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PubMed1983

The corneal endothelium following photocoagulation: induced decompensation.

The wide-field specular microscope was used to study retrospectively the corneal endothelia of six patients. Each patient had recovered from an episode of corneal decompensation in one eye, which consisted of subepithelial edema, punctate staining, iritis, and a fixed dilated pupil, following retinal photocoagulation with the xenon arc. In each case, the normal and the previously decompensated eyes were found to have equal endothelial cell counts and indistinguishable cell morphology. Nothing was seen to suggest why these corneas should have decompensated. It is concluded that photocoagulation-induced corneal decompensation did not produce permanent morphological changes in corneal endothelial cells. Possible mechanisms of corneal decompensation are discussed.

Adult↗

PubMedDate not supplied

[Long-term effect of brace treatment on spinal decompensation in idiopathic scoliosis. A comparison of Milwaukee brace--Chêneau corset].

Spinal decompensation is a statistically important factor in idiopathic scoliosis. In our study we compared longterm influence of brace-treatment by Milwaukee brace and Chêneau-Orthosis. Twenty-six patients treated by Milwaukee Brace and 21 treated by Chêneau-Orthosis were followed up with an average of 7.8 (Milwaukee) and 4 (Chêneau) years. No correlation was found between spinal decompensation, expression and localisation of the major curve. Further we didn't find any correlation between spinal decompensation and development of the major curve under therapy. Chêneau-Orthosis showed better results significantly. In 61.9% of all patients decreased of spinal decompensation to 35% of the initial value was seen. With Milwaukee Brace only 38.5% of the patients did improve to 46.6% of the initial value. A prediction for development of spinal decompensation under therapy was not possible.

Braces↗

PubMed1997

Effects of naturally acquired decompensated mitral valve regurgitation on the renin-angiotensin-aldosterone system and atrial natriuretic peptide concentration in dogs.

OBJECTIVE: To investigate activity of the renin-angiotensin-aldosterone system and N-terminal pro-atrial natriuretic peptide (NT-proANP) during development of clinical signs of decompensated mitral valve regurgitation (MR). ANIMALS: 11 Cavalier King Charles Spaniels with advanced MR attributable to chronic valvular disease. PROCEDURE: Dogs were subjected to repeated examinations at 6-month intervals until signs of decompensation had developed (end point). Data acquired at end point were compared with data obtained from examinations 1 year and 1 to 6 months before decompensation. Each examination included physical examination, collection of venous blood, thoracic radiography, and echocardiography. RESULTS: Echocardiographic measurements of left atrial-to-aortic root ratio and left ventricular end diastolic diameter increased considerably during the study, whereas left ventricular end systolic diameter remained unchanged. The increase in cardiac size was associated with increased plasma concentration of NT-proANP. In contrast, plasma concentrations of aldosterone and angiotensin II were reduced at decompensation (aldosterone compared with the 2 earlier examinations and angiotensin II compared with values obtained 1 to 6 months before), despite decreased plasma protein concentration and hematocrit, suggesting fluid retention. The urine-to-plasma creatinine ratio was reduced at end point. CONCLUSION AND CLINICAL IMPLICATIONS: Early decompensated MR in dogs was not associated with increased circulating renin-angiotensin-aldosterone system activity, which may be caused by increased activity of ANP, and may be important for future therapeutic strategies of MR.

Aldosterone↗

PubMed2006

Utility of impedance cardiography for the identification of short-term risk of clinical decompensation in stable patients with chronic heart failure.

OBJECTIVES: This study sought to assess the potential utility of impedance cardiography (ICG) in predicting clinical deterioration in ambulatory patients with heart failure (HF). BACKGROUND: Impedance cardiography uses changes in thoracic electrical impedance to estimate hemodynamic variables, but its ability to predict clinical events has not been evaluated. METHODS: We prospectively evaluated 212 stable patients with HF and a recent episode of clinical decompensation who underwent serial clinical evaluation and blinded ICG testing every 2 weeks for 26 weeks and were followed up for the occurrence of death or worsening HF requiring hospitalization or emergent care. RESULTS: During the study, 59 patients experienced 104 episodes of decompensated HF (16 deaths, 78 hospitalizations, and 10 emergency visits). Multivariate analysis identified 6 clinical and ICG variables that independently predicted an event within 14 days of assessment. These included three clinical variables (visual analog score, New York Heart Association functional class, and systolic blood pressure) and three ICG parameters (velocity index, thoracic fluid content index, and left ventricular ejection time). The three ICG parameters combined into a composite score was a powerful predictor of an event during the next 14 days (p = 0.0002). Visits with a high-risk composite score had 2.5 times greater likelihood and those with a low-risk score had a 70% lower likelihood of a near-term event compared with visits at intermediate risk. CONCLUSIONS: These results suggest that when performed at regular intervals in stable patients with HF with a recent episode of clinical decompensation, ICG can identify patients at increased near-term risk of recurrent decompensation.

