Aortic Wall Tension Research Articles

Coronary Perfusion Pressure during Antegrade Cardioplegia in On-Pump CABG Patients.

ObjectiveThe aim of this study was to investigate whether aortic tension estimated by palpation and cardioplegia infusion line pressure provide results equivalent to those obtained with direct aortic intraluminal pressure measurement.MethodsSixty consecutive patients who underwent coronary artery bypass graft surgeries with extracorporeal circulation were analyzed. Sanguineous cardioplegic solution in a ratio of 4:1 was administered using a triple lumen antegrade cannula. After crossclamping, cardioplegia was infused and aortic root pressure was recorded by surgeon (A) considering the aortic tension he felt in his fingertips. At the same time, another surgeon (B) recorded his results for the same measurement. Concomitantly, the anesthesiologist recorded intraluminal pressure in the aortic root and the perfusionist recorded delta pressure in cardioplegia infusion line. None of the participants involved in these measurements was allowed to be informed about the values provided by the other examiners.ResultsThe Bland-Altman test showed that a considerable variation between aortic wall tension was found as measured by palpation and by intraluminal pressure, with a bias of -9.911±18.75% (95% limits of agreement: -46.7 to 26.9). No strong correlation was observed between intraluminal pressure and cardioplegia line pressure (Spearman's r=0.61, 95% confidence interval 0.5-0.7; P<0.0001).ConclusionThese findings reinforce that cardioplegia infusion should be controlled by measuring intraluminal pressure, and that palpation and cardioplegia line pressure are inaccurate methods, the latter should always be used to complement intraluminal measurement to ensure greater safety in handling the cardioplegia circuit.

Abstract 135: Thoracic Aortic Wall Tension Regulates microRNA-133a Abundance

Background: MicroRNA-133a (miR133a) is a small non-coding RNA, which represses the translation of multiple mRNAs. This laboratory has reported an inverse relationship between aortic diameter and miR133a abundance in aortic tissue from patients with thoracic aortic aneurysm (TAA); as diameter increased, the abundance of miR133a decreased. Given that wall tension at a given pressure increases with increasing vessel diameter (Law of LaPlace), this study tested the hypothesis that elevated aortic wall tension results in a loss of miR-133a. Methods/Results: TAA was induced in wild type mice using an established murine model (0.5M CaCl 2 application, 15 min). MiR133a abundance (QPCR) was reduced in TAA tissue (3-wk TAA, 42.1±8.6% p&lt;0.05 vs mice without TAA (100%)). In two in vivo models of elevated wall tension ( simulated hypertension ): 1) ANGII (angiotensin II infusion; 1.44mg/kg/day), and 2) BPH2 (spontaneously hypertensive mice, The Jackson Laboratory, Stock #003005), miR133a levels were decreased compared to normotensive controls (ANGII: 53.0±4.3%; BPH2: 51.7±7.0%; p&lt;0.05 vs normotensive control (100%)). Aortic rings from wild type mice were hung on parallel wires in an ex vivo tissue myograph at 0.7 g, then ANGII (100nM) was added to the tissue baths, which generated increased tension (1.21±0.15g) and resulted in reduced tissue miR133a abundance (46.0±12%; p&lt;0.05 vs no AngII,). Furthermore, increased tension alone (1.5g, 3 hr) resulted in decreased tissue miR133a abundance (39.0±7.0%; p&lt;0.05 vs 0.7 g tension). Isolated primary aortic cell lines (fibroblasts (FB) and smooth muscle cells (SMC)) were exposed to biaxial cyclic stretch for 3 hr. FB miR133a was reduced (62.8±8.3%; p&lt;0.05 vs unstretched control (100%)), while SMC miR133a abundance remained unchanged. Conclusion: The significance of these unique findings is 2-fold: First, tension alone was sufficient to decrease miR133a abundance in aortic tissue. Second, increased tension reduced miR133a abundance in FB, a cell type that is responsible for extracellular matrix remodeling. These findings suggest changes in wall tension alone ( hypertension ) may be associated with pathological extracellular matrix remodeling, in part, through the loss of miR133a in fibroblasts.

Pressure dependency of aortic pulse wave velocity in vivo is not affected by vasoactive substances that alter aortic wall tension ex vivo.

