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F C Monson

Publications and source records attributed to F C Monson.

30 records · Page 2Linked to original sources
PubMed1993

3H-thymidine uptake by the rat urinary bladder after induction of diabetes mellitus.

Streptozotocin-induced diabetes mellitus causes diuresis, increases in bladder mass and changes in micturition. Temporal changes in micturition and bladder mass after induction of diabetes with streptozotocin were monitored and correlated with DNA synthesis and 3H-thymidine incorporation. There were increases in water consumption, urine excretion, urinary frequency, and mean and maximal micturition volume within 1 day after induction of diabetes. These parameters reached maximal values within 6 to 11 days and were maintained at 30 and 60 days. Bladder mass was significantly elevated by 7 days and did not increase further with increasing duration of diabetes. DNA concentration was decreased in bladders from 4, 7 and 14 day diabetics. 3H-thymidine incorporation into DNA increased within 2 days after induction of diabetes, reached maximal values at 4 to 7 days and declined to control values by 14 days. Autoradiography showed intense labelling of the urothelium one day after induction of diabetes, with labelling remaining high up to day 7. Connective tissue and smooth muscle labelling were slower to develop. Labelling of smooth muscle was transient, appearing only on days 4 and 7. The time course of the events was consistent with the hypothesis that bladder distension or increasing micturition volume stimulates thymidine incorporation into DNA, resulting in an increase in bladder mass.

Animals↗
PubMed1993

The influence of acute overdistension on rat bladder function and DNA synthesis.

Prolonged micturition problems are often encountered after long-term bladder overdistension caused by urinary retention. In animal studies, damage to the bladder wall innervation has been found following overdistension. Experimentally, acute overdistension has also been implicated in the pathogenesis of the response to partial outlet obstruction. In the present study we investigated the influence of overdistension on micturition volume and frequency, on in vitro bladder function using the whole bladder model and on 3H-thymidine uptake, localization and DNA synthesis. Overdistension was induced for 3 hours by forced diuresis and balloon obstruction. Another group of rats was catheterized for 3 hours but received no diuretic, nor was the balloon inflated. An additional group of controls was neither anesthetized nor catheterized. Overdistension caused a gradual increase in bladder mass which was maximal at 7 days. During the first 24 hours following overdistension, the frequency of micturition decreased, but normalized thereafter. A progressive decrease in the response to field stimulation was noted between 16 hours and 7 days following overdistension and remained at this level until 21 days. There were, however, no significant differences in the responses to carbachol, ATP and KCl. There was a 30% reduction in the ability of field stimulation to empty the bladder 16 hours after overdistension, but no impairment of the emptying ability of carbachol. Overdistension was followed by a significant increase in 3H-thymidine uptake, which was maximal at 2 days. 3H-thymidine labelling increased rapidly after overdistension and was maximal within 16 hours in the urothelium. In smooth muscle, connective tissue and lamina propria, maximal labelling occurred at 2 days. Catheterization alone caused a mild distension which was associated with a small, but statistically significant, increase in 3H-thymidine incorporation into DNA within 16 hours. The labelling was located primarily in the urothelium. Overdistension causes a proliferative reaction within the bladder wall. Its initial effects occur within the urothelium, and the later involvement of the subendothelial smooth muscle and connective tissue is directly proportional to the degree of bladder distension. Three weeks following overdistension, the bladder's functional state was not completely recovered, although the urinary bladder was found to have a good capacity to adapt and compensate for the stress-induced changes caused by overdistension. It is, therefore, clear that overdistension may have long-lasting effects on the bladder.

Animals↗
PubMed1992

Effect of outlet obstruction on 3H-thymidine uptake: a biochemical and radioautographic study.

