Pressure-diameter Data Research Articles

Comparative analysis of arterial compliance in mice genetically null for cathepsins K, L, or S

Cysteine cathepsins are potent proteases implicated in cardiovascular disease for degrading extracellular matrix (ECM) whose structure and integrity determine the mechanical behavior of arteries. Cathepsin knockout mouse models fed atherogenic diets have been used to study their roles in cardiovascular disease, but the impacts of cathepsin knockout on non-atherosclerotic arterial mechanics are scarce. We examine arterial mechanics in several cathepsin knockout mouse lines (CatK−/−, CatL−/−ApoE−/− and CatS−/−ApoE−/−) and controls (C57/Bl6, apolipoprotein E−/−). Common carotid arteries of three month-old mice were isolated and underwent biaxial mechanical testing and opening angle tests. Measured wall thicknesses and pressure-diameter curves were fed into a 4-fiber constitutive model to assess differences in material properties. Pressure-diameter data revealed CatL−/−ApoE−/− arteries were smaller in caliber compared to CatK−/−, CatS−/−ApoE−/− and ApoE−/− controls and were less compliant than ApoE−/− and CatS−/−ApoE−/− arteries at lower pressures, where elastin governs the mechanical response. CatK−/− arteries showed increased in vivo axial stretches compared to CatL−/−ApoE−/− and CatS−/−ApoE−/− arteries. CatL−/−ApoE−/− arteries were less compliant than ApoE−/− and CatS−/−ApoE−/− arteries pressurized to sub-diastolic pressures. 4-fiber and unified fiber distribution models were able to capture arteries’ nonlinear mechanical responses; calculated material parameters suggested that ApoE−/− arteries had increased axial parameters compared to CatL−/−ApoE−/− and CatS−/−ApoE−/− arteries. Taken together, the data suggests that loss of the potent collagenase catK increases axial and circumferential arterial compliance, while knockout of the elastase catL decreased circumferential arterial compliance, and knockout of the elastase catS showed no impact on carotid arterial mechanics.

A structural approach to 3D-printing arterial phantoms with physiologically comparable mechanical characteristics: Preliminary observations.

Pulse wave behavior is important in cardiovascular pathophysiology and arterial phantoms are valuable for studying arterial function. The ability of phantoms to replicate complex arterial elasticity and anatomy is limited by available materials and techniques. The feasibility of improving phantom performance using functional structure designs producible with practical 3D printing technologies was investigated. A novel corrugated wall approach to separate phantom function from material properties was investigated with a series of designs printed from polyester-polyurethane using a low-cost open-source fused filament fabrication 3D printer. Nonpulsatile pressure-diameter data was collected, and a mock circulatory system was used to observe phantom pulse wave behavior and obtain pulse wave velocities. The measured range of nonpulsatile Peterson elastic strain modulus was 5.6–19 to 12.4–33.0 kPa over pressures of 5–35 mmHg for the most to least compliant designs respectively. Pulse wave velocities of 1.5–5 m s−1 over mean pressures of 7–55 mmHg were observed, comparing favorably to reported in vivo pulmonary artery measurements of 1–4 m s−1 across mammals. Phantoms stiffened with increasing pressure in a manner consistent with arteries, and phantom wall elasticity appeared to vary between designs. Using a functional structure approach, practical low-cost 3D-printed production of simple arterial phantoms with mechanical properties that closely match the pulmonary artery is possible. Further functional structure design development to expand the pressure range and physiologic utility of dir"ectly 3D-printed phantoms appears warranted.

Variation of Passive Biomechanical Properties of the Small Intestine along Its Length: Microstructure-Based Characterization.

