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F C Monson

Publications and source records attributed to F C Monson.

At least 19 recordsLinked to original sources

Evidence for a unique elastic sheath surrounding the vesicular arteries of the rabbit urinary bladder--studies of the microvasculature with microscopy and vascular corrosion casting.

Because the urinary bladder stores and releases urine, its normal function includes filling and emptying, accompanied by distension and relaxation. It is known that chronic distension compromises blood flow. Recent studies of the rabbit bladder vasculature have described specializations of that vasculature that appear to enhance blood flow in the bladder wall during distension. The present report describes the location, orientation, and structure of an elastic sheath surrounding the vesicular arteries, which may represent one of these specializations. The location, vasculature, and structure of an accessory elastic sheath surrounding the vesicular arteries of the rabbit bladder is described using light and electron microscopy, India ink injection, and vascular corrosion casting. The common iliac arteries of rabbits were cannulated to permit perfusion of the distal vasculature including the urinary bladder. After the bladder vasculature was visually cleared of blood by perfusion with buffered saline, one of the following procedures was used: 1) for light or electron microscopy, the bladder was perfuse-fixed with buffered 2% glutaraldehyde; 2) the bladder vasculature was filled with India ink for vessel tracing; or 3) corrosion casts of the bladder vasculature were prepared by infusion of a Mercox resin mixture. Casts, cleaned of tissue with KOH, and water and formic acid rinses, are dried, and mounted for routine scanning electron microscopy. The presence of an accessory sheath surrounding the main vesicular arteries and some of their branches in the basal two thirds of the urinary bladder was observed on India ink injected specimens and confirmed by micrographs and vascular corrosion casts. The sheath consists of elastic and collagenous fibers and is separated from the tunica media of the arteries by a loose connective tissue layer of variable width. The sheath is circumscribed by a layer of fine blood vessels. The vesicular arteries undulate within the sheath to an extent which is dependent upon the degree of distension of the bladder. This sheath likely represents a specialization which permits the bladder vasculature to accommodate expansion and contraction of the wall during normal filling and emptying. Undulations or coiling of the vesicular arteries within the loose connective tissue core of the sheath increase with bladder contraction, and apparently the sheath simply holds the artery in position during such coiling. The sheath, may represent a modification of the external elastic lamina found in some muscular arteries.

Animal Structures

Structure and blood supply of intrinsic lymph nodes in the wall of the rabbit urinary bladder--studies with light microscopy, electron microscopy, and vascular corrosion casting.

The urinary bladder is especially subject to infection by virtue of its direct connection to the external urethral opening, and it is natural to anticipate the presence of a well-developed immunological mechanism to respond to this potential threat. The present study describes small, very highly vascular lymph nodes located in the wall of the rabbit bladder, which may be involved in a local response to foreign antigens. The vasculature and structure of these lymph nodes was described using a combination of vascular corrosion casting, ink injection, and light and electron microscopy. The distal abdominal aorta was cannulated, and after clearing the bladder vasculature with buffered saline, one of the following procedures was used: 1) the bladder was perfuse-fixed in preparation for light and electron microscopy; 2) the bladder vasculature was filled with India ink for vessel tracing; or 3) vascular corrosion casts of the vasculature were prepared by infusing resin comprised of a mixture of Mercox, methyl methacrylate monomer, and catalyst. The resulting casts were cleaned with KOH, formic acid, and water in preparation for scanning electron microscopy. Vascular casts and India ink injections revealed the presence of a number of isolated capillary tufts consisting of clusters of one to five "glomeruli," closely associated with the major vesicular vessels along the lateral walls of the bladder, and supplied by tertiary branches of these vessels. Light and electron microscopy showed that the capillary tufts represented the blood supply to small, ovoid lymph nodes located near the serosal surface of the bladder wall and usually restricted to the basal half of the bladder. These nodes were encapsulated and exhibited subcapsular sinuses, numerous small blood vessels, a limited number of high endothelial cells, and, occasionally, nerves and a follicular substructure. The nodes contained abundant lymphocytes, stellate stromal cells, macrophages, and eosinophils, but lacked the obvious cortical and medullary organization and germinal centers often seen in larger lymph nodes. Vascular corrosion casts, vascular ink injections, and microscopic examination confirmed the presence of small, highly vascular lymph nodes closely associated with the main vesicular vessels along the lateral walls of the rabbit bladder. A follicular substructure of the nodes appears to correspond with the "glomerular" capillary arrangement within the nodes as seen with corrosion casts. The rich blood supply may be indicative of the high metabolic demand of lymphatic tissue, and may be altered in response to the level of activity of the node. The close association between the lymphatic tissue and the rich blood supply to the nodes may allow a rapid mobilization of lymphocytes during a local immune response to foreign agents.

