Gastric response to severe head injury.
We studied the gastric response to severe head injury and multiple trauma in 53 patients admitted to the surgical intensive care unit at the University of Louisville. Twenty-two of the 32 patients with severe head injury could have endoscopy. Each patient had gastritis or duodenitis. Patients with severe head injury had a slightly higher rate of gastric acid secretion than did the other trauma patients without severe head injury, but the difference was not significant. Serum gastrin levels were normal in both groups and did not correlate with intracranial pressure. Pancreatic polypeptide levels were significantly higher in patients with severe head injury compared with the control trauma patients without head injury. Elevations in pancreatic polypeptide may be linked to increases in intracranial pressure. We conclude that erosive gastritis occurs commonly in patients with severe head injury and that severe head injury is associated with a marked increase in pancreatic polypeptide levels in the fasted, nongut-stimulated state. Gastrin levels are within normal limits. Head injury appears to specifically increase pancreatic polypeptide release, probably by influencing autonomic centers in the mid brain. Because the cephalic phase of pancreatic polypeptide release is vagalcholinergic, the data are consistent with the hypothesis that severe head injury increases vagal activity. Participation of vagal adrenergic fibers in this process cannot be excluded.
D000293:Adolescent; D000328:Adult; D000368:Aged; D006259:Craniocerebral Trauma / Q000503:physiopathology*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D006801:Humans; D007427:Intracranial Pressure; D008297:Male; D008875:Middle Aged; D010191:Pancreatic Polypeptide / Q000378:metabolism*; D013270:Stomach / Q000294:innervation; D014630:Vagus Nerve / Q000503:physiopathology
D010191:Pancreatic Polypeptide