Multiaxial testing of the small intestinal wall is critical for understanding its biomechanical properties and defining material models, but limited data and material models are available. The aim of the present study was to develop a microstructure-based material model for the small intestine and test whether there was a significant variation in the passive biomechanical properties along the length of the organ. Rat tissue was cut into eight segments that underwent inflation/extension testing, and their nonlinearly hyper-elastic and anisotropic response was characterized by a fiber-reinforced model. Extensive parametric analysis showed a non-significant contribution to the model of the isotropic matrix and circumferential-fiber family, leading also to severe over-parameterization. Such issues were not apparent with the reduced neo-Hookean and (axial and diagonal)-fiber family model, that provided equally accurate fitting results. Absence from the model of either the axial or diagonal-fiber families led to ill representations of the force- and pressure-diameter data, respectively. The primary direction of anisotropy, designated by the estimated orientation angle of diagonal-fiber families, was about 35° to the axial direction, corroborating prior microscopic observations of submucosal collagen-fiber orientation. The estimated model parameters varied across and within the duodenum, jejunum, and ileum, corroborating histologically assessed segmental differences in layer thicknesses.

Comparison of in vivo vs. ex situ obtained material properties of sheep common carotid artery

Patient-specific biomechanical modelling can improve preoperative surgical planning. This requires patient-specific geometry as well as patient-specific material properties as input. The latter are, however, still quite challenging to estimate in vivo.This study focuses on the estimation of the mechanical properties of the arterial wall. Firstly, in vivo pressure, diameter and thickness of the arterial wall were acquired for sheep common carotid arteries. Next, the animals were sacrificed and the tissue was stored for mechanical testing. Planar biaxial tests were performed to obtain experimental stress-stretch curves. Finally, parameters for the hyperelastic Mooney–Rivlin and Gasser–Ogden–Holzapfel (GOH) material model were estimated based on the in vivo obtained pressure-diameter data as well as on the ex situ experimental stress-stretch curves.Both material models were able to capture the in vivo behaviour of the tissue. However, in the ex situ case only the GOH model provided satisfactory results. When comparing different fitting approaches, in vivo vs. ex situ, each of them showed its own advantages and disadvantages. The in vivo approach estimates the properties of the tissue in its physiological state while the ex situ approach allows to apply different loadings to properly capture the anisotropy of the tissue. Both of them could be further enhanced by improving the estimation of the stress-free state, i.e. by adding residual circumferential stresses in vivo and by accounting for the flattening effect of the tested samples ex vivo.• Competing interests: none declared• Word count: 4716

Blood pressure in the Greenland shark as estimated from ventral aortic elasticity

We conducted in vitro inflations of freshly excised ventral aortas of the Greenland shark, Somniosus microcephalus, and used pressure-diameter data to estimate the point of transition from high to low compliance, which has been shown to occur at the mean blood pressure in other vertebrates including fishes. We also determined the pressure at which the modulus of elasticity of the aorta reached 0.4 MPa, as occurs at the compliance transition in other species. From these analyses, we predict the average ventral aortic blood pressure in S. microcephalus to be about 2.3-2.8 kPa, much lower than reported for other sharks. Our results support the idea that this species is slow moving and has a relatively low aerobic metabolism. Histological investigation of the ventral aorta shows that elastic fibres are present in relatively low abundance and loosely connected, consistent with this aorta having high compliance at a relatively low blood pressure.

Evaluation of pulmonary artery wall properties in congenital heart disease patients using cardiac magnetic resonance

Congenital heart disease patients (CHD) with complex right heart disease are often left with residual lesions that result in right ventricular (RV)-pulmonary artery (PA) dysfunction post surgery. The appropriate timing of re-intervention to correct these lesions is difficult to determine due to lack of suitable quantifiable diagnostic techniques. The PA wall (material) properties characterize the mechanical behavior of the PAs and thus, contribute significantly to the RV-PA function. Therefore, the arterial wall properties of the main PA (MPA), left PA (LPA), and right PA (RPA) of three CHD subjects with normal RV-PA function and anatomy were quantified using retrospective pressure-diameter data as input to a constitutive (material) model. Intra-vessel (MPA vs branched PAs) and inter-subject variability was observed in the wall properties and consequently, the arterial wall compliance and stress-stretch characteristics. The LPA was least compliant in comparison to the MPA and RPA. Also, the circumferential and axial stress in the PAs increased with the subject's age. Therefore, monitoring the wall properties of the individual PAs may provide valuable longitudinal (time-dependent) information on disease progression of CHD patients.

