(1/740) Fibrocartilage in tendons and ligaments--an adaptation to compressive load.

Where tendons and ligaments are subject to compression, they are frequently fibrocartilaginous. This occurs at 2 principal sites: where tendons (and sometimes ligaments) wrap around bony or fibrous pulleys, and in the region where they attach to bone, i.e. at their entheses. Wrap-around tendons are most characteristic of the limbs and are commonly wider at their point of bony contact so that the pressure is reduced. The most fibrocartilaginous tendons are heavily loaded and permanently bent around their pulleys. There is often pronounced interweaving of collagen fibres that prevents the tendons from splaying apart under compression. The fibrocartilage can be located within fascicles, or in endo- or epitenon (where it may protect blood vessels from compression or allow fascicles to slide). Fibrocartilage cells are commonly packed with intermediate filaments which could be involved in transducing mechanical load. The ECM often contains aggrecan which allows the tendon to imbibe water and withstand compression. Type II collagen may also be present, particularly in tendons that are heavily loaded. Fibrocartilage is a dynamic tissue that disappears when the tendons are rerouted surgically and can be maintained in vitro when discs of tendon are compressed. Finite element analyses provide a good correlation between its distribution and levels of compressive stress, but at some locations fibrocartilage is a sign of pathology. Enthesis fibrocartilage is most typical of tendons or ligaments that attach to the epiphyses of long bones where it may also be accompanied by sesamoid and periosteal fibrocartilages. It is characteristic of sites where the angle of attachment changes throughout the range of joint movement and it reduces wear and tear by dissipating stress concentration at the bony interface. There is a good correlation between the distribution of fibrocartilage within an enthesis and the levels of compressive stress. The complex interlocking between calcified fibrocartilage and bone contributes to the mechanical strength of the enthesis and cartilage-like molecules (e.g. aggrecan and type II collagen) in the ECM contribute to its ability to withstand compression. Pathological changes are common and are known as enthesopathies.  (+info)

(2/740) Investigation of distal aortic compliance and vasodilator responsiveness in heart failure due to proximal aortic stenosis in the guinea pig.

Hypotension and syncope are recognized features of chronic aortic stenosis. This study examined vasomotor responses and dynamic compliance in isolated abdominal aortae after chronic constriction of the ascending aorta. Guinea pigs underwent constriction of the ascending aorta or sham operation. Sections of descending aorta were removed for studies of contractile performance and compliance. Dynamic compliance was measured using a feedback-controlled pulsatile pressure system at frequencies of 0.5, 1.5 and 2.5 Hz and mean pressures from 40 to 100 mmHg. Chronic (149+/-6 days) aortic constriction resulted in significant increases in organ weight/body weight ratios for left ventricle (58%), right ventricle (100%) and lung (61%). The presence of heart failure was indicated by increased lung weights, left ventricular end-diastolic pressure and systemic vascular resistance, reduced cardiac output and increased levels of plasma atrial natriuretic peptide (166%), adrenaline (x20), noradrenaline (106%) and dopamine (x3). Aortic rings showed similar constrictor responses to phenylephrine and angiotensin II, but maximal vasodilator responses to acetylcholine and isoprenaline were significantly increased (144% and 48% respectively). Dilator responses to sodium nitroprusside, forskolin and cromokalim were unchanged. Compliance of all vessels decreased with increasing pulsatile frequency and to a lesser extent with increased mean pressure, but were similar in aortic-constricted and control groups. Chronic constriction of the ascending aorta resulted in heart failure and increased vasodilator responses to acetylcholine and isoprenaline in the distal aorta while dynamic compliance was unchanged. We hypothesize that increased endothelium-mediated vasodilatation may contribute to hypotension and syncope in patients with left ventricular outflow obstruction.  (+info)

(3/740) Balloon-artery interactions during stent placement: a finite element analysis approach to pressure, compliance, and stent design as contributors to vascular injury.

Endovascular stents expand the arterial lumen more than balloon angioplasty and reduce rates of restenosis after coronary angioplasty in selected patients. Understanding the factors involved in vascular injury imposed during stent deployment may allow optimization of stent design and stent-placement protocols so as to limit vascular injury and perhaps reduce restenosis. Addressing the hypothesis that a previously undescribed mechanism of vascular injury during stent deployment is balloon-artery interaction, we have used finite element analysis to model how balloon-artery contact stress and area depend on stent-strut geometry, balloon compliance, and inflation pressure. We also examined superficial injury during deployment of stents of varied design in vivo and in a phantom model ex vivo to show that balloon-induced damage can be modulated by altering stent design. Our results show that higher inflation pressures, wider stent-strut openings, and more compliant balloon materials cause markedly larger surface-contact areas and contact stresses between stent struts. Appreciating that the contact stress and contact area are functions of placement pressure, stent geometry, and balloon compliance may help direct development of novel stent designs and stent-deployment protocols so as to minimize vascular injury during stenting and perhaps to optimize long-term outcomes.  (+info)

(4/740) Physiological changes in blood glucose do not affect gastric compliance and perception in normal subjects.