Adult↗

PubMed2005

Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials.

CONTEXT: Nesiritide improves symptoms in patients with acutely decompensated heart failure compared with placebo and appears to be safer than dobutamine. Its short-term safety relative to standard diuretic and vasodilator therapies is less clear. OBJECTIVE: To investigate the safety of nesiritide relative to noninotrope-based control therapies, primarily consisting of diuretics or vasodilators. DATA SOURCES: Primary reports of completed clinical trials as of December 2004 were obtained from the US Food and Drug Administration (FDA), the study sponsor (Scios Inc), a PubMed literature search using the terms nesiritide, clinical trials, and humans, and a manual search of annual meetings of 3 heart associations. STUDY SELECTION: Of 12 randomized controlled trials evaluating nesiritide, 3 met all inclusion criteria: randomized double-blind study of patients with acutely decompensated heart failure, therapy administered as single infusion (> or =6 hours), inotrope not mandated as control, and reported 30-day mortality. DATA EXTRACTION: Data were extracted from FDA and sponsor documents and corroborated with published articles when available. Thirty-day survival was assessed by meta-analysis using a fixed-effects model and time-dependent risk by Kaplan-Meier analysis with Cox proportional hazards regression modeling. Where deaths were described within a range of days after treatment, an extreme assumption was made favoring nesiritide over control therapy, an approach relevant to the time-dependent analyses. DATA SYNTHESIS: In the 3 trials, 485 patients were randomized to nesiritide and 377 to control therapy. Death within 30 days tended to occur more often among patients randomized to nesiritide therapy (35 [7.2%] of 485 vs 15 [4.0%] of 377 patients; risk ratio from meta-analysis, 1.74; 95% confidence interval [CI], 0.97-3.12; P = .059; and hazard ratio after adjusting for study, 1.80; 95% CI, 0.98-3.31; P = .057). CONCLUSIONS: Compared with noninotrope-based control therapy, nesiritide may be associated with an increased risk of death after treatment for acutely decompensated heart failure. The possibility of an increased risk of death should be investigated in a large-scale, adequately powered, controlled trial before routine use of nesiritide for acutely decompensated heart failure.

Diuretics↗

PubMed2000

Maximizing management of patients with decompensated heart failure.

Patients with decompensated congestive heart failure can be categorized into those with either acute or chronic presentations. Patients with acute decompensated heart failure most often have an acute injury that affects either myocardial performance (i.e., myocardial infarction) or valvular/chamber integrity (mitral regurgitation, ventricular septal rupture), which leads to an acute rise in left ventricular (LV) filling pressures resulting in pulmonary edema and dyspnea. Therapy for these patients is aimed at treating the underlying cause of the myocardial injury as well as pharmacologic strategies to reduce LV filling pressures and to improve cardiac performance. In contrast, the therapy of patients presenting with decompensated heart failure in the setting of chronic LV systolic dysfunction, treated with angiotensin-converting enzyme inhibitors, digoxin, diuretics, and may be beta blockers, represent a poorly defined clinical entity that lacks clear guidelines for treatment. These patients can present with symptoms of volume overload and/or low cardiac output without evidence for a volume overloaded state. Potential diagnostic and therapeutic approaches include (1) a pulmonary artery catheter for invasive hemodynamic monitoring, (2) intravenous inotropic therapy, (3) LV mechanical assist device therapy, and (4) cardiac transplantation. This review presents some of the advantages and disadvantages of each of these interventions for patients with chronic systolic dysfunction who present with decompensated symptoms and require specialized management in the hospital setting.

Acute Disease↗

PubMed2005

HIV coinfection shortens the survival of patients with hepatitis C virus-related decompensated cirrhosis.

