Urology · 1999
Demonstration of a "renogastric reflex" after rapid distension of renal pelvis and ureter in nonanesthetized patients.
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Shafik A
Аннотация
OBJECTIVES: Renal or ureteral diseases are often associated with nausea, vomiting, and abdominal pain. The aim of the current study was to investigate the cause of gastric manifestations that accompany renoureteral disorders.
METHODS: A 3F balloon-tipped catheter was introduced by means of a flexible cystoscope into the renal pelvis of 14 healthy volunteers (mean age 38.6 years; 10 men, 4 women), and the effect of rapid and slow renal pelvic and ureteral distension on the pyloric sphincter, gastric corpus, lower esophageal sphincter, and esophagus was recorded. The renal pelvis and ureter were then anesthetized and the tests repeated.
RESULTS: Rapid renal pelvic distension effected a significant rise in pressure in the renal pelvis at the 6-mL distension and above and in the pyloric sphincter at 10 and 1 2 mL. Loin and epigastric pain as well as nausea in all subjects and vomiting in 5 occurred at the 10 and 1 2-mL distensions. Slow renal pelvic distension caused a renal pelvic pressure rise at the 8-mL distension and above but no pressure changes in the pyloric sphincter or gastric corpus; loin pain, but not nausea or vomiting, occurred. Rapid ureteral distension at 1 mL was associated with loin and epigastric pain in all subjects and vomiting in 3. No epigastric pain, nausea, or vomiting occurred with slow ureteral distension. Renal pelvic or ureteral distension, slow or rapid, caused no pressure changes in the lower esophageal sphincter or esophagus. Distension of the anesthetized renal pelvis or ureter effected no gastric or esophageal pressure changes and no nausea or vomiting.
CONCLUSIONS: The study demonstrated the possible existence of a reflex relationship between the distension of the renal pelvis and ureter and the pressure of the pyloric sphincter. This reflex effect was reproducible and did not occur when the anesthetized renal pelvis or ureter was distended. We call this reflex relationship the "renogastric reflex" and suggest that it explains the cause of gastric manifestations that might occur with renoureteral disorders.
METHODS: A 3F balloon-tipped catheter was introduced by means of a flexible cystoscope into the renal pelvis of 14 healthy volunteers (mean age 38.6 years; 10 men, 4 women), and the effect of rapid and slow renal pelvic and ureteral distension on the pyloric sphincter, gastric corpus, lower esophageal sphincter, and esophagus was recorded. The renal pelvis and ureter were then anesthetized and the tests repeated.
RESULTS: Rapid renal pelvic distension effected a significant rise in pressure in the renal pelvis at the 6-mL distension and above and in the pyloric sphincter at 10 and 1 2 mL. Loin and epigastric pain as well as nausea in all subjects and vomiting in 5 occurred at the 10 and 1 2-mL distensions. Slow renal pelvic distension caused a renal pelvic pressure rise at the 8-mL distension and above but no pressure changes in the pyloric sphincter or gastric corpus; loin pain, but not nausea or vomiting, occurred. Rapid ureteral distension at 1 mL was associated with loin and epigastric pain in all subjects and vomiting in 3. No epigastric pain, nausea, or vomiting occurred with slow ureteral distension. Renal pelvic or ureteral distension, slow or rapid, caused no pressure changes in the lower esophageal sphincter or esophagus. Distension of the anesthetized renal pelvis or ureter effected no gastric or esophageal pressure changes and no nausea or vomiting.
CONCLUSIONS: The study demonstrated the possible existence of a reflex relationship between the distension of the renal pelvis and ureter and the pressure of the pyloric sphincter. This reflex effect was reproducible and did not occur when the anesthetized renal pelvis or ureter was distended. We call this reflex relationship the "renogastric reflex" and suggest that it explains the cause of gastric manifestations that might occur with renoureteral disorders.