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Circumferential Wall Stress (circumferential + wall_stress)
Selected AbstractsCOMPARISON OF ANGIOTENSIN II-INDUCED BLOOD PRESSURE AND STRUCTURAL CHANGES IN FISCHER 344 AND WISTAR KYOTO RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2004Jocelyne Blanc SUMMARY 1.,The purpose of the present study was to evaluate the blood pressure (BP) response, the BP and heart rate (HR) components of the startle reaction and the structure of the carotid artery and the aorta during chronic infusion of angiotensin (Ang) II in Fischer 344 (F344) compared with Wistar Kyoto (WKY) rats, two in-bred normotensive contrasted strains. 2.,Osmotic mini-pumps filled with saline vehicle or AngII (120 ng/kg per min) were implanted subcutaneously in 8-week-old normotensive rats and infused for 4 weeks in F344 rats (saline, n = 10; AngII, n = 10) and WKY rats (saline, n = 10; AngII, n = 9). Basal BP, HR and the responses to an acoustic startle stimulus (duration 0.7 s, 115 dB) were recorded in conscious rats. The structure of the carotid artery and aorta was determined in 4% formaldehyde-fixed arteries. 3.,Compared with WKY rats, vehicle-treated F344 rats had lower bodyweight (BW; 266 ± 7 vs 299 ± 9 g; P < 0.05) and heart weight (0.80 ± 0.02 vs 0.98 ± 0.04 g; P < 0.05) and higher aortic systolic BP (SBP; 131 ± 1 vs 123 ± 5 mmHg; P < 0.001) and diastolic BP (98 ± 3 vs 89 ± 2 mmHg; P < 0.001). In F344 rats, compared with the WKY rats, the wall thickness/BW ratio was increased in the carotid artery (156 ± 9 vs 131 ± 6 nm/g; P < 0.05) and abdominal aorta (264 ± 13 vs 217 ± 12 nm/g; P < 0.05) and decreased in the thoracic aorta (246 ± 13 vs 275 ± 8 nm/g; P < 0.05). There was no difference in elastin and collagen density. Angiotensin II differentially enhanced BP in both strains: (SBP: 163 ± 5 and 132 ± 4 mmHg in F344 and WKY rats, respectively; Pstrain × treatment < 0.05). Circumferential wall stress was increased in the aorta of F344 rats compared with WKY rats (1176 ± 39 vs 956 ± 12 kPa (P < 0.001) and 1107 ± 42 vs 813 ± 12 kPa (P < 0.001) in thoracic and abdominal aortas, respectively). The startle response was amplified in F344 rats, with enhanced increases in SBP and pulse pressure (PP) and bradycardia compared with responses of WKY rats (+44 ± 9 mmHg, +10 ± 2 mmHg and ,40 ± 17 b.p.m., respectively, in F344 rats vs+28 ± 4 mmHg, + 4 ± 2 mmHg and ,19 ± 10 b.p.m. in WKY rats, respectively; Pstrain < 0.05 for BP and PP). The startle response was not affected by AngII. 4.,These results indicate a higher BP producing an increase in wall thickness in F344 rats compared with WKY rats. We propose that an increase in sympathetic nervous activity causes these haemodynamic differences, as suggested by the excessive increase in BP during an acoustic startle stimulus. Angiotensin II increased BP in F344 rats, but did not exaggerate the increase in BP during the startle reaction. [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] Assessment of left ventricular systolic function using tissue Doppler imaging in children after successful repair of aortic coarctationCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 1 2010Tomasz Florianczyk Summary Aim:, Assessment of left ventricular systolic function in children after the successful repair of aortic coarctation using tissue Doppler imaging (TDI). Methods:, The study group consisted of 32 patients (mean age 12·0 ± 4·2 years) after the aortic coarctation repair. The TDI parameters and the conventional echocardiographic endocardial and midwall indices of the left ventricular systolic function were analysed and compared with the results obtained from 34 healthy children. Results:, The systolic mitral annulus motion velocity, systolic myocardial velocity of the medial segment of the left ventricular septal wall, left ventricular strain and Strain Rate (SR) in the study group were significantly higher than in the control group, respectively: 6·92 ± 0·75 cm s,1 versus 6·45 ± 0·83 cm s,1; 5·82 ± 1·03 cm s,1 versus 5·08 ± 1·11 cm s,1; ,28·67 ± 6·04% versus ,22·53 ± 6·44% and ,3·20 ± 0·76 s,1 versus ,2·39 ± 0·49 s,1. Except midwall shortening fraction the conventional endocardial and midwall echocardiographic indices in the study group were significantly higher in comparison to the healthy controls. The left ventricular systolic meridional fibre stress and end-systolic circumferential wall stress did not differ between the examined groups. There were no differences of the TDI or conventional parameters between hypertensive and normotensive patients. Conclusions:, Left ventricular systolic performance in children after the surgical repair of aortic coarctation reveals tendency to rise in late follow-up despite a satisfactory result after surgery. Higher systolic strain and SR in children treated due to coarctation of the aorta may suggest the increased preserved left ventricular performance despite normalization of afterload. [source] Physiological determinants of the variation in left ventricular mass from early adolescence to late adulthood in healthy subjectsCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 4 2007Peter A. Cain Summary Background:, The physiological determinants of left ventricular mass (LVM) measured by cardiac magnetic resonance (CMR) imaging are not well defined as prior investigators have studied either adults or adolescents in isolation or have not strictly excluded hypertension or accounted for the effects of exercise habits, haemodynamic, demographic, or body shape characteristics. Methods:, Ninety-seven healthy volunteers (11,81 years, 51 males) underwent CMR. All parameters [unstandardized and adjusted for body surface area (BSA)] were analysed according to gender and by adolescence versus adulthood (adolescents <20 years, adults ,20 years). The influence of haemodynamic factors, exercise and demographic factors on LVM were determined with multivariate linear regression. Results:, Left ventricular mass rose during adolescence and declined in adulthood. LVM and LVMBSA were higher in males both in adults (LVM: 188 ± 22 versus 140 ± 21 g, P<0·001; LVMBSA: 94 ± 11 versus 80 ± 11 g m,2, P<0·001) and in adolescents when adjusted for BSA (LVM: 128 ± 29 versus 107 ± 20 g, P = 0·063; LVMBSA: 82 ± 8 versus 71 ± 10 g m,2, P = 0·025). In adults, systolic blood pressure (SBP) and self-reported physical activity increased while meridional and circumferential wall stress were constant with age. Multivariate regression analysis revealed age, gender and BSA as the major determinants of LVM (global R2 = 0·68). Conclusions:, Normal LVM shows variation over a broad age range in both genders with a rise in adolescence and subsequent decline with increasing age in adulthood despite an increase in SBP and physical activity. BSA, age and gender were found to be major contributors to the variation in LVM in healthy adults, while haemodynamic factors, exercise and wall stress were not. [source] | ||||||||||