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Wall Tension (wall + tension)
Selected AbstractsLeft ventricular hypertrophy in rats with biliary cirrhosisHEPATOLOGY, Issue 3 2003Javier Inserte Portal hypertension induces neuroendocrine activation and a hyperkinetic circulation state. This study investigated the consequences of portal hypertension on heart structure and function. Intrahepatic portal hypertension was induced in male Sprague-Dawley rats by chronic bile duct ligation (CBDL). Six weeks later, CBDL rats showed higher plasma angiotensin-II and endothelin-1 (P < .01), 56% reduction in peripheral resistance and 73% reduction in pulmonary resistance (P < .01), 87% increase in cardiac index and 30% increase in heart weight (P < .01), and increased myocardial nitric oxide (NO) synthesis. In CBDL rats, macroscopic analysis demonstrated a 30% (P < .01) increase in cross-sectional area of the left ventricular (LV) wall without changes in the LV cavity or in the right ventricle (RV). Histomorphometric analysis revealed increased cell width (12%, P < .01) of cardiomyocytes from the LV of CBDL rats, but no differences in myocardial collagen content. Myocytes isolated from the LV were wider (12%) and longer (8%) than right ventricular myocytes (P < .01) in CBDL rats but not in controls. CBDL rats showed an increased expression of ANF and CK-B genes (P < .01). Isolated perfused CBDL hearts showed pressure/end-diastolic pressure curves and response to isoproterenol identical to sham hearts, although generated wall tension was reduced because of the increased wall thickness. Coronary resistance was markedly reduced. This reduction was abolished by inhibition of NO synthesis with N -nitro-L-arginine. Expression of eNOS was increased in CBDL hearts. In conclusion, portal hypertension associated to biliary cirrhosis induces marked LV hypertrophy and increased myocardial NO synthesis without detectable fibrosis or functional impairment. This observation could be relevant to patients with cirrhosis. [source] Increasing intra-abdominal pressure increases pressure, volume, and wall tension in esophageal varicesHEPATOLOGY, Issue 4 2002Angels Escorsell Many daily activities cause acute elevations of intra-abdominal pressure (IAP). In portal hypertensive cirrhotic patients, increased IAP increases absolute portal pressure and azygos blood flow, suggesting that it may have detrimental consequences at the esophageal varices. The aim of this study was to investigate the effects of increased IAP on variceal pressure, size, and wall tension. Endosonography and a noninvasive endoscopic pressure gauge were used to measure variceal pressure, radius, wall tension, and volume in baseline conditions and after increasing IAP by 10 mm Hg using an inflatable girdle in 14 patients with cirrhosis and esophageal varices. Increasing IAP markedly increased variceal pressure (from 13.3 ± 4.2 to 17.4 ± 4.6 mm Hg; P = .0001) and radius (from 2.9 ± 1.0 to 3.9 ± 1.1 mm; P = .0001). Consequently, wall tension dramatically increased (from 38.7 ± 13.6 to 65.9 ± 23.8 mm Hg · mm, +78%; P = .0001). Variceal volume increased significantly from 1,264 ± 759 to 2,025 ± 1,129 mm3 (P = .0001). In conclusion, in portal hypertensive cirrhotic patients, increases in IAP have deleterious effects on variceal hemodynamics, markedly increasing the volume, pressure, and wall tension of the varices. Increases in IAP may contribute to the progressive dilatation that precedes the rupture of the varices in portal hypertension. [source] Ventricular Volume Reduction ProceduresJOURNAL OF CARDIAC SURGERY, Issue 2003Akira T. Kawaguchi M.D. Other volume reduction procedures have become popular with renewed interest in ventricular reshaping to improve function. Although recent refined selection criteria have improved survival with PLV, earlier unpredictable results prompted less invasive procedures based on the same physiologic concept of reducing radius or wall tension by wrapping, piercing, or clasping. These new techniques are not only less invasive but also reversible and adjustable and appear safer for less symptomatic patients at risk of progressive heart failure. Nonetheless, mechanisms of action and degrees of volume reduction and/or restriction need to be delineated before widespread clinical application. (J CARD SURG 2003;18 (Suppl 2):S69-S75) [source] A Theoretical Model for the Myogenic Response Based on the Length,Tension Characteristics