Participation of regional sympathetic outflows in the centrogenic pulmonary pathology

In anesthetized and vagotomized rats, a mechanical cerebral compression (CC) evoked systemic arterial hypertension (SAH) and pulmonary venous hypertension (PVH) followed by massive pulmonary hemorrhagic edema (PHE). The hemodynamic and pulmonary changes induced by CC were more pronounced in the right heart bypass (RHB) preparation (venous return to reservoir and constant pulmonary inflow). Additional observations in RHB included a marked reduction in reservoir volume (RV) without significant change in pulmonary vascular resistance (PVR). In either natural circulation or RHB, an upper thoracic sympathectomy did not affect the SAH, RV reduction, and PVR change, but reduced the PVH and PHE by approximately one-third. Such effects were not attributed to cardiac denervation, because beta 1-adrenergic blockade (metaprolol) did not alter the CC-induced PHE. Splanchnic denervation greatly diminished the SAH and prevented the RV reduction, PVH, and PHE. The results suggest that the centrogenic PHE is initiated from an intense arteriolar constriction, principally in the splanchnic beds. The latter causes left heart failure leading to volume and pressure loading and blood loss in the lungs. Direct sympathetic impulses to the lungs do not affect the PVR and RV changes and are not essential for the genesis of PHE. However, they may alter the vascular compliance and thereby exacerbate the PVH and PHE when passive accumulation of blood is produced in the lungs.