Biomechanical Characterization of Ascending Aortic Aneurysms

Ascending thoracic aortic aneurysms (ATAAs) are a silent disease, ultimately leading to dissection or rupture of the arterial wall. There is a growing consensus that diameter information is insufficient to assess rupture risk, whereas wall stress and strength provide a more reliable estimate. The latter parameters cannot be measured directly and must be inferred through biomechanical assessment, requiring a thorough knowledge of the mechanical behaviour of the tissue. However, for healthy and aneurysmal ascending aortic tissues, this knowledge remains scarce. This study provides the geometrical and mechanical properties of the ATAA of six patients with unprecedented detail. Prior to their ATAA repair, pressure and diameter were acquired non-invasively, from which the distensibility coefficient, pressure-strain modulus and wall stress were calculated. Uniaxial tensile tests on the resected tissue yielded ultimate stress and stretch values. Parameters for the Holzapfel-Gasser-Ogden material model were estimated based on the pre-operative pressure-diameter data and the post-operative stress-stretch curves from planar biaxial tensile tests. Our results confirmed that mechanical or geometrical information alone cannot provide sufficient rupture risk estimation. The ratio of physiological to ultimate wall stress seems a more promising parameter. However, wall stress estimation suffers from uncertainties in wall thickness measurement, for which our results show large variability, between patients but also between measurement methods. Our results also show a large strength variability, a value which cannot be measured non-invasively. Future work should therefore be directed towards improved accuracy of wall thickness estimation, but also towards the large-scale collection of ATAA wall strength data.

Abstract 515: Comparison of Aging and Disturbed Flow Effects on Arterial Wall Biomechanics

Introduction: Arterial stiffness is an age related disease that doubles ones cardiovascular mortality and functions as an intermediary step in the formation of atherosclerosis. We have recently demonstrated that low and oscillatory wall shear stress, termed disturbed flow (d-flow), leads to arterial stiffness in otherwise normal arteries. Since d-flow has been linked to atherosclerotic plaque formation, our objective is to compare the carotid artery mechanics of 12 week arteries exposed to 4 weeks of d-flow to that of untreated 80 week old s129 mice. We hypothesize that low and oscillatory shear governs the remodeling of the arteries in a way that mimics the effect of arterial stiffening associated with aging. Materials and Methods: We used a partial carotid ligation model in 12-week-old s129 male (n=3) and female (n=3) mice. 4 weeks post surgery we euthanized the animals and performed biaxial extension-inflation biomechanical testing, confocal imaging, histological studies and opening angle studies on the left (partially ligated) carotid artery (LCA) and right (non-ligated) carotid artery (RCA) in order to characterize their biomechanical behavior. The same testing was performed on s129 80-week-old male animals (n=4). Pressure-diameter (P-d) data were collected from cyclic pressurization ramps from 0 to 160 mmHg at constant axial extension levels ranging from 1.3 to 1.9. Compliance was calculated at the in-vivo axial stretch level of 1.7 for both age groups. Intima media thickness was analyzed from H&E stained histological slides. Results were compared with the unpaired, two-tailed t-test and significance was taken at p<0.05. Results and Conclusions: Partial ligation for 4 weeks drastically decreased the compliance of the 12-week-old left carotid in a way that exactly follows the stiffening of the arteries in the 80-week-old mice. The compliance of the non-manipulated right carotid arteries reflected the age related difference in the stiffness of young vs old arteries with statistical difference in the 30 - 90 mmHg range. We have established that low shear stress and oscillatory flow promote the increase in arterial stiffening in the partially ligated young mice in a way that mimics the age-related decrease in arterial compliance in old mice.

Non-invasive, energy-based assessment of patient-specific material properties of arterial tissue.

The mechanical properties of human biological tissue vary greatly. The determination of arterial material properties should be based on experimental data, i.e. diameter, length, intramural pressure, axial force and stress-free geometry. Currently, clinical data provide only non-invasively measured pressure-diameter data for superficial arteries (e.g. common carotid and femoral artery). The lack of information forces us to take into account certain assumptions regarding the in situ configuration to estimate material properties in vivo. This paper proposes a new, non-invasive, energy-based approach for arterial material property estimation. This approach is compared with an approach proposed in the literature. For this purpose, a simplified finite element model of an artery was used as a mock experimental situation. This method enables exact knowledge of the actual material properties, thereby allowing a quantitative evaluation of material property estimation approaches. The results show that imposing conditions on strain energy can provide a good estimation of the material properties from the non-invasively measured pressure and diameter data.