Experimental outlet obstruction in the rabbit is characterized by a rapid and substantial increase in urinary bladder mass. Although it is clear that both the smooth muscle and connective tissue compartments are increasing in mass, there is little information on the mechanisms by which this increase in mass occurs. As an initial investigation in this process, urinary bladders from normal and obstructed NZW rabbits were exposed in vitro to tritiated thymidine (3H-TdR) in order to determine which populations of cells are induced to synthesize DNA following outlet obstruction, and when, after obstruction, such synthesis occurs. Biochemical analysis of nucleic acids was performed on each specimen to determine total and radioactive DNA. These analyses showed a marked increase in DNA synthesis at 24 hours following obstruction which remained relatively high through seven days after obstruction. There was a decline in labelling at 14 days. Incorporation of radioactive label peaked at three days and declined to control levels by 14 days. Samples of tissue were taken from each subject and processed for radioautography. At 24 hours after obstruction, significant numbers of cells of the basal cell layer of the urothelium are observed to be actively involved in DNA synthesis, while the other two tissue compartments (muscularis and connective tissue) show no significant changes when compared to normal specimens. Connective tissue, on the other hand, showed significantly increased levels of labelling above control level from three to 14 days after obstruction. Smooth muscle cells were observed to be frequently labelled in only one of the experimental bladders observed three days after obstruction.

Animals↗
PubMed1992

Effects of acute in vitro overdistension of the rabbit urinary bladder on DNA synthesis.

Urinary bladder outflow obstruction induces a myriad of structural and functional changes in the organ. Among the morphological responses to outlet obstruction is both hyperplasia and hypertrophy of specific cellular elements. The initial event which has been implicated in the initiation of the response to outflow obstruction is an initial period of high intravesical pressure and subsequent distention of the bladder. In a previous study, it was shown that at one day following partial outlet obstruction there was a marked increase in thymidine labelling of the urothelium, at 3-5 days, the labeling shifted from the urothelium to the interstitial and serosal elements. The current study was designed to determine if acute distention of the urinary bladder can induce an increase in DNA synthesis (3H-thymidine incorporation), and localize the increased DNA synthesis via autoradiography of 3H-thymidine. In this study, the bladders of adult male New Zealand white rabbits were mounted in isolated in vitro baths. Each control bladder was filled to either 5 or 20 ml. with saline, or distended to 120% of capacity. The bladders were incubated for 7 hours at which time 3H-thymidine was placed both within and outside the bladder for an additional one hour. At the end of the time the bladder was divided at the ureteral orifices into bladder body and base, and each body and base divided into two sections. One section of bladder body and base was quantitatively analyzed for both labelled and unlabelled DNA; the second section was fixed and prepared for autoradiography. The results can be summarized as follows: 1) Acute overdistention for 8 hours induced a slight decrease in the DNA concentration which was mediated by edema of the bladder wall. 2) Acute overdistention induced a 5-fold increase in 3H-thymidine incorporation in the bladder body and a 3-fold increase in the bladder base. Radioautoradiography of the overdistended bladders showed significant and substantial labelling which was confined to the urothelial basal cells. The control bladders showed little or no labelling. These results are consistent with the theory that acute distention following partial outlet obstruction initiates the proliferative response of the bladder to outlet obstruction, and the urothelium is the initial target of the proliferative response. Functionally, the proliferative response may serve to maintain the structural as well as functional integrity of the bladder.

Animals↗
PubMed1991

Indigocarmine as a quantitative indicator of urothelial integrity.

There is increasing evidence that the urothelium of the bladder mucosa prevents the penetration of solutes from the urine into the bladder wall. In the current study, in vivo treatments of rabbit urinary bladder with DMSO, acetone and overdistension resulted in damage to the physical integrity of the bladder mucosa as quantitated by the penetration of the dye indigocarmine (1% in saline) into submucosal tissues. Penetration of the dye can be quantitated, because the dye can be extracted from the tissue and measured spectrophotometrically. Indigocarmine does not penetrate normal, control, bladder mucosae. Bladders treated with gentle 20, 30 and 50% acetone washes for one minute permit dye penetration which is proportional to the acetone concentration utilized. Intravesical 50% DMSO ("RIMSO 50") administration permits modest dye penetration. Distension by slow filling with saline to volumes 90% of capacity and greater causes a marked increase in dye penetration which is proportional to the magnitude of overdistension. Although pretreatment of the bladder with heparin did not reduce the dye penetration following acetone administration, it completely abolished penetration of the dye following overdistension. Indigocarmine is potentially useful as both a quantitative and qualitative indicator of bladder mucosal integrity.