Marked hyperglycemia (blood glucose approximately 14 mmol/l) slows gastric emptying and affects the perception of sensations arising from the gut. Elevation of blood glucose within the physiological range also slows gastric emptying. This study aimed to determine whether physiological changes in blood glucose affect proximal gastric compliance and/or the perception of gastric distension in the fasting state. Paired studies were conducted in 10 fasting healthy volunteers. On a single day, isovolumetric and isobaric distensions of the proximal stomach were performed using an electronic barostat while the blood glucose concentration was maintained at 4 and 9 mmol/l in random order. Sensations were quantified using visual analog scales. The blood glucose concentration had no effect on the pressure-volume relationship during either isovolumetric or isobaric distensions or the perception of gastric distension. At both blood glucose concentrations, the perceptions of fullness, nausea, bloating, and abdominal discomfort, but not hunger or desire to eat, were related to intrabag volume (P +info)

(5/740) Aortic pressure-diameter relationship assessed by intravascular ultrasound: experimental validation in dogs.

Intravascular ultrasound (IVUS) has emerged as an important diagnostic method for evaluating vessel diameter and vessel wall motion. To evaluate the validity of IVUS in assessing changes in the pressure-diameter relationship we compared measurements of abdominal aortic diameters derived from IVUS with those simultaneously obtained at the same site using implanted sonomicrometers in five chronically instrumented conscious dogs and in seven acutely instrumented anesthetized dogs. Five hundred eighty beats were analyzed to obtain peak systolic and end-diastolic diameters and to calculate aortic compliance at different blood pressure levels induced either by an aortic pneumatic cuff or by intravenous injections of nitroglycerin or norepinephrine. IVUS agreed closely with sonomicrometer measurements at different blood pressure levels. However, IVUS slightly but significantly underestimated aortic diameters by 0.6 +/- 0.7 mm for systolic diameters (P < 0.001) and by 0.7 +/- 0.6 mm for diastolic diameters (P < 0.001) compared with the sonomicrometer measurements. We conclude that IVUS is a feasible and reliable method to measure dynamic changes in aortic dimensions and has the potential to provide ready access to assess aortic compliance in humans.  (+info)

(6/740) The compliance of collagen gels regulates transforming growth factor-beta induction of alpha-smooth muscle actin in fibroblasts.

Wound contraction is mediated by myofibroblasts, specialized fibroblasts that appear in large numbers as the wound matures and when resistance to contractile forces increases. We considered that the regulation of myofibroblast differentiation by wound-healing cytokines may be dependent on the resistance of the connective tissue matrix to deformation. We examined transforming growth factor-beta1 (TGF-beta1) induction of the putative fibroblast contractile marker, alpha-smooth muscle actin (alpha-SMA), and the regulation of this process by the compliance of collagen substrates. Cells were cultured in three different types of collagen gels with wide variations of mechanical compliance as assessed by deformation testing. The resistance to collagen gel deformation determined the levels of intracellular tension as shown by staining for actin stress fibers. For cells plated on thin films of collagen-coated plastic (ie, minimal compliance and maximal intracellular tension), TGF-beta1 (10 ng/ml; 6 days) increased alpha-SMA protein content by ninefold as detected by Western blots but did not affect beta-actin content. Western blots of cells in anchored collagen gels (moderate compliance and tension) also showed a TGF-beta1-induced increase of alpha-SMA content, but the effect was greatly reduced compared with collagen-coated plastic (<3-fold increase). In floating collagen gels (high compliance and low tension), there were only minimal differences of alpha-SMA protein. Northern analyses for alpha-SMA and beta-actin indicated that TGF-beta1 selectively increased mRNA for alpha-SMA similar to the reported protein levels. In pulse-chase experiments, [35S]methionine-labeled intracellular alpha-SMA decayed most rapidly in floating gels, less rapidly in anchored gels, and not at all in collagen plates after TGF-beta1 treatment. TGF-beta1 increased alpha2 and beta1 integrin content by 50% in cells on collagen plates, but the increase was less marked on anchored gels and was undetectable in floating gels. When intracellular tension on collagen substrates was reduced by preincubating cells with blocking antibodies to the alpha2 and beta1 integrin subunits, TGF-beta1 failed to increase alpha-SMA protein content in all three types of collagen matrices. These data indicate that TGF-beta1-induced increases of alpha-SMA content are dependent on the resistance of the substrate to deformation and that the generation of intracellular tension is a central determinant of contractile cytoskeletal gene expression.  (+info)

(7/740) Assessment of arterial compliance by carotid midwall strain-stress relation in normotensive adults.