A mechanistic collagen recruitment model can explain passive property differences in resistance arteries from salt sensitive, fawn hooded and brown norway rats on low salt diets

A mechanistic model for collagen recruitment and passive response was developed which predicts the stress of elastin and collagen fibers in middle cerebral arteries based on available pressure‐diameter data for salt sensitive (SS/JrHsdMcwi, n=8), fawn hooded (FHH/EurMcwi, n=11) and brown norway (BN/NHsdMcwi, n=10) male rats, all maintained on a low salt (0.4% NaCl) diet. In this model, which describes total vessel wall stress as a sum of elastin and collagen stresses, a Weibull distribution function is assumed to describe gradual recruitment of collagen fibers in the vessel wall. It was found that the peak recruitment strain parameter for collagen was relatively invariant within each rat strain based on independent analysis of the experimental data. Subsequently with the peak recruitment strain parameter fixed, the remaining parameters describing ratios of cross sectional elastin and collagen area to total vessel wall area and shape of the recruitment distribution can be determined by fitting the model to experimental data. Applying this model to SS, BN and FH rat data shows that average elastin tension is 2.91 N/m for BN, 2.9 N/m for FH and 3.2N/m for SS and average collagen tension is 49.3 N/m for BN, 76.0 N/m for FH and 86.0 N/m for SS. Therefore we can conclude that cerebral arteries of the SS rat have stiffer passive properties than those of FH and BN rats, even before onset of any difference in hypertensive phenotype.

Relaxin regulates vascular wall remodeling and passive mechanical properties in mice

Administration of recombinant human relaxin (rhRLX) to conscious rats increases global arterial compliance, and small renal arteries (SRA) isolated from these rats demonstrate increased passive compliance. Here we characterize relaxin-induced vascular remodeling and examine its functional relevance. SRA and external iliac arteries (EIA) were examined in rhRLX-treated (1.0 μg/h for 5 days) and relaxin knockout mice. Arterial geometric remodeling and compositional remodeling were quantified using immunohistochemical and biochemical techniques. Vascular mechanical properties were quantified using an ex vivo preparation wherein pressure-diameter data were obtained at various axial lengths. Compared with vehicle-treated mice, SRA from rhRLX-treated mice showed outward geometric remodeling (increased unstressed wall area and wall-to-lumen area ratio), increased smooth muscle cell (SMC) density, reduction in collagen-to-total protein ratio, and unchanged elastin-to-tissue dry weight ratio. Compared with wild-type mice, relaxin knockout mice exhibited the opposite pattern: decreased unstressed wall area and wall-to-lumen area ratio, decreased SMC density, and increased collagen-to-total protein ratio. Although tissue biaxial strain energy of SRA was not different between rhRLX- and vehicle-treated groups at low-to-physiological circumferential and axial strains, it was lower for the rhRLX-treated group at the highest circumferential strain. In contrast to SRA, relaxin administration was not associated with any vascular remodeling or changes in passive mechanics of EIA. Thus relaxin induces both geometric and compositional remodeling in vessel-specific manner. Relaxin-induced geometric remodeling of SRA is responsible for the increase in passive compliance under low-to-physiological levels of circumferential and axial strains, and compositional remodeling becomes functionally relevant only under high circumferential strain.

In vivo measurement of proximal pulmonary artery elastic modulus in the neonatal calf model of pulmonary hypertension: development and ex vivo validation