The impact of human immunodeficiency virus (HIV) coinfection on the survival of patients with hepatitis C virus (HCV)-related end-stage liver disease (ESLD) is unknown. Because HIV infection is no longer considered an absolute contraindication for liver transplantation in some countries, it has become a priority to address this topic. The objective of this study was to compare the survival of HIV-infected and HIV-uninfected patients with decompensated cirrhosis due to HCV. In a retrospective cohort study, the survival of 1,037 HCV monoinfected and 180 HCV/HIV-coinfected patients with cirrhosis after the first hepatic decompensation was analyzed. Of the group, 386 (37%) HCV-monoinfected and 100 (56%) HCV/HIV-coinfected subjects died during the follow-up. The median survival time of HIV-infected and HIV-uninfected patients was 16 and 48 months, respectively (P < .001). The relative risk (95% CI) of death for HIV-infected patients was 2.26 (1.51-3.38). Other independent predictors of survival were age older than 63 years (2.25 [1.53-3.31]); Child-Turcotte-Pugh class B versus class A (1.95 [1.41-2.68]) and class C versus class A (2.78 [1.66-4.70]); hepatitis D virus infection (1.56 [1.12-4.77]); model for end-stage liver disease score, (1.05 [1.01-1-11]); more than one simultaneous decompensation (1.23 [1.12-3.33]); and the type of the first hepatic decompensation, with a poorer prognosis associated with encephalopathy compared with portal hypertensive gastrointestinal bleeding (2.03 [1.26-3.10]). In conclusion, HIV coinfection reduces considerably the survival of patients with HCV-related ESLD independently of other markers of poor prognosis. This fact must be taken into account to establish the adequate timing of liver transplantation in HIV-coinfected subjects.

Adult↗

PubMed1986

Survival and prognostic indicators in compensated and decompensated cirrhosis.

Six-year survival of cirrhosis was assessed in a series of 1155 consecutive patients (751 men, 404 women). Among the men, 33% were alcoholics and 18% were HBsAg positive; corresponding figures for the women were 15% and 6% respectively. Features of decompensation at first presentation were observed in 63% of the patients. Six-year survival was 54% in compensated and 21% in decompensated patients. No significant differences in survival were found between alcoholics and nonalcoholics. Leading causes of death were liver failure (49%), hepatocellular carcinoma (22%), and bleeding (13%). The prognostic role of 21 variables was evaluated separately in compensated and decompensated patients by the Cox's regression model. The following variables were found to be significant predictors of death risk in compensated patients: male sex, HBsAg positivity, age, prothrombin time prolongation, and esophageal varices. In decompensated disease the significant indicators of death risk were: hepatocellular carcinoma, encephalopathy, hemorrhage, SGOT, esophageal varices, gamma globulins, prothrombin time prolongation, continued abuse of alcohol, HBsAg positivity, gamma glutamyl transpeptidase, and cholinesterase. A simple prognostic index based upon the relative risk coefficient of the significant variables is suggested.

Carcinoma, Hepatocellular↗

PubMed1990

The contribution of protein catabolism to metabolic decompensation in 3-hydroxy-3-methylglutaric aciduria.

Leucine and protein metabolism were studied using stable isotope techniques in 6-year-old twins with 3-hydroxy-3-methylglutaric aciduria during acute metabolic decompensation. The decompensation was preceded by prolonged fasting in twin 1 and by an upper respiratory infection in twin 2. Twin 2 was also studied when well (control study). During infection, leucine oxidation (36 mumol/kg per hour), protein catabolism (6.0 g/kg per day) and urinary excretion of major leucine metabolites (104 mumol/kg per hour) were all increased compared with the control study (16 mumol/kg per hour, 4.7 g/kg per day and 28 mumol/kg per hour respectively). During fasting, leucine oxidation (18 mumol/kg per hour) was unchanged and protein catabolism (4.1 g/kg per day) was decreased despite substantially increased urinary metabolite excretion (87 mumol/kg per hour) compared with the control study. These results indicate that protein mobilisation and leucine oxidation played important roles in metabolic decompensation during infection but not during fasting. It is likely that the increased metabolite excretion during fasting arose primarily from fatty acid catabolism, indicating the importance of this substrate in metabolic decompensation in 3-hydroxy-3-methylglutaric aciduria.

Amino Acid Metabolism, Inborn Errors↗

PubMed2003

MR diffusion imaging and MR spectroscopy of maple syrup urine disease during acute metabolic decompensation.