Aortic stiffness, a predictive parameter in cardiovascular medicine, is blood pressure dependent and experimentally requires isobaric measurement for meaningful comparison. Vasoactive drug administration to change peripheral resistance and blood pressure allows such isobaric comparison but may alter large conduit artery wall tension, directly changing aortic stiffness. This study quantifies effects of sodium nitroprusside (SNP, vasodilator) and phenylephrine (PE, vasoconstrictor) on aortic stiffness measured by aortic pulse wave velocity (aPWV) assessed by invasive pressure catheterization in anaesthetized Sprague-Dawley rats (n = 7). This was compared with nondrug-dependent alteration of blood pressure through reduced venous return induced by partial vena cava occlusion. In vivo drug concentration was estimated by modeling clearance rates. Ex vivo responses of excised thoracic and abdominal aortic rings to drugs was measured using myography. SNP administration did not alter aPWV compared with venous occlusion (P = 0.21-0.87). There was a 5% difference in aPWV with PE administration compared with venous occlusion (P < 0.05). The estimated in vivo maximum concentration of PE (7.0 ± 1.8 ×10(-7) M) and SNP (4.2 ± 0.6 ×10(-7) M) caused ex vivo equivalent contraction of 52 mmHg (thoracic) and 112 mmHg (abdominal) and relaxation of 96% (both abdominal and thoracic), respectively, despite having a negligible effect on aPWV in vivo. This study demonstrates that vasoactive drugs administered to alter systemic blood pressure have a negligible effect on aPWV and provide a useful tool to study pressure-normalized and pressure-dependent aPWV in large conduit arteries in vivo. However, similar drug concentrations affect aortic ring wall tension ex vivo. Future studies investigating in vivo and ex vivo kinetics will need to elucidate mechanisms for this marked difference.

Abstract 540: Mineralocorticoid Receptor Antagonism Prevents The Aortic Dilatation And Extracellular Matrix Degradation Induced By Beta-adrenoceptor Overactivation

Chronic stimulation of β-adrenoceptor (β-AR) and activation of renin-angiotensin-aldosterone system are common feature of cardiovascular diseases as heart failure and hypertension. β-AR overactivation induces cardiac remodeling, which contribute to cardiac dysfunction. However, it is unknown whether it alters arterial structure. Here, we demonstrated that β-AR overactivation induced by isoproterenol (ISO) treatment in Wistar rats (0.3 mg/kg/day, for 7 days) compared to control group (vs. CT, *p&lt;0.05) increased thoracic aortic lumen area (CT: 1.8±0.06 vs. ISO: 2.3±0.08* mm2) and internal diameter (ID) (CT: 1.63±0.28 vs. ISO: 1.77±0.08* mm), without changes on wall thickness (wt). ISO caused disorganization and rupture of elastin fibers (Score; CT: 1.53±0.07 vs. ISO: 2.52±0.27*) and reduced aortic collagen deposition measured by picrosiuris red (CT: 56±3 vs. ISO: 32±2* A.U./vessel area). These alterations induced by ISO were associated with increased phosphorylation of extracellular signal-regulated kinase 1/2 (p-ERK/ ERK; CT: 0.75±0.07 vs. ISO: 0.95±0.05* A.U.); increased matrix metalloproteinase (MMP)-2 activity evaluated by zymography (CT: 4.0±0.9 vs. ISO: 10.8±1.2* A.U.); and reduced protein expression of TIMP-2 (CT: 0.95 ±0.07 vs. ISO: 0.48±0.08* A.U.) and collagen I/III (CT: 0.9±0.08 vs. ISO: 0.6±0.06* A.U.). ISO treatment did not change mean arterial pressure (MAP); however, it increased the mechanical forces circumferential wall tension (CWT= MAPxID/2; CT: 10.1±0.35 vs. ISO: 11.6±0.35* 103dyn/cm) and tensile stress (TS=CWT/wt; CT: 102±6 vs. ISO: 121±6* 104dyn/cm2) on aorta. The co-treatment with spironolactone (SPI, 200 mg/kg/day), a mineralocorticoid receptor (MR) antagonist prevented the ISO-induced aortic structural changes, MMP-2 and ERK1/2 activation, as well as the reductions on collagen and TIMP-2 expression. However, SPI did not modify MAP, CWS or TS. The results suggest that β-AR overactivation induces an aneurysm-like thoracic aortic remodeling characterized by vessel dilatation and extracellular matrix degradation, associated with MMP-2 and ERK1/2 activation. This remodeling and signaling were prevented by MR antagonist, independently of changes on aortic wall tension and tensile stress.