Examining left ventricular midwall as opposed to endocardial mechanics enhances understanding of left ventricular function in individuals with abnormal cardiac geometry. Accordingly, we used carotid ultrasound and applanation tonometry of arterial pressure to derive carotid midwall strain and its relation to carotid peak-systolic and end-diastolic stresses in 82 apparently normal, employed subjects (56 men, 26 women; median age, 47 years; 70% white; 21% overweight) with no evidence of coronary or valvular heart disease. Regression equations relating carotid luminal and midwall strain to the increment in carotid stress during systole (Deltacarotid stress) were used to predict strain for the observed Deltastress. Observed/predicted carotid luminal or midwall strain was calculated as a measure of carotid luminal or midwall strain for imposed stress, termed stress-corrected strain. Midwall carotid strain was similar in women and men but was negatively related to older age (r=-0.35, P=0.001) and higher body mass index (r=-0.31, P=0.005) and brachial and carotid blood pressure (r=-0.30 to -0.45, all P<0.01). The pulsatile change in arterial load, measured by Deltacarotid stress, was positively related to midwall strain (r=0. 44, P<0.001) more closely than was carotid luminal strain. Regression analyses revealed that carotid midwall strain was positively related to Deltastress, with additional negative relations to age and carotid diastolic diameter (all P<0.001). Stress-corrected carotid midwall strain was strongly and negatively correlated with midwall elastic modulus and Young's modulus (both r=-0.77, P<0.001), followed by elastic modulus (r=-0.74, P<0.001), midwall Young's modulus (r=-0.73, P<0.001), midwall stiffness index (r=-0.70, P<0.001), and stiffness index (r=-0.66, P<0.001). Thus, in normal adults, carotid midwall strain is unrelated to gender, is positively related to pulsatile carotid load as measured by Deltacarotid stress, and is negatively related to age, overweight, and standard measures of arterial stiffness.  (+info)

(8/740) Assessment of arterial compliance by carotid midwall strain-stress relation in hypertension.

To elucidate the relations between arterial hypertrophy and compliance in hypertension, we studied 205 unmedicated hypertensive patients (129 men and 76 women) and 82 normotensive adults (56 men and 26 women) from an employed population by carotid ultrasound, noninvasive applanation tonometry, and echocardiography. Carotid midwall strain and circumferential stress were calculated at end diastole and peak systole. The relations of luminal and midwall strain to the increment in circumferential stress from end diastole to peak systole (Deltacarotid stress in normal subjects) were used to calculate ratios of observed/predicted carotid luminal and midwall strain. Mean stress-corrected luminal strain (82+/-26%) and midwall strain (78+/-23%) were lower (both P<0.001) in hypertensive patients than in normal adults. Stress-corrected luminal strain identified 14% of hypertensive patients with low arterial compliance, while stress-corrected midwall strain was low in 18% of patients. Patients with subnormal carotid midwall strain were older (61+/-12 versus 54+/-12 years, P<0.01) and had larger carotid diameters (6. 6+/-0.8 versus 5.7+/-0.8 mm, P=0.002) and higher brachial pulse pressures (71+/-25 versus 63+/-17 mm Hg, P<0.05) than other patients. Patients with arterial hypertrophy had lower stress-corrected midwall strain than those without hypertrophy (70+/-24% versus 79+/-23%, P=0.05), whereas no difference was observed in stress-corrected luminal strain (P=0.40). Stress-corrected midwall strain tended to be lower in patients with discrete atherosclerotic plaques than in those without (74+/-20% versus 79+/-24%, P=0.15). Compared with patients with normal left ventricular geometry, those with concentric hypertrophy had larger carotid diameters (6.6+/-0.7 versus 5.8+/-0.9 mm, P<0.05) and lower stress-corrected luminal strain (62+/-11% versus 85+/-25%, P<0.05) and midwall strain (59+/-10% versus 81+/-22%, P<0.05). Therefore, stress-corrected midwall strain identifies patients with reduced arterial compliance, increased arterial wall thickness, and abnormal left ventricular geometry better than conventional measures based on arterial lumen diameters.  (+info)