of the lung. Methylprednisolone sodium succinate (MPSS) has been advocated for post-traumatic fat embolism to prevent acute lung injury. We used the BCA procedure to produce acute fat and marrow embolism, and tested the efficacy of MPSS (30 mg · kg-1) in preventing physiological and pathological markers of acute lung injury. Dogs (n = 6) pre-treated with MPSS demonstrated similar acute increases in pulmonary artery pressure (PAP) within one minute of BCA (17.8 ± 7.3 mm Hg) as the untreated (control n = 7) dogs (18.6 ± 12.6). Pulmonary vascular resistance (PVR) increased to the same degree in both groups (455 ± 323 and 319 ± 137 dyne · sec · cm-5) and PaO2 decreased by 18.3 ±6.4 mmHg in the control group as opposed to 12.4 ± 7.7 mmHg in the MPSS group within five minutes of BCA. Circulating arterial and mixed venous plasma concentrations of thromboxane B2 (TxB2) increased within one minute of BCA in both groups with no increase in the transpulmonary gradient. Arterial plasma 6-keto prostaglandin Flα (6-keto PGFlα) increased (0.91 ± 0.29 ng · ml-1 and 0.87 ± 0.43 ng · ml-1) in both groups one minute after BCA. Mixed venous 6-keto PGFlα plasma concentration also increased, but a significant transpulmonary 6-keto PGFlα gradient was found. We conclude that acute fat and marrow embolism after BCA is associated with increased levels of TxB2 and 6-keto PGFlα. The source of the 6-keto PGFlα after acute pulmonary fat embolism is the lung and neither the acute haemodynamic changes nor the prostanoid response are inhibited by MPSS. © 1991 Canadian Anesthesiologists.