Neural Structures Involved in the Genesis of ‘Preoptic Pulmonary Edema,’ Gastric Erosions and Behavior Changes

Abstract

Lung edema resulting from preoptic lesions in rats, previously described by Gamble and Patton, was further studied. Mid-line lesions dorsal to the chiasm cause lung edema more consistently than the lateral preoptic lesions described by Gamble and Patton. Vagotomy does not prevent development of lung edema following preoptic lesions. Cervical spinal transection, however, completely prevents development of preoptic lung edema. The evidence suggests that edemagenic impulses traverse the sympathetic outflow, but their effector organs are unknown. Hypothalamic transections dorsal to the chiasm cause lung edema and increased running. Similar transections 1–3 mm caudal to the chiasm are ineffective. Indeed, mid-line lesions in the caudal hypothalamus prevent development of lung edema and hyperactivity when preoptic lesions are inflicted. The evidence suggests that ‘preoptic pulmonary edema’ is a release phenomenon, and that the edemagenic impulses arise from postchiasmatic hypothalamic structures which are normally held in abeyance by the preoptic region. Hemorrhagic gastric erosions were sometimes observed in animals autopsied after preoptic lesions. Neither spinal transection nor caudal hypothalamic lesions diminish the incidence of gastric lesions. Vagotomy, however, prevents development of gastric lesions following preoptic lesions.