Animals↗
PubMed1990

Effect of bladder outlet obstruction on the morphology, physiology, and pharmacology of the bladder.

Bladder outlet obstruction secondary to benign prostatic hyperplasia induces numerous changes in bladder morphology, physiology, and pharmacology. These changes have been studied experimentally in various animal models, and while each species has advantages and disadvantages, it is unclear which is most like man. It has been shown that tissue hypertrophy leading to an increase in tissue mass develops rapidly after bladder outlet obstruction. Ischemia induced by the obstruction results in acute muscle dysfunction. The degree of functional impairment is directly related to the degree of tissue hypertrophy. However, the bladder contractile apparatus appears to have a surprising regenerative ability, such that recovery of bladder function becomes obvious 14 days after obstruction. Urodynamic changes include an increase in urinary frequency and voiding pressure and a decrease in voided volume. Clinically, involuntary bladder contractions are often present. Determination of which of these specific aspects of outlet obstruction the investigator is interested in studying will dictate the selection of the most appropriate animal model.

Animals↗
PubMed1990

Diagnosis of interstitial cystitis.

We reviewed clinical and histological findings in 55 patients with interstitial cystitis and 21 with voiding dysfunction secondary to other pathological conditions. Of our interstitial cystitis patients 36% would fail to meet the research definition proposed at a recent National Institutes of Health workshop. Detrusor mastocytosis was present in 64% of our interstitial cystitis patients compared to 80% of the noninterstitial cystitis group. There was no statistically significant difference in mean detrusor mast cell counts between interstitial cystitis and noninterstitial cystitis patients. Biopsies of 12 patients who did meet the proposed National Institutes of Health research definition were evaluated by immunohistochemical techniques. Early results are inconclusive. These studies indicate that interstitial cystitis is a complex disease whose diagnosis presently still must be made from a symptom complex rather than from objective histological criteria, including mastocytosis or the presence of any specific immunoreactive cell.

Cell Count↗
PubMed1990

The functional effects of long-term outlet obstruction on the rabbit urinary bladder.

The current study investigated the relationship between duration of outlet obstruction, magnitude of bladder mass, and functional dysfunction on the rabbit urinary bladder. Following the production of obstruction with the "cuff model", bladder wet weight increased to twice control weight within one week, and then slowly to four times control weight by one month, and remained at this level for the six month period. Bladder capacity decreased significantly by one week but returned to control volumes by one month. The in vitro ability of the bladder to empty in response to field stimulation and bethanechol decreased significantly in the one and two week obstructed bladders and remained decreased for six months. One of the major observations of this study was the relatively large variation of bladder weight and histology observed for the one to six month obstructed rabbits. Although the bladders with mild mass increase (less than 3 gm./kg. body weight) had normal distribution of urothelium and muscular elements, the bladders with moderate mass increase (3 to 6 gm./kg.) had thick extrinsic connective tissue deposits and the bladders with severe mass increase (greater than 6 gm./kg.) had thick extrinsic and intrinsic connective tissue deposits and muscular degeneration. The percentage occurrence of mild, moderate and severe mass increase was approximately the same (58%, 30% and 12%, respectively) for the one, three, and six month groups. The bladders with mild mass increase had normal bladder capacities and increased pressure responses to field stimulation and bethanechol. The bladders with moderate-to-severe mass increase showed enlarged bladder capacities and had progressively smaller pressure responses. As the magnitude of bladder mass increased, the ability of the bladder to empty in response to field stimulation and bethanechol decreased proportionally. We conclude that the functional impairment of the bladder is related to the amount of extrinsic and intrinsic connective tissue and the degree of muscle degeneration.

Adenosine Triphosphate↗
PubMed1989

Effect of chronic ischemia on glucose metabolism of rabbit urinary bladder.