of Vascular Smooth MuscleMICROCIRCULATION, Issue 4 2005BRIAN E. CARLSON ABSTRACT Objective: A theoretical model is developed to describe the myogenic response of resistance vessels to changes in intravascular pressure, based on a consideration of the active and passive length,tension characteristics of vascular smooth muscle (VSM). The dependence of model parameters on vessel diameter is examined. Methods: The vessel wall is represented mechanically as a nonlinear passive component in parallel with an active contractile component. The level of VSM tone is assumed to have a sigmoidal dependence on circumferential wall tension or stress. Model parameters are optimized for each of 18 independent experimental data sets previously obtained using pressure or wire myograph systems. Results: Close fits between model predictions and experimental data are found in each case. An alternative formulation in which VSM tone depends on circumferential wall stress is found also to be consistent with available data. Significant trends in model parameters as a function of diameter are found. Conclusions: The results support the hypothesis that circumferential tension or stress in the wall provides the signal for myogenic responses. The model provides a basis for simulating steady-state myogenic responses in vascular networks containing a range of vessel diameters. [source] Bladder wall tension during physiological voiding and in patients with an unstable detrusor or bladder outlet obstructionBJU INTERNATIONAL, Issue 6 2003S. Bross OBJECTIVE To develop and evaluate a new clinical method for measuring bladder wall tension (BWT) on detrusor contraction during physiological voiding and under pathological conditions, as in experimental trials during subvesical obstruction the ability to generate pressure increases, whereas the contractile force per cross-sectional area of detrusor muscle decreases. PATIENTS AND METHODS In all, 24 patients were divided into three equal groups: group 1 (mean age 58, sd 8.6 years) comprised men with bladder outlet obstruction in accordance with the Abrams-Griffiths nomogram; group 2 (four men and four women, 56, sd 7.2 years) had detrusor instability; and group 3 (54, sd 9.6 years) had normal bladder emptying. BWT, as the detrusor force per cross-sectional area of bladder tissue (in N/cm2), was calculated after a urodynamic evaluation and ultrasonographic estimate of bladder wall thickness. RESULTS In all patients it was possible to measure BWT; the mean (sd) maximum BWT in group 1 was 9.8 (3.9) N/cm2, in group 2 during bladder instability was 11.7 (2.6) N/cm2 and in group 3 was 2.8 (0.5) N/cm2. CONCLUSIONS Estimating BWT in humans is possible by combining a urodynamic evaluation with an ultrasonographic estimate of bladder wall thickness. Further clinical research should elucidate the clinical relevance of BWT under comparable conditions. [source] Role Of Protein Kinase C In Myogenic Calcium, Contraction Coupling Of Rat Cannulated Mesenteric Small ArteriesCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2001Jos Pm Wesselman SUMMARY 1. The present study was designed to determine the role of protein kinase C (PKC) in the myogenic response of small arteries. In particular, we tested whether inhibition of PKC reverses the previously found pressure-induced elevation of contractile element calcium sensitivity. 2. Rat mesenteric small arteries were cannulated and pressurized. The internal diameter was continuously monitored with a video camera and intracellular calcium levels were measured by means of fura-2. Myogenic responses were observed when the pressure was raised stepwise from 20 to 60 and then to 100 mmHg in physiological saline solution and during application of phenylephrine (0.1 or 1 ,mol/L) or potassium (36 mmol/L). 3. The PKC inhibitors H-7 (20 ,mol/L), staurosporine (100 nmol/L) and calphostin C (10 nmol/L) all completely abolished the myogenic response. Whereas staurosporine caused an ongoing reduction in intracellular calcium, pressure-induced calcium transients were not affected by either H-7 or calphostin C. In particular, the slope of the wall tension,calcium relationship remained similar in the presence of both H-7 and calphostin C, despite an upward shift of this relationship to higher calcium levels in the case of calphostin C. 4. These results show that activity of PKC isoform(s) is essential for myogenic calcium,contraction coupling. [source] | ||||||||||