Aortic Root Size and Prevalence of Aortic Regurgitation in Elite Strength Trained Athletes

Athletes involved in mainly static or isometric exercise (e.g., weight lifting, power lifting, and bodybuilding) develop pressure overloads due to the high systemic arterial pressure found in this type of exercise. It is hypothesized that chronically elevated aortic wall tension in strength-trained athletes is associated with aortic dilatation and regurgitation. The aim of this study was to evaluate aortic root size and the prevalence of aortic regurgitation in elite strength-trained athletes. The cohort included 100 male athletes (mean age 22.1 +/- 3.6 years; all were finalists or medalists in the country) and 128 healthy age- and height-matched subjects (the control group). Aortic root diameters at end-diastole were measured at 4 locations: (1) the aortic annulus, (2) the sinuses of Valsalva, (3) the sinotubular junction, and (4) the maximal diameter of the proximal ascending aorta. Aortic root diameters at all levels were significantly greater in the strength-trained athletes (p <0.05 for all comparisons). When the strength-trained athletes were divided into quartiles of duration of high-intensity strength training (first quartile: <18 months; second quartile: >18 and <36 months; third quartile: >36 and <54 months; fourth quartile: >54 months), progressive enlargement was found at all aortic diameters. In conclusion, aortic root diameters in all segments of the aortic root were significantly greater in elite strength-trained athletes compared with an age- and height-matched population.

Hipervolemia mais tríplice oclusão vascular no tratamento da lesão traumática da veia cava retro-hepática e veias hepáticas

BACKGROUND: Liver vascular isolation is essential for the treatment of the retrohepatic vena cava and hepatic veins. Triple vessel occlusion (TVO - occlusion of the portal triad, the inferior vena cava above the renal veins and within the pericardium) is the easiest isolation method for the surgeon. Unfortunately, this technique cannot be applied to hypovolemic and/or shock (cardiac arrest) patients as it compromises venous return. OBJECTIVES: Our objective is to demonstrate that in the above mentioned patients, establishing a previous hypervolemic state allows the safe use of TVO. METHODS: The method includes efficient injury tamponade with aggressive fluid replacement until normal blood volume is reached (resuscitation). Normal blood volume is recognized by a return of arterial blood pressure to normal levels, inferior vena cava filling and an increase in aortic wall tension. Following this procedure, hypervolemia is obtained by the rapid additional infusion of 1.500 to 2.000 ml of fluids. TVO in this situation does not alter the heart rhythm and maintains a clear operative field which is essential for hepatotomy, venorrhaphy and or venous ligation. RESULTS: Three patients were successfully operated.

Aortic Wall Tension as a Predictive Factor for Abdominal Aortic Aneurysm Rupture: Improving the Selection of Patients for Abdominal Aortic Aneurysm Repair

Aortic wall tension was determined in 40 patients to assess its predictive value in abdominal aortic aneurysm (AAA) rupture. A 3-year retrospective analysis of 243 patients with ruptured AAAs and 45 patients with intact AAAs was conducted. The 288 patient sample was limited to the 40 patients with an abdominal CT scan investigation. Aortic wall tension was calculated using blood pressure data and measurements from computerized tomographic (CT) images of 26 patients with intact AAAs and 14 patients with ruptured AAAs in accordance with LaPlace's Law for wall tension: P x R/W, where P = mean arterial pressure (MAP), R = radius of the vessel, and W = wall thickness of the vessel. The wall tension was approximated with the more readily accessible patient parameters of AAA diameter, MAP, height, and weight. This approximation was termed the body mass index (BMI)-pressure approximation for tension (BPAT), which is AAA diameter/BMI x MAP. Data were analyzed using one-sided t-tests, chi-squared tests, and a regression analysis for the relationship between aortic wall tension and the BPAT. AAA wall tension is a significant predictor of pending rupture. BPAT used to approximate the actual tension in the AAA wall is a more sensitive predictor of rupture than aneurysm diameter alone. A prospective study has been initiated to validate these conclusions.