Maple syrup urine disease (MSUD) is an inborn error of amino acid metabolism, which affects the brain tissue resulting in impairment or death if untreated. Imaging studies have shown reversible brain edema during acute metabolic decompensation. The purpose of this paper is to describe the diffusion-weighted imaging (DWI) and spectroscopy findings during metabolic decompensation and to assess the value of these findings in the prediction of patient outcome. Six patients with the diagnosis of MSUD underwent conventional MR imaging with DWI during acute presentation with metabolic decompensation. Spectroscopy with long TE was performed in four of the six patients. Follow-up examinations were performed after clinical and metabolic recovery. DWI demonstrated marked restriction of proton diffusion compatible with cytotoxic or intramyelinic sheath edema in the brainstem, basal ganglia, thalami, cerebellar and periventricular white matter and the cerebral cortex. This was accompanied by the presence of an abnormal branched-chain amino acids (BCAA) and branched-chain alpha-keto acids (BCKA) peak at 0.9 ppm as well as elevated lactate on proton spectroscopy in all four patients. The changes in all six patients were reversed with treatment without evidence of volume loss or persistent tissue damage. The presence of cytotoxic or intramyelinic edema as evidenced by restricted water diffusion on DWI, with the presence of lactate on spectroscopy, could imply imminent cell death. However, in the context of metabolic decompensation in MSUD, it appears that changes in cell osmolarity and metabolism can reverse completely after metabolic correction.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

PubMed2004

Quality of care and outcomes in acute decompensated heart failure: The ADHERE Registry.

Despite 1 million or more annual hospitalizations, the management of acute decompensated heart failure remains largely empiric. Data are lacking regarding patient characteristics, usual comorbidities, commonly used treatment strategies, clinical outcomes, and adherence to recently published quality indicators. The Acute Decompensated Heart Failure National Registry (ADHERE(R)) has been established to capture data regarding the presentation, management, and expected outcomes of acute decompensated heart failure. The size of the registry and its web-based platform allow for evaluation of compliance with quality indicators, assessment of mortality risk, and correlation of parenteral treatment strategies with clinical outcomes. More than 100,000 patient episodes have been recorded in the registry. These patient data have been reviewed and reveal important findings regarding acute decompensated heart failure and potential opportunities to improve the quality of care.

Acute Disease↗

PubMed1991

Systemic and renal production of thromboxane A2 and prostacyclin in decompensated liver disease and hepatorenal syndrome.

To assess the role of altered renal and systemic production of thromboxane A2 and prostacyclin in the hepatorenal syndrome, urinary excretion of their major renal and extrarenal metabolites was measured in patients with compensated and decompensated liver disease, chronic renal failure, and hepatorenal syndrome. Urinary excretion rates of all prostanoids (renal and extrarenal) were increased in subjects with liver disease compared with normal controls. Moreover, they were considerably higher in subjects with severe hepatic decompensation but good renal function compared with those with hepatorenal syndrome. In contrast, the excretion rate of all metabolites was reduced in patients with chronic renal failure. The excretion rate of all metabolites was markedly elevated during the early stages of hepatorenal syndrome and decreased in parallel with creatinine clearance. When corrected for creatinine clearance, there was a strong correlation between prostanoid excretion and serum bilirubin in subjects with liver disease; there was no difference, however, in the excretion of renal and extrarenal prostanoids between hepatorenal syndrome and severe hepatic decompensation. It is concluded that hepatic decompensation is associated with a progressive increase in prostanoid excretion but that changes in production of prostacyclin or thromboxane A2 are unlikely to be major factors in the pathogenesis of the hepatorenal syndrome.

Adult↗

PubMed2006

Inferior corneal decompensation following laser peripheral iridotomy in the superior iris.

PURPOSE: To describe a previously unreported clinical entity of inferior corneal decompensation occurring as a long-term complication of superior laser peripheral iridotomy. DESIGN: Retrospective, non-comparative observational case series. METHODS: Chart review of 14 subjects (16 eyes) with inferior corneal decompensation. RESULTS: All patients were Chinese, most were females (71.4%), and the mean age was 69.5 +/- 8.1 year. The mean interval from iridotomy to the onset of inferior corneal decompensation was 66.1 +/- 34.0 months. The most common indication for laser iridotomy was for prophylaxis, either in the fellow eye of acute angle closure (43.8%) or for occludable angles (12.5%). CONCLUSIONS: Corneal decompensation in the inferior part of the cornea at a site remote from the iridotomy is a rare but important complication of laser iridotomy. Because many of the laser iridotomies were performed prophylactically in eyes without glaucoma, patients may need to be warned of this risk.