The effect of chronic ischemia on glucose metabolism of the rabbit urinary bladder was studied. Unilateral ischemia was produced by ligation of one of the two vesical arteries which supply the rabbit bladder. Two weeks after the operation, the in vitro glucose metabolism of normal bladder tissue was compared to the glucose metabolism of tissue isolated from both the ischemic side and contralateral (non-ischemic) side of the ischemic bladder. The results can be summarized as follows: 1) ischemic and contralateral side bladder tissues contained less glycogen than normal; 2) glucose utilization was higher in the ischemic and contralateral side tissues; 3) ischemic and contralateral side tissues incorporated more glucose into lactate and produced more total lactate than normal tissues; 4) whereas contralateral side tissue produced more 14CO2 than ischemic side tissue, the ability of normal bladder tissue to form 14CO2 is significantly higher than both ischemic and contralateral side tissues; 5) the degree of reduced CO2 production correlated well with previous studies on the contractile response of smooth muscle strips isolated from the ischemic and contralateral sides, and the reduced functional ability of the in vitro whole bladder to empty; 6) histologically, smooth muscle degeneration and necrosis is only present on the ischemic side of the bladder although the contralateral side shows signs of generalized degeneration and edema. In general, we conclude that although only the ischemic tissue demonstrated major smooth muscle degeneration and necrosis, unilateral ischemia resulted in marked alterations in glucose metabolism on both the ischemic and contralateral sides.

Animals↗
PubMed1988

Effect of chronic nitrofurantoin on the rabbit urinary bladder.

Interstitial cystitis is a pathological condition whose symptoms mimic urinary tract infection and include urgency, frequency, and moderate to severe pain. Many more women than men are affected, with antibiotic therapy being the usual first treatment approach based on symptomology. Some clinicians believe that chronic antibiotic therapy may play an etiological role in interstitial cystitis; however neither clinical nor experimental data support their opinion. The implied pathogenesis of antibiotic injury is an alteration of the bladder mucosa and its protective mucin coating to allow urine-mediated damage to the bladder wall. The purpose of this study is to evaluate rabbit urinary bladder function and morphology during chronic nitrofurantoin administration. The results demonstrate that up to twelve months of chronic nitrofurantoin administration produce no changes in 1) bacterial adherence to the rabbit bladder mucosa, 2) specific antibacterial adherence activity of the bladder mucin, and 3) ultrastructure of the mucosa, submucosa, and muscularis.

Animals↗
PubMed1988

The effects of short-term in-vivo ischemia on the contractile function of the rabbit urinary bladder.

The proper functioning of any smooth muscle requires adequate perfusion with oxygen and nutrients. Ischemia compromises both these factors and results in dysfunction, the extent depending on the degree and duration of ischemia. This study determined the effects of one, two and four weeks in vivo ischemia on the capacity, compliance and contractile function of the rabbit urinary bladder. Morphological changes were also studied with light microscopy. Different degrees of ischemia were achieved as follows. In the unilateral group the vesical artery was tied on one side and the animals were sacrificed at one week or two weeks. In the bilateral group the vesical arteries on both sides were tied and the animals were sacrificed one week later. In the bilateral staged group the vesical artery was tied on one side and after one week the contralateral artery was ligated, and the animals sacrificed one week after the second procedure. Muscle strips were studied for contractile response, with a distinction being made between the ipsilateral and contralateral side of vessel ligation in the unilateral group. The results were as follows. 1) In the unilateral group there was a 72% reduction in the contractile response of the dome of the bladder to bethanecol on the side of vessel ligation and a 32% reduction on the contralateral side. The response to methoxamine on the base was reduced by 44%, with no difference between the ipsilateral and contralateral side. 2) Bilateral vessel ligation resulted in a 97% reduction in contractile response to bethanechol on the dome and a 75% in the response of the base to methoxamine. 3) Staged bilateral ligation resulted in a 69% reduction in the contractile response of the dome to bethanechol and a 18% reduction in the response of the base to methoxamine. Ischemia caused a marked reduction in the compliance and capacity of the bladder in all the three groups, with the most marked changes in the bilateral group. Multiple spontaneous contractions were noted in the three groups during the filling phase of the cystometrograms. Histological features correlated well with the functional changes in the different groups.

Animals↗