A standardized treatment protocol for blood pressure management in transport patients with a reported diagnosis of acute aortic dissection or symptomatic aortic aneurysm

Reprint no. 74/l/21 0 The use of standardized treatment protocols (SIR) are a common practice in the air medical industry. These proto cols provide nonphysician flight crews with specific guidelines on the medical management of the patients they transport. Although implementation of protocols is widely accepted, evaluating their application and reporting their effectiveness is relatively rare. On June 12, 1995, Stanford Health Services (SHS) Life Flight/Medical Transport programs instituted a compre hensive set of STPs designed to provide medical guidelines for the RN/RN crew that transported patients. One of the more aggressive protocols addressed the blood pressure (BP) management of pa tients with a reported diagnosis of acute aortic dissection or symptomatic aortic aneurysm. Initially, a quality assurance evaluation was performed to ascertain how effective the crews were in applying the protocol. To determine whether ap plication of the protocol had a significant effect on BP outcomes, a second analysis was performed to compare BP manage ment provided by SHS transporting crews versus nonSHS crews that brought inter-facility transfers to SHS. Emergent medical management in aortic dissections focuses on minimizing the aortic forces that can exacerbate the dissection. For symptomatic aneurysms, management is aimed at decreasing aortic wall tension to prevent rupture. Both goals can be achieved through pharmacologic intervention using a fast-acting

Aortic medial necrosis with or without thrombosis in rabbits treated with Russell's viper venom and angiotensin II

The aim of the present study is primarily to re-examine an animal model of acute myocardial infarction (AMI) and arterial thrombosis, developed by Constantinides and his colleagues in the 1960s, in both heritable hyperlipidemic rabbits and normal rabbits because they did not study these rabbits. The groups in this study consisted of 29 normal rabbits and 29 Watanabe heritable hyperlipidemic (WHHL) rabbits. These rabbits were administered Russell's viper venom (RVV) as a procoagulant, intraperitoneally with serotonin or angiotensin II or saline, intravenously. As a control, 10 normal and 17 WHHL rabbits were administered intravenously with either angiotensin II or saline. These treatments were given on 2 successive days. AMI lesion was found in 8 of 29 normal and 7 of 29 WHHL rabbits receiving RVV and angiotensin or serotonin. Angiotensin II promoted the incidence of aortic thrombosis associated with segmental medial necrosis and an intimal disruption in WHHL rabbits receiving RVV. In the normal rabbits, angiotensin II in addition to RVV induced segmental medial necrosis of the aorta, but angiotensin II alone did not. Thus, we postulated that a synergistic effect of RVV as a cytotoxic substance and a sudden increase in the aortic wall tension by angiotensin II might thus result in acute aortic medial necrosis. The conclusion was that no close correlation between coronary arteriosclerosis and AMI was found in this animal model. The intravenous administration of angiotensin promoted aortic medial necrosis even in normal rabbits treated with RVV and then accelerated aortic thrombosis in the WHHL rabbits treated with RVV.

Effects of neural stimuli on blood flow through vasa vasorum in dogs.

The purpose of this study was to determine whether neural stimuli alter blood flow through vasa vasorum in the thoracic aorta. We measured flow with microspheres in anesthetized dogs and observed responses to sympathetic stimulation and baroreceptor stimulation. During these interventions, changes in arterial pressure were prevented with propranolol or an arterial reservoir, to minimize indirect effects on vasa vasorum mediated through changes in aortic wall tension. Electrical stimulation of the stellate ganglion at 10 Hz reduced blood flow to vasa vasorum in the thoracic aorta from 11 +/- 1.6 (mean +/- SE to 6.8 +/- 1.1 ml/min per 100 g (p less than 0.05). Aortic diameter, measured with a sonomicrometer technique, did not change during sympathetic stimulation. Thus, the reduction in blood flow through vasa vasorum during sympathetic stimulation appears to be a direct effect, and not the result of constriction of the aorta and compression of vasa. To determine effects of physiological alterations in neurogenic vasoconstrictor activity, we examined responses to stimulation of carotid baroreceptors. When pressure in isolated, perfused carotid sinus baroreceptors was raised from 81 +/- 3 to 198 +/- 2 mm Hg, blood flow to vasa vasorum of the thoracic aorta increased from 3.7 +/- 0.6 to 10 +/- 2.2 ml/min per 100 g (P less than 0.05). We conclude that vasa vasorum are responsive to neural stimuli, since they constrict during sympathetic stimulation and dilate in response to baroreceptor stimulation.