Animals

Partial bladder outlet obstruction in the fetal rabbit.

PURPOSE: We developed and tested an animal model of bladder dysfunction due to posterior urethral valves using partial outlet obstruction of the fetal rabbit bladder. MATERIALS AND METHODS: Partial bladder outlet obstruction of fetal rabbit bladders was created on day 23 of gestation. Of the litter of 8 to 10 fetuses half was obstructed and the remainder served as controls. The doe and fetuses were sacrificed on day 30 of gestation (full term 31 to 32 days) and the fetal bladders were removed. Bladders that had doubled in weight from the average bladder weight of the control littermates were deemed sufficiently obstructed. Hematoxylin and eosin staining was performed and bladder strip response to 32 Hz. field stimulation, 200 microM. bethanechol and 200 mM. potassium chloride was measured. RESULTS: Average body weight did not differ between the control and obstructed fetuses, indicating that surgery did not hinder fetal development. Hematoxylin and eosin staining confirmed smooth muscle cell hypertrophy and increased connective tissue in the obstructed bladders. Obstructed bladder strips responded significantly less to field stimulation, and significantly more to bethanechol and potassium chloride (mean plus or minus standard deviation 5.18 +/- 1.52, 6.29 +/- 1.3 and 10.15 +/- 2.18 x force per/100 mg. tissue, respectively)than control bladder strips (9.0 +/- 1.19, 3.5 +/- 0.46 and 6.16 +/- 1.33 x force per/100 mg. tissue, respectively) suggesting that denervation supersensitivity may have resulted from obstruction. CONCLUSIONS: Partial outlet obstruction of the fetal rabbit bladder results in bladder hypertrophy and dysfunction but these changes are markedly different from those in the adult rabbit. Since rabbit fetal development is delayed compared to human fetal development, this model can be used to assess the consequences of posterior urethral valves.

Animals

Hyperplasia in the rabbit bladder urothelium following partial outlet obstruction. Autoradiographic evidence.

Previous experiments have shown that adult male rabbits subjected to partial outlet obstruction or overdistension and acutely labeled, 24 h later, in vivo or in vitro with 3H-Thymidine(3H-TdR) show high levels of incorporated radioactivity in bladder epithelium when they are visualized with autoradiography. To test the hypothesis that such labeling represents the onset of a wave of proliferation (that is, true hyperplasia), we injected 3H-TdR subcutaneously in two normal and three partially obstructed New Zealand White male rabbits on each of days One, Two or Three following obstruction. Bladders were excised on the seventh day(D) following obstruction or the sixth day after injection of normals. Under these conditions, cells labeled with 3H-TdR had the opportunity to proliferate, after labelling, for 6(OneD and Normals), 5(TwoD) or 4(ThreeD) days respectively. After processing tissues for autoradiography, normal bladders showed only trace levels of labeling. Animals exposed to 3H-TdR one day after obstruction, when large numbers of basal cells of the urothelium are known to incorporate 3HTdR (i.e., synthesize DNA), showed labeling in most layers of the urothelium seven days after injection, but levels of labeling in bladders injected TwoD or ThreeD were lower than those injected OneD after obstruction. The smaller numbers of urothelial cells labeled by 3H-TdR in TwoD bladders were found in clusters where one or two alternate or adjacent layers of cells were labeled. Obstructed animals injected ThreeD after surgery showed even less labeling. This evidence clearly supports the hypothesis that DNA synthesis that occurs in the urothelium within 24 h after obstruction is followed by proliferation, because by the seventh day, labeling can be found at all levels of the urothelium. The decline of labeling in TwoD and ThreeD animals suggests that the proliferative stimulus probably operates only during the first 24 h after insult. The data suggest that a substantial fraction of the urothelium enters one or more rounds of proliferation following obstruction and support the contention that hyperplasia does occur.

Animals

Microvasculature of the rabbit urinary bladder.

