Post-prostatectomy syndrome (PPS) is characterized by hyponatremia aft
er absorption of glycine irrigant. To study the pathogenesis of this s
yndrome, adult male rats with ligated ureters were infused over 15 min
utes with 7.5 ml/100 g body weight of isosmotic glycine (N = 9) or man
nitol (N = 9) and were compared to non-infused, ureter-ligated control
s (N = 9). Immediately post-infusion, plasma sodium had decreased simi
larly in glycine- and mannitol-infused animals (111 +/- 2 vs. 106 +/-
1 mmol/liter), but plasma osmolality remained at control levels in bot
h groups (285 +/- 1 vs. 288 +/- 1 mOsm/kg). Two hours post-infusion, h
yponatremia was stable in the mannitol group (108 +/- 1 mmol/liter), b
ut in the glycine group plasma sodium increased significantly (to 120
+/- 1 mmol/liter). Plasma osmolality two hours post-infusion was maint
ained in both the glycine (287 +/- 2) and mannitol (292 +/- 2) groups.
Brain water in glycine-infused animals (3.90 +/- 0.01 liter/kg dry wt
) was not significantly different from the mannitol-infused group (3.8
5 +/- 0.01) and only 1.8% higher than non-infused controls (3.83 +/- 0
.02). Brain tissue glycine did not differ between the three groups. In
contrast, muscle water two hours post-infusion in the glycine group w
as 6% higher than mannitol-infused and 13% higher than non-infused ani
mals. Muscle glycine content in the glycine group (67 +/- 4 mM/kg dry
tissue) was increased when compared to both mannitol-infused (25 +/- 1
) and non-infused (20 +/- 1) groups. Plasma ammonia and brain glutamin
e were significantly increased in glycine-infused animals. In a second
set of studies, infusion of 7.5 ml/100 g body weight of 1.5% (200 mmo
l/liter) glycine caused only a non-significant increase in brain water
. In conclusion, in a model of PPS in rats, acute hyponatremia induced
by intravenous isosmotic glycine did not decrease plasma osmolality.
Hyponatremia induced by isosmotic or hypoosmotic glycine caused minima
l brain edema.