The pathophysiology of postictal pulmonary edema was investigated by inducing seizures with bicuculline in nine paralyzed, halothane-anesthetized sheep and measuring of pulmonary lymphatic flow, pulmonary arterial and left atrial pressures, and lymph and plasma albumin concentration. Pulmonary microvascular pressure and transcapillary albumin conductance were calculated. Seizures transiently (less than 15 min) elevated microvascular pressure in all animals; lymph flow increased greater than twofold in response to the increased hydrostatic driving force. However, the elevation in lymph flow, with a stable lymph-to-plasma protein ratio and doubled transcapillary albumin conductance, persisted for the duration of the experiment, more than 3 h after microvascular pressure returned to base line. These changes were neurally mediated because they were blocked by cervical spinal cord transection in four additional animals.
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