BACKGROUND: The urinary bladder requires a rich blood supply to maintain its functions, the storage and release of urine. Specialized properties of the bladder vasculature might be anticipated to ensure the integrity of this blood supply, because it is known that blood flow is reduced by distension during bladder filling. However, the bladder vasculature has been described in detail only at the gross level. A comprehensive, three-dimensional view of the blood supply to the bladder wall is presented here. METHODS: The microvasculature of the bladder of male New Zealand white rabbits was described using the combination of vascular corrosion casting, alkali digestion, light microscopy, and scanning and transmission electron microscopy. Following administration of an anticoagulant and an overdose of anesthetic, the abdominal aorta was cannulated just above the inferior mesenteric artery to permit flushing of the distal vasculature. The bladder vasculature was cleared of blood with buffered saline and then either perfuse-fixed with buffered 2% glutaraldehyde and sectioned, or filled with "Mercox" resin to prepare vascular corrosion casts. Casts were cleaned with NaOH, formic acid, and water. In some cases fixed bladders were partially digested with NaOH to expose the mucosal capillary plexus. RESULTS: The bladder is supplied with blood by single, left and right vesicular branches of the internal or external iliac arteries. The serpentine vesicular arteries extend along the lateral borders of the bladder from base to apex just deep to the serosal surface and send dorsal and ventral branches to supply the dorsal and ventral bladder walls. Veins accompany the arteries and exhibit numerous valves. A very dense complex of vessels at the apex of the bladder apparently serves to accommodate bladder distension. The muscularis and submucosa contains few vessels, but the mucosa is well vascularized. An especially dense capillary plexus is present in the lamina propria at its junction with the transitional epithelium. In the relaxed bladder these capillaries lie in grooves formed by the basal layers of the epithelium. The endothelial cells of these capillaries display few cytoplasmic vesicles and are continuous or fenestrated. These capillaries are often invested with pericytes. The mucosal capillary plexus may be associated with an epithelial transport function or may be necessary for urothelial metabolism or maintenance of the barrier function of the urothelium. Unusual capillary tufts, possibly associated with vascular lymphatic tissue, are found associated with the main vessels on the lateral walls in the basal half of the bladder. CONCLUSIONS: These methods present a clear, comprehensive, three-dimensional view of the microvasculature of the bladder wall. They also identify several unique features of this vasculature and provide a basis for studies of the response of this vasculature to pathologic states and experimental manipulation.

Animals

Bladder function in experimental outlet obstruction: pharmacologic responses to alterations in innervation, energetics, calcium mobilization, and genetics.

The two functions of the urinary bladder is to store urine at low intravesical pressures, and to periodically expel the urine through a coordinated contraction of the bladder and relaxation of the urethra. To a large extent, urinary bladder function depends upon the underlying structure of the organ as a whole, particularly on the inter-relationships among the smooth muscle, connective tissue, and neuronal elements. An alteration in the ratio of connective tissue to smooth muscle, for example, can significantly alter compliance and functional capacity, structurally impairing the bladder's ability to empty efficiently and fully. Thus, a change in structural compartmentation can affect bladder function independent of autonomic receptor density, response to receptor stimulation, and the contractile capabilities of the smooth muscle elements. Similarly, a selective alteration in either the afferent or efferent innervation of the bladder or urethra can induce significant alterations in the structural interrelationships between smooth muscle and connective elements. In addition, the bladder responds rapidly to alterations in urine volume and urethral resistance with marked changes in bladder and urethral structure and function, and these changes are under the controls of specific genes that are known to control cellular growth, hypertrophy, and hyperplasia. A knowledge of the mechanisms that control the response to specific forms of stress may lead to novel therapies for specific disease states.

Animals

Contractility and phenotype transitions in serosal thickening of obstructed rabbit bladder.

Partial outlet obstruction of rabbit bladder induces serosal thickening and smooth muscle (SM) cell hypertrophy that are accompanied by phenotypic changes in the expression of cytoskeletal and cytocontractile proteins. In the present study, we compare the observed progressive phenotypic changes with the contractile responses of strips of the thickened serosa. At 15 days after partial outlet obstruction, although cells in thickened serosa demonstrate the presence of nonmuscle (NM) myosin of A-like type, vimentin, and SM alpha-actin, no contractile responses of this tissue were noted. At later times (30 days), this tissue expressed in addition SM myosin, and this pattern was paralleled by the development of KCl-stimulated contractility. It is only after 60 days that the serosa demonstrated the expression of desmin, phosphoglucomutase (PGM)-related protein, and was locally negative for NM myosin, indicating a maturation toward adult SM cells. Concomitant to this phenotypic change, the response to KCl increased, and a bethanechol-stimulated contractile response developed. At no time period did the serosal layer react with anti-synaptophysin or anti-neurofilament proteins nor did the strips respond to field stimulation (via release of neurotransmitters), showing that SM cell differentiation and development of contractile responses during serosal thickening are independent of innervation.