Developing clinical work suggests that vascular stiffening plays a role in the progression of pulmonary hypertension (PH), while recent studies in animal models of hypoxic PH have found significant proximal vascular stiffening in the diseased population. Here, we develop and validate a minimally invasive, clinically realizable method to estimate the local elastic modulus of the proximal pulmonary arteries from pressure-diameter (PD) data. PD measurements were made in the main pulmonary arteries of 16 calves; lumen diameter was assessed using color M-mode tissue Doppler imaging ultrasound, while pressure was measured via catheter. Two methods corresponding to thin-walled pressure vessel theory ("thin") and Lame's equation for a thick-walled cylinder ("thick") were used to approximate the artery elastic modulus from PD measurements. The harvested arteries were tested independently to determine their "true" ex vivo elastic modulus and stiffness. Both approximations displayed excellent correlation with ex vivo elastic modulus of the calf main pulmonary artery (thin r(2) = 0.811; thick r(2) = 0.844; both P < 0.01). Bland-Altman analysis indicated that the thick-walled approximation has better overall agreement with ex vivo modulus. The approximations displayed quantitatively distinct regression slopes that were statistically different (P = 0.02). The elastic modulus of the main pulmonary artery can be reasonably estimated from combined color M-mode tissue Doppler imaging ultrasound and catheter pressure measurements in calves. Such measurements may be a valuable tool in the diagnosis and treatment of human PH.

Mechanisms of Arterial Remodeling in Hypertension

Diverse data collected over the past 4 decades suggest the existence of a mechanical homeostasis across multiple length and time scales in the vasculature. For example,1 stress fibers within endothelial and vascular smooth muscle cells appear to disassemble and then reassemble in a mechanically preferred manner when perturbed from a normal value of mechanical stress or strain; focal adhesions in smooth muscle cells and fibroblasts tend to increase in area in response to local increases in mechanical loading so as to maintain the stress constant at a preferred value; fibroblasts tend to increase the tractions that they exert on the extracellular matrix when external loads are decreased from a preferred value, thus suggesting an attempt to enforce a “tensional homeostasis”; vascular smooth muscle cells tend to relengthen to their normal, preferred values when an arteriole is forced into a vasoconstricted state for an extended period; and arteries tend to decrease in caliber in response to sustained decreases in flow-induced wall shear stress, to increase in thickness in response to sustained increases in pressure-induced circumferential stress, and to lengthen in response to extension-induced increases in axial stress. Although changes in the cytoskeleton and integrins occur within minutes, changes at the cell-cell and cell-matrix levels occur over hours, and those at the vessel level occur over days to weeks or months. Hence, despite marked differences in length scales (dimensions from nanometers to centimeters) and time scales (durations from minutes to months), mechanobiological control mechanisms in the vasculature tend to restore values of stress or strain toward preferred (homeostatic) values in response to diverse perturbations from normal.2–5 Biomechanics and mechanobiology thus play key roles in vascular development, tissue maintenance in maturity, normal adaptations, aging, disease progression, and responses to injury or clinical interventions. A current challenge in hypertension research is to …

Towards in vivo aorta material identification and stress estimation.

This paper addresses the problem of constructing a mechanical model for the abdominal aorta and calibrating its parameters to in vivo measurable data. The aorta is modeled as a pseudoelastic, thick-walled, orthotropic, residually stressed cylindrical tube, subjected to an internal pressure. The model parameters are determined by stating a minimization problem for the model pressure and computing the optimal solution by a minimization algorithm. The data used in this study is in vivo pressure-diameter data for the abdominal aorta of a 24-year-old man. The results show that the axial, circumferential and radial stresses have magnitudes in the span 0 to 180 kPa. Furthermore, the results show that it is possible to determine model parameters directly from in vivo measurable data. In particular, the parameters describing the residual stress distribution can be obtained without interventional procedures.

Assessment of aortic line of elasticity using polynomial regression analysis.

The aim of this study was to assess the sigmoid line of elasticity in the human aorta. The pressure-diameter relation was measured in the descending aorta in 120 subjects. In an additional group of 6 subjects, transient vena caval occlusion produced 5 sets of pressure-diameter data. We found that the best fit curve of the pooled pressure-diameter data was a third-order polynomial. A polynomial equation was used to calculate the sigmoid line of elasticity in the entire population and after the administration of diltiazem (15 patients) or enalaprilat (10 patients). The sigmoid line of elasticity was significantly different with respect to age (P<0.001), history of hypertension (P<0.004), and hypercholesterolemia (P<0.02). The difference between the transition point and the peak systolic pressure was increased in normal subjects compared with patients (P<0.0001). The sigmoid line shifted leftward and upward with diltiazem, but it remained unchanged with enalaprilat. During an average of 3 years of follow-up, 19 of 88 patients developed stroke (n=4), unstable angina (n=8), acute myocardial infarction (n=4), or acute pulmonary edema (n=3). This approach provides a quantitative evaluation of the aortic line of elasticity, which can differentiate the intrinsic from the extrinsic aortic elastic properties. Furthermore, it is a powerful and independent risk factor for cardiovascular events.