Aged↗

PubMed2004

Measures of heart period variability as predictors of mortality in hospitalized patients with decompensated congestive heart failure.

Depressed heart rate variability (HRV) is a powerful independent predictor of a poor outcome in patients with chronic and stable congestive heart failure (CHF). However, the prognostic value of HRV analysis in patients hospitalized for decompensated CHF is not known. The aim of this study was to investigate whether HRV parameters obtained during admission for decompensated CHF could predict survival after hospital discharge. We studied 199 patients (131 men, aged 60 +/- 14 years) with a previous diagnosis of New York Heart Association class III or IV CHF who were admitted to the hospital for decompensated CHF. Twenty-four-hour Holter recordings were obtained on admission, and measures of HRV were calculated in the time and frequency domain. During a mean follow-up of 312 +/- 150 days, 40 patients (21.1%) died. Kaplan-Meier analysis indicated that patients with SD of the RR intervals over a 24-hour period (p = 0.027), SD of all 5-minute mean RR intervals (p = 0.043), total power (p = 0.022), and ultra-low-frequency power (p = 0.008) in the lower tertile were at a higher risk of death. In a multivariate Cox regression model, the same indexes in the lower tertile were independent predictors of mortality: SD of the RR intervals over a 24-hour period (risk ratio [RR] 2.2, 95% confidence interval [CI] 1.05 to 4.3, p = 0.036), SD of all 5-minute mean RR intervals (RR 2.1, 95% CI 1.05 to 4.2, p = 0.04), total power (RR 2.2, 95% CI 1.08 to 4.2, p = 0.03), and ultra-low-frequency power (RR 2.6, 95% CI 1.3 to 5.3, p = 0.007). Therefore, the severity of autonomic perturbations during hospital admission for CHF decompensation, as reflected by measures of overall HRV, can predict survival after hospital discharge. Together with previous studies, our findings suggest that indexes of overall HRV provide useful prognostic information in the full spectrum of CHF severity.

Arrhythmias, Cardiac↗

PubMed2004

Elevated blood urea nitrogen level as a predictor of mortality in patients admitted for decompensated heart failure.

BACKGROUND: Hospitalization for decompensated heart failure is associated with high mortality after discharge. In heart failure, renal function involves both cardiovascular and hemodynamic properties. We studied the relation between renal dysfunction and mortality in patients admitted for decompensated heart failure. METHODS: The prognostic importance of four measures of renal function-blood urea nitrogen, serum creatinine, blood urea nitrogen/creatinine ratio, and estimated creatinine clearance-was evaluated in 541 patients (mean [+/- SD] age, 63 +/- 14 years; 377 men [70%]) with a previous diagnosis of heart failure (96% with New York Heart Association class III or IV symptoms) who were admitted for clinical decompensation. RESULTS: During a mean follow-up of 343 +/- 185 days, 177 patients (33%) died. In multivariable Cox regression models, the risk of all-cause mortality increased with each quartile of blood urea nitrogen, with an adjusted relative risk of 2.3 in patients in the upper compared with the lower quartiles (95% confidence interval [CI]: 1.3 to 4.1; P = 0.005). Creatinine and estimated creatinine clearance were not significant predictors of mortality after adjustment for other covariates. Blood urea nitrogen/creatinine ratio yielded similar prognostic information as blood urea nitrogen (adjusted relative risk = 2.3; 95% CI: 1.4 to 3.8; P = 0.0007 for patients in the upper compared with the lower quartiles). CONCLUSION: Blood urea nitrogen is a simple clinical variable that provides useful prognostic information in patients admitted for decompensated heart failure. In this setting, elevated blood urea nitrogen levels probably reflect the cumulative effects of hemodynamic and neurohormonal alterations that result in renal hypoperfusion.

Aged↗

PubMed2004

Risk stratification after hospitalization for decompensated heart failure.