Animals

Genetic and cellular characteristics of bladder outlet obstruction.

Urinary bladder outlet obstruction is a common medical problem. In order to understand the effects of outlet obstruction on bladder morphology, physiology, and pharmacology, several animal models of obstruction have been developed using a variety of species. Although there are marked differences in bladder size, capacity, compliance, physiology, and pharmacology among these species, responses to outlet obstruction have many common characteristics. This article will be separated into six areas: introduction, genetic factors mediating the response during the initial period of partial outlet obstruction and overdistension, cytostructural alterations that accompany compensated bladder function, alterations in innervation accompanying bladder hypertrophy secondary to partial outlet obstruction, alterations in calcium translocation during bladder hypertrophy, and metabolic factors involved in the response to partial outlet obstruction.

Animals

Stimulation of DNA synthesis in rabbit bladder wall after partial outlet obstruction and acute overdistension.

Partial outlet obstruction of the rabbit urethrovesical junction (UVJ) has been used to induce pathology in the urinary bladder characteristic of obstructive damage observed in humans. The purpose of the experiments reported here was to compare the 3H-thymidine (3H-TdR) labelling of DNA in urinary bladders of male New Zealand White (NZW) rabbits subjected to partial outlet obstruction or overdistension. A total of 18 animals was used. Two normal controls, and 12 partially obstructed animals (at 1 day [D], 3D, 5D, 7D, 14D, and 21D) were injected (i.v.) with 3H-TdR at a dose of 0.5 microCi/g body weight. An additional 4 were overdistended to volumes 120% of maximum intravesical pressure, immediately emptied via the catheter, and injected with 3H-TdR 24 hr (1D) later. All animals were sacrificed up to 3.5 hr after injection of the label. DNA-associated radioactivity reached a peak at 3D after obstruction and was reduced substantially by 5D, although the level of incorporation remained well above control levels out to 21D. Levels of 3H-TdR incorporation 1D after overdistension bladders were about half of that found 1D following partial obstruction. The distribution of 3H-TdR labelled DNA in tissues was demonstrated by radioautography of histologic sections. One day following obstruction, 3H-Tdr incorporation was localized in the urothelium. Labelling of urothelium subsequent to 1D was reduced but remained above control levels until 21D. Labelled smooth muscle nuclei were observed only in control and 3D bladders, and they were measured at similar frequencies. Labelling of both intrinsic connective tissue (ICT) (mucosal, submucosal, and mural) and extrinsic connective tissue (ECT) (serosal) peaked at 3D after obstruction and declined thereafter but not to control levels. Labelling of ECT was, of course, limited to those bladders in which ECT was present (i.e., 3-21D). While the distribution of labelled cells in radioautograms was more variable 1D after obstruction than 1D after overdistension, the general cellular and biochemical responses to overdistension, as measured by DNA synthesis, are similar to those observed after partial outlet obstruction. Since the first sequela of obstruction is acute distension, these data support the assertion that the initial overdistension of the bladder initiates the cellular response to obstruction.

Animals

3H-thymidine uptake by the rat urinary bladder after partial outflow obstruction.

Partial outflow obstruction induces marked changes in detrusor contractile function and morphology. One common finding in all experimental animal models of outflow obstruction is a significant increase in bladder mass. It is not clear which tissue compartments undergo hypertrophy, hyperplasia, or both. The present study was designed to evaluate the time-related changes in 3H-thymidine uptake and distribution within each tissue compartment induced by partial outflow obstruction using autoradiography. Partial outlet obstruction in rats induced a mild 2-fold increase in mass over a 14 day period. DNA synthesis increased significantly at 1 day following surgery, and remained increased through 7 days. DNA synthesis returned to control levels by 14 days. Distribution studies (using autoradiography) demonstrated a marked increase in the number of labelled urothelium cells at 1 and 3 days after obstruction. Sham surgery also initiated an increase in the number of labelled cells in the urothelium at 1 day. Although both sham and obstructive surgeries induced substantial increases in the labelling of cells within the connective tissue components, the magnitude of the increase in labelled connective tissue cells of the obstructed bladders was greater than that of the sham group. The number of labelled smooth muscle cells of the obstructed bladder increased significantly at 3, 5, and 7 days. However, there were no changes in smooth muscle incorporation of 3H-thymidine by the sham groups. In conclusion, partial outflow obstruction induced time-dependent increases in bladder wall proliferation. The urothelium and connective tissue were the compartments first affected, followed by smooth muscle.