Experimental Approaches on Measuring the Mechanical Properties and Constitutive Laws of Arterial Walls

Studies on the elastic properties of arterial walls which have been done for the past two decades are surveyed briefly. After several in vitro and in vivo experimental methods and clinical techniques for the measurements of the mechanical behavior of arterial walls have been reviewed, data obtained of the basic characteristics of the arterial wall, including wall incompressibility and anisotropy, are discussed. The author then reviews constitutive laws proposed for the description of stress-strain relationships of arterial walls and methods for the parametric expression of pressure-diameter data, and shows data on the effects of aging and vascular diseases on arterial mechanics. Finally, residual stress in the arterial wall is discussed.

Mechanics and composition of cerebral arterioles in renal and spontaneously hypertensive rats.

The purpose of this study was to examine effects of hypertension on mechanics of cerebral arterioles in nongenetic and genetic models of chronic hypertension. Pressure (servo null) and diameter were measured in pial arterioles of anesthetized renal hypertensive rats (one-kidney, one clip), uninephrectomized normotensive rats, spontaneously hypertensive rats, and normotensive Wistar-Kyoto rats. During maximal dilatation with EDTA, external diameter of pial arterioles at 70 mm Hg pial arteriolar pressure was not significantly different in renal hypertensive and normotensive rats (86 +/- 5 [mean +/- SEM] versus 84 +/- 4 microns) but was less in spontaneously hypertensive rats than in Wistar-Kyoto rats (81 +/- 3 versus 92 +/- 3 microns; p < 0.05). Cross-sectional area of the arteriolar wall (histological) was greater in renal hypertensive than in normotensive rats (1,360 +/- 131 versus 952 +/- 89 microns 2; p < 0.05) and in spontaneously hypertensive rats than in Wistar-Kyoto rats (1,294 +/- 97 versus 817 +/- 86 microns 2; p < 0.05). The stress-strain relation obtained from pressure-diameter data during maximal dilatation with EDTA indicated that distensibility of pial arterioles, when fully relaxed, was greater in renal hypertensive and spontaneously hypertensive rats than in normotensive and Wistar-Kyoto rats. We used point-counting stereology to quantitate composition of pial arterioles in renal hypertensive rats. Cross-sectional area of smooth muscle and elastin was significantly greater in renal hypertensive than in normotensive rats (smooth muscle, 947 +/- 108 versus 620 +/- 62 microns 2; elastin, 101 +/- 11 versus 55 +/- 6 microns 2; p < 0.05), whereas cross-sectional area of collagen and basement membrane was not significantly different in the two groups (collagen, 6 +/- 1 versus 5 +/- 1 microns 2; basement membrane, 120 +/- 12 versus 104 +/- 8 microns 2). Thus, we conclude that 1) cerebral arterioles undergo hypertrophy in both renal hypertensive and spontaneously hypertensive rats; 2) cerebral arterioles in renal hypertensive rats do not undergo "remodeling" with a reduction in external diameter, whereas external diameter is smaller in spontaneously hypertensive than in Wistar-Kyoto rats; 3) distensibility of cerebral arterioles, when fully relaxed, is increased in renal hypertensive rats and is greater in spontaneously hypertensive than in Wistar-Kyoto rats; and 4) the distensible components of the arteriolar wall are increased disproportionately in cerebral arterioles of renal hypertensive rats, which may contribute to increases in arteriolar distensibility.

