Effects of Streptozotocin-Induced Diabetes on Bladder Function in the Rat

Abstract

Streptozotocin-induced (STZ, 60 mg./kg. I.V.) diabetic male rats underwent cystometrographic (CMG) and electrophysiologic evaluations under urethane anesthesia (1.2 gm./kg.) to determine whether the neural pathways to the urinary bladder are altered in these animals. Diabetic rats (n = 6) in comparison to controls (n = 8) had significantly greater micturition volumes (3.0 +/- 0.8 ml. vs. 0.7 +/- 0.4 ml., p less than 0.001), bladder compliances (0.51 +/- 0.15 cm. H2O/ml. vs. 0.12 +/- 0.09 cm. H2O/ml., p less than 0.001) and bladder weights (225.2 +/- 21.4 mg. vs. 112.2 +/- 18.0 mg., p less than 0.01). No differences were noted in: 1) the thresholds or conduction velocities of axons in the bladder postganglionic nerves, 2) transmission in the major ganglion or 3) the latencies for firing in the supraspinal parasympathetic reflex pathway to the bladder. However, the supraspinal reflex, which was facilitated by bladder distension in 38% of control rats, was not facilitated in any diabetic rats. Another apparent difference in diabetic rats was the absence of spinal reflex response which was noted in 38% of control animals. This study confirmed that CMG changes in STZ-induced diabetic rats are similar to those observed clinically in patients with diabetic autonomic neuropathy, and in addition raise the possibility that these changes are produced by a defect in autonomic reflexes. It is also clear that alterations of the micturition reflex pathway in diabetic rats are distinct from those associated with another type of enlarged, abnormal bladder induced by bladder outlet obstruction.

Protective effect of cyanidin‐3‐O‐β‐D‐glucopyranoside fraction from mulberry fruit pigment against oxidative damage in streptozotocin‐induced diabetic rat bladder

“…In practice, the functional studies in STZ rat model have demonstrated a relationship between polyuria and alterations in bladder volume, rate of filling, and bladder stretching. Increased bladder work and distension leads to progressive remodeling and deterioration of the bladder 35, 36…”

Nitrergic relaxations and phenylephrine contractions are not compromised in isolated urethra in a rat model of diabetes

“…This suggests deficits in the upstream neuronal pathways innervating the urethra. In support for this, histological (size of cell bodies), neurochemical (reduction of Substance P, increase in NGF, and other peptides) and functional (ion channels) alterations in the primary afferent neurons in the dorsal root ganglia and/or efferent neurons in the major pelvic ganglia have been previously reported (Santicioli et al, 1987;Steers et al, 1990Steers et al, , 1994Sasaki et al, 2002;Yang et al, 2008). In addition, recent findings investigating synaptic transmission in the major pelvic ganglion of the obese type 2 diabetic mice identified altered pre-synaptic regulation of transmitter release (Tompkins et al, 2013).…”

Decreased urinary bladder apoptosis in a rabbit model of diabetes mellitus

“…Morphological, histological and functional alterations in autonomic neurotransmission have been reported in diabetes [9]. In addition, there is evidence that diabetes is associated with increased bladder weight [12]. This is thought to be secondary to diabetes-induced diuresis, which, in turn, leads to increased bladder weight [12].…”

“…In addition, there is evidence that diabetes is associated with increased bladder weight [12]. This is thought to be secondary to diabetes-induced diuresis, which, in turn, leads to increased bladder weight [12]. The increase in bladder weight has, in itself, been attributed to increased cellular proliferation, in particular, urothelial cell proliferation [5].…”

“…In addition to this effect, it has been demonstrated in a rat model of diabetes that there is a time-dependent increase in bladder distension/increased micturition volume, which stimulates thymidine incorporation into DNA. This is an indication of increased cellular proliferation, leading in increased bladder weight [12].…”