Animals

Rabbit as a model of urinary bladder function.

Micturition is a complex neuromuscular process. Although control mechanisms have been identified at several levels of the central nervous system and spinal cord, the final pathway in the control of micturition is the autonomic innervation of the urinary bladder and related structures. Following this line of reasoning further, micturition is ultimately dependent on the ability of the urinary bladder to both contract and generate intravesical pressure, and to modify its shape in such a way as to efficiently expel its contents without leaving a high residual volume. In order to understand the various elements of micturition, a wide variety of both in vivo and in vitro animal models has been developed. In many cases, animal models have been utilized to describe the effect of specific experimental pathologies on the lower urinary tract. The current review of the use of the rabbit in urological research is not meant to be a comprehensive treatise on the topic, but should provide a rational description of the how this species can be utilized to study both normal and pathological function.

Aging

Update on bladder smooth-muscle physiology.

The urinary bladder responds to distension induced by a number of different stresses with rapid and substantial increases in bladder mass and concomitant alterations in the contractile responses to neuronal stimulation, pharmacological simulation by autonomic agonists, and membrane depolarization. Furosemide, sucrose, or diabetes-induced diuresis, as well as outlet obstruction and overdistension all produce similar effects on the bladder. Accompanying the increases in bladder mass and contractile changes are increases in DNA synthesis and [3H]-thymidine uptake. Autoradiographic studies have localized the increased DNA synthesis following bladder distension initially to the urothelium, followed by slower increases in labelling of the lamina propria and extramural connective tissue. The net result of these compartmental differences in DNA synthesis is a reorganization of the structural relationships between smooth-muscle cells, the connective-tissue matrix, and the extrinsic connective-tissue lamina. This may contribute to the functional changes which occur after severe overdistension. Increases in the expression of heat-shock protein-70, basic fibroblast growth factor, N-ras, and c-myc, and decreases in transforming growth factor-beta occurred acutely after obstruction, suggesting that these changes may play a role in obstruction-induced bladder hypertrophy. Removal of the obstruction induces apoptosis of urothelial and connective tissue elements in the bladder, accompanied by increases in transforming growth factor-beta and decreases in basic fibroblast growth factor genes, and a reversal of the bladder dysfunction. Therefore the bladder hyperplasia after outlet obstruction and the regression following removal of the obstruction seem to be directly opposing processes governed by gene expression.

Animals

Effect of slow and rapid cystometry on in vitro rat urinary bladder DNA synthesis.

1. Partial outflow obstruction induces marked changes in detrusor contractile function and morphology. One common finding in all experimental animal models of partial outflow obstruction is a significant increase in bladder mass. 2. Previous studies have demonstrated that partial outlet obstruction induces a rapid and substantial increase in [3H]thymidine incorporation into virtually all cellular elements of the bladder. 3. The present study was designed to investigate the [3H]thymidine uptake and localization induced by exposure of the in vitro whole rat bladder model to various intravesical pressures and rates of intravesical infusion. 4. The results are as follows: (a) There were no differences in DNA concentration between control and other groups. (b) Slow infusion induced a mild increase in DNA synthesis ([3H]thymidine incorporation) at 0.5 ml and a significantly greater level of DNA synthesis at 1.6 ml. (c) [3H]thymidine incorporation was significantly increased by exposure to 7.5 cm H2O, 15 cm H2O, and 30 cm H2O. (d) Exposure to 60 cm H2O and 90 cm H2O did not initiate an increase in [3H]thymidine incorporation. (e) Autoradiography showed that all tissue elements (urothelium, connective tissue, smooth muscle) participated in the response.

Animals

Temporal changes in rabbit urinary bladder function and DNA synthesis during chronic treatment with furosemide.