Adjuvant N-(2-mercaptopropionyl)-glycine in blood cardioplegia does not improve myocardial protection in ischemically damaged hearts

Oxyradicals potentially limit the myocardial protection provided by blood cardioplegia in ischemically damaged hearts. We tested the hypothesis that the addition to blood cardioplegic solution of a new oxyradical scavenger--N-(2-mercaptopropionyl)-glycine--would result in improved left ventricular performance and oxygen consumption compared to that resulting from the use of blood cardioplegia alone. Gauges and transducer-tipped catheters for left ventricular minor axis ultrasonic dimension were placed in 17 open-chest dogs, and instantaneous left ventricular pressure-diameter data were acquired by computer. The aorta was crossclamped for 30 minutes during total vented bypass to induce ischemic injury. The heart was reoxygenated and protected by multidose, hypothermic blood cardioplegic solution alone (n = 9) or enhanced with 0.0132 mmol N-(2-mercaptopropionyl)-glycine (n = 8) for 1 hour of cardioplegia-induced arrest. Preischemic and postischemic left ventricular performance was measured by slope changes in end-systolic pressure-diameter relations induced by gradual afterload reduction during right heart bypass. When blood cardioplegia alone was used, postischemic left ventricular systolic performance was depressed by 73.2% +/- 10.0% (166.8 +/- 56.1 mm Hg/mm versus 25.1 +/- 7.0 mm Hg/mm). N-(2-mercaptopropionyl)-glycine did not significantly attenuate this functional depression (62.7% +/- 9.0%, 146.6 +/- 67.6 mm Hg/mm versus 33.6 +/- 11.9 mm Hg/mm). The postischemic end-diastolic pressure-diameter relation was shifted to the right, whereas chamber stiffness was increased comparably, with or without N-(2-mercaptopropionyl)-glycine. Postischemic oxygen consumption in the beating working state, calculated from left ventricular blood flow (measured by microspheres) and arterial-coronary sinus oxygen extraction, averaged 7.8 +/- 0.9 ml O2/100 gm/min with blood cardioplegia alone and 7.5 +/- 1.0 ml O2/100 gm/min with N-(2-mercaptopropionyl)-glycine, and was unchanged from paired preischemic values in both groups. We conclude (1) that N-(2-mercaptopropionyl)-glycine added to blood cardioplegic solution in the dose and delivery regimen tested did not improve ventricular systolic and diastolic performance compared with blood cardioplegia alone and (2) that postischemic oxygen consumption may not parallel the extent of left ventricular functional recovery.

In situ study of active and passive mechanical properties of rat tail artery.

The present study constitutes an effort to close the gap still existing between in vivo and in vitro experiments in vascular mechanics. Active and passive mechanical properties of the rat tail artery were studied in situ under conditions as close as possible to the natural in vivo state of the vessel. At constant pressure levels, changes in diameter as caused after dilatation by papaverine and constriction by norepinephrine, were automatically and continuously registered using a contact free measurement technique (Video Dimension Analyzer). In order to check consistency of the in situ findings with analogous results from in vitro studies, pressure-diameter and stress-strain data were compared with results from our own and other authors. The results show that, quite similarly to in vitro, the maximum isobaric response of the tail artery in situ occurs in the physiological pressure range of some 100 mm Hg. Although the results focus the attention on the importance of both the experimental protocols and the definitions used, they confirm the validity of in vitro investigations as a powerful tool in arterial rheology.

Changes in arterial wall properties during development and maintenance of renal hypertension.

Segments of carotid and tail arteries were used to determine the effects of two-kidney Goldblatt hypertension on mechanical properties and chemical contents. Arteries were obtained after 4 and 12 wk of hypertension. Systolic pressures averaged 129 mmHg in control animals and 150 mmHg in hypertensive ones. Pressure-diameter data were recorded under conditions of active (145 mM K+) and passive (0 Ca2+ and 2 mM EGTA) smooth muscle. Small increases in passive stiffness were found after 4 and 12 wk in the carotid arteries of hypertensive animals, but no significant change occurred in the tail arteries. Small but significant decreases in total connective tissue content of these arteries were found after 12 wk of hypertension. Maximum values of active stress response were significantly larger in carotid arteries from hypertensive animals at both 4 and 12 wk of hypertension. No significant differences were found for the tail arteries. The K+ content of the carotid but not the tail artery was larger for the hypertensive animals. When corrected for differences in relative cell content most of the differences in active force development were eliminated. The differences in passive mechanics can not be explained on the basis of the changes in connective tissue content. The active smooth muscle responses and content changes suggest that they are directly related to the moderate elevation of arterial pressure.