BACKGROUND: Decompensated heart failure (HF) is among the most common indications for hospitalization in the United States, but little is known about features on admission that predict adverse events. We used data from the Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) study to develop a model that would predict outcomes in patients with decompensated HF. METHODS AND RESULTS: OPTIME-CHF randomized 949 patients hospitalized with decompensated HF for 48 to 72 hours of infusion of either milrinone or placebo. We used multivariable modeling to evaluate variables on admission that would be predictive of 60-day mortality or the composite of death or rehospitalization at 60 days. Variables at presentation that predicted death at 60 days were increased age, lower systolic blood pressure, New York Heart Association class IV symptoms, elevated blood urea nitrogen (BUN), and decreased sodium. Predictors of the composite of death or rehospitalization within 60 days were the number of HF hospitalizations in the preceding 12 months, elevated BUN, lower systolic blood pressure, decreased hemoglobin, and a history of percutaneous coronary intervention (PCI). The discriminatory power of the model was substantial for the mortality model (c-index .77) but less for the composite endpoint (c-index .69). CONCLUSIONS: Risk stratification of patients with decompensated HF may be accomplished using easily assessed clinical variables. Further research into the validity of this model in independent samples will potentially aid in the development of risk stratification strategies.

Aged↗

PubMed2006

Heart rate turbulence and death due to cardiac decompensation in patients with chronic heart failure.

BACKGROUND: As treatment strategies for patients with chronic heart failure (HF) become more sophisticated, identifying patients at high risk of death and predicting mode of death is important. The aim of this study was to explore the potential utility of heart rate turbulence (HRT) to identify patients with HF at high risk of death. METHODS AND RESULTS: In a prospective study, 553 ambulant outpatients age 63+/-10 with symptoms of HF and evidence of cardiac dysfunction were recruited. All patients underwent 24-h Holter ECG recordings, which were analysed for arrhythmias, heart rate variability and HRT a measurement that is thought to quantify cardiac autonomic regulatory mechanisms. Baseline chest radiograph, biochemistry and 12-lead electrocardiograms were also obtained. In patients with HRT measurements at 5 years follow up, 146 patients had died, 59 due to decompensated HF. Independent predictors of death from decompensated HF at 5-year follow up (Cox proportional hazard model) were HRT slope (HR for 10% increment 0.84, 95% CI 0.77-0.91), serum sodium (HR for 10% increment 0.75, 95% CI 0.62-0.91) and serum creatinine (for 10% increment HR 1.14, 95% CI 1.08-1.19) all P<0.01. These 3 variables combined had excellent discrimination between patients dying of decompensated HF and other patients, C-statistic=0.82. CONCLUSIONS: In patients with mild-to-moderate HF, HRT slope is an independent predictor of death due to decompensated HF. HRT may have the potential to help tailor therapy in this patient group.

Aged↗

PubMed2001

The decompensated detrusor IV: experimental bladder outlet obstruction and its functional correlation to the expression of the ryanodine and voltage operated calcium channels.

PURPOSE: Calcium ion homeostasis has a significant role in smooth muscle function. Its regulation requires complex storage and release mechanisms via ion pumps and channels located within intracellular storage sites (sarcoplasmic reticulum) and at the plasma membrane. A prominent component of the sarcoplasmic reticulum is the ryanodine sensitive ion channel which releases calcium from the sarcoplasmic reticulum into the cytosol. At the level of the plasma membrane the voltage operated calcium channel (dihydropyridine sensitive) serves to allow an influx of extracellular calcium. Our prior studies have shown a loss of sarcoplasmic endoplasmic reticulum Ca++Mg++ATPase expression following outlet obstruction. In this study we correlate ryanodine and voltage operated calcium channel protein expression with bladder function following partial outlet obstruction. MATERIALS AND METHODS: Standardized partial bladder outlet obstructions were created in adult New Zealand white rabbits, which were divided into control, sham operated and obstructed groups. Muscle strip studies further subcategorized the obstructed group into compensated (force greater than 50% of control) and decompensated (force less than 50% of control) and were correlated with in vivo determinations of voiding frequency and voided volumes. Microsomal membrane protein fractions were prepared from the same bladder tissue and were used for Western blot analysis using specific monoclonal antibodies. RESULTS: Increased voiding frequency and decreased voided volumes correlated with the definitions of compensated and decompensated. The Western blots revealed a near disappearance of ryanodine expression in the decompensated group with minimal changes in the expression of the voltage operated calcium channel. CONCLUSIONS: Bladder performance as measured in vivo and in vitro after outlet obstruction is influenced in part by smooth muscle cell ability to maintain calcium homeostasis via the sarcoplasmic reticulum. Bladder decompensation is highly associated with a loss of sarcoplasmic reticulum function with lesser changes taking place in those calcium regulatory proteins at the plasma membrane.

Animals↗