In a preliminary study we showed that 14 days of furosemide infusion in rabbits caused increases in bladder mass and contractile responses of bladder body strips to field stimulation, bethanechol, ATP and KCl. The present study investigated the temporal effects of furosemide-induced diuresis on micturition, bladder mass, bladder wall proliferation activity and DNA synthesis. In addition, contractile responses of bladder body strips were monitored. Furosemide-containing osmotic pumps were implanted in male New Zealand White rabbits. Micturition was monitored for 7 days. Biochemical analyses were done 3, 7 and 14 days after implantation. Contractile responses were measured at 3 and 7 days. Polyuria and polydipsia started within 1 day after implantation of furosemide-containing osmotic pumps and continued at the same level for 7 days. Bladder mass was significantly increased at 3 and 7 days. Diuresis stimulated 3H-thymidine uptake and caused an increase in bladder DNA concentration at 3 days. However, both DNA concentrations and 3H-thymidine levels returned to control levels by 7 days. Contractile responses to field stimulation and agonists were increased at 7 days but unchanged at 3 days. The data confirm that modest increases in bladder mass and the ensuing increases in contractile function are a normal and beneficial physiological response to diuresis.

Adenosine Triphosphate

What is the most accurate way to study the active properties of bladder smooth muscle?

There is often disagreement over the optimal method by which to study the active properties of smooth muscle. While some favor setting smooth muscle strips at a resting or passive tension of 1 g, others have argued in favor of determining the Lo or optimal length for maximal force generation for each individual strip. Setting each strip to its individual Lo is tedious, especially if one is dealing with multiple strips during one experiment. Is it possible to study smooth muscle strips at an average length at which most strips of similar dimensions exhibit their maximal force, and if this method is used to what extent does it underestimate the maximal force generated? When comparing bladder, smooth muscle strips 1 cm long from pregnant versus virginal rabbits, the average length at which maximal force was generated was 2.41 and 2.45 cm, respectively (p = n.s.). Studying all strips at a length of 2.5 cm (2.5 x the slack length) would have resulted in a 10% underestimate of the maximal force within each group (p = n.s.). We conclude that comparative bladder smooth muscle strip studies can be accurately carried out at an average fixed length provided that preliminary studies are done to determine the length-tension relationships for the specific experimental situation.

Animals

Expression of constitutive heat shock protein-70 in normal (non-stressed) rabbit urinary bladder tissue.

The expression of constitutive HSP-70 in the urinary bladder was determined by SDS-PAGE and western blotting using a mouse monoclonal antibody against HSP-70. The western blot analysis showed that the mouse anti-HSP-70 cross-reacted with a 70 kDa protein present in the extracts of the urinary bladder muscle and mucosa. Densitometric scanning of the western blots allowed us to specifically quantitate the relative amounts of the HSP-70. The quantitation of the HSP-70 by combining immunoblotting and densitometry using a laser scanner is reproducible and this technique requires only a small amount of tissue. The amounts of HSP-70 can be estimated from a standard curve of nanogram(ng) of HSP-70 vs absorption from the immunoblots. The amounts of HSP-70 in the muscular and mucosal layers in the body of the urinary bladder are more than those in the base of the bladder. The presence of HSP-70 in the muscle and mucosal epithelium of the bladder was demonstrated by immunohistochemical analysis of freshly removed tissue from the base and the body of bladder from normal animals.

Animals

Urothelial permeability of the isolated whole bladder.

The urothelium of the bladder presents an effective barrier to the penetration of solutes from the urine into the bladder wall. Previously, we have demonstrated that the dye indigocarmine can be utilized intravesically to study urothelial permeability. In general, intravesical indigocarmine (administered in vivo) will not penetrate the bladder wall unless the urothelium is damaged by overdistension, acetone administration, or mechanical damage. Unfortunately, using in vivo methodologies, one is limited in the study of the effect of specific conditions and permeations on bladder permeability. In the current study an isolated in vitro whole bladder model was developed to quantitatively study the permeability of the bladder urothelium. In these studies, the penetration of indigocarmine into and through the bladder wall was quantitated under various conditions. The in vitro bladder was filled by infusing 1% indigocarmine in saline in a step-wise manner at the rate of 10 ml in 10 minutes followed by a stabilization period of 10 minutes. Samples were taken from the bath at 20 minutes intervals for spectrophotometrical analysis of the dye. At the end of experiment the bladder was washed in saline for 10 minutes, and stored and extracted in formalin. In general, no indigocarmine penetrated the urothelium until the in vitro capacity was reached and exceeded. At intravesical volumes greater than capacity, the dye concentration in the bath increased very rapidly, even though the integrity of the bladder wall remained intact. In bladders treated with a gentle 50% acetone wash for 1 minute the dye started to penetrate into the bath at intravesical volumes of 25% of capacity and increased rapidly thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetone

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