Influence of vascular smooth muscle on contractile mechanics and elasticity of arteries.

ARTICLESInfluence of vascular smooth muscle on contractile mechanics and elasticity of arteriesPB Dobrin, and AA RovickPB Dobrin, and AA RovickPublished Online:01 Dec 1969https://doi.org/10.1152/ajplegacy.1969.217.6.1644MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByCuffless blood-pressure estimation method using a heart-rate variability-derived parameter5 September 2018 | Physiological Measurement, Vol. 39, No. 9A multiphysics approach for modeling early atherosclerosis20 November 2017 | Biomechanics and Modeling in Mechanobiology, Vol. 17, No. 3Pressure dependency of aortic pulse wave velocity in vivo is not affected by vasoactive substances that alter aortic wall tension ex vivoMark Butlin, George Lindesay, Kayla D. Viegas, and Alberto P. Avolio15 May 2015 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 308, No. 10Modeling flow in collecting lymphatic vessels: one-dimensional flow through a series of contractile elementsA. J. Macdonald, K. P. Arkill, G. R. Tabor, N. G. McHale, and C. P. Winlove1 July 2008 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 295, No. 1Length-tension relationships of small arteries, veins, and lymphatics from the rat mesenteric microcirculationRong-zhen Zhang, Anatoliy A. Gashev, David C. Zawieja, and Michael J. Davis1 April 2007 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 292, No. 4Biomechanical proprieties of decellularized porcine common carotid arteriesSylvain Roy, Paolo Silacci, and Nikolaos Stergiopulos1 October 2005 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 289, No. 4A constitutive formulation of arterial mechanics including vascular smooth muscle toneMartin A. Zulliger, Alexander Rachev, and Nikos Stergiopulos1 September 2004 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 287, No. 3Mechanical Properties of Rat Middle Cerebral Arteries With and Without Myogenic Tone9 March 2004 | Journal of Biomechanical Engineering, Vol. 126, No. 1Effects of ischemia and myogenic activity on active and passive mechanical properties of rat cerebral arteriesRebecca J. Coulson, Naomi C. Chesler, Lisa Vitullo, and Marilyn J. Cipolla1 December 2002 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 283, No. 6Angiotensin II contributes to arterial compliance in congestive heart failureSilvia G. Lage, Liliane Kopel, Caio C. J. Medeiros, Ricardo T. Carvalho, and Mark A. Creager1 October 2002 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 283, No. 4Endothelium-dependent arterial wall tone elasticity modulated by blood viscosityEdmundo I. Cabrera Fischer, Ricardo L. Armentano, Franco M. Pessana, Sebastián Graf, Luis Romero, Alejandra I. Christen, Alain Simon, and Jaime Levenson1 February 2002 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 282, No. 2Smooth muscle relaxation and local hydraulic impedance properties of the aortaBernard P. Cholley, Roberto M. Lang, Claudia E. Korcarz, and Sanjeev G. Shroff1 June 2001 | Journal of Applied Physiology, Vol. 90, No. 6Mechanical properties of mesenteric arteries in diabetic rats: consequences of outward remodelingFrancy R. L. Crijns, Bruce H. R. Wolffenbuttel, Jo G. R. de Mey, and Harry A. J. Struijker Boudier1 May 1999 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 276, No. 5Arterial response during cold pressor test in borderline hypertensionA. B. Lafleche, B. M. Pannier, B. Laloux, and M. E. Safar1 August 1998 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 275, No. 2Estrogen replacement, vascular distensibility, and blood pressures in postmenopausal womenRonald E. De Meersman, Adrienne S. Zion, Elsa G. V. Giardina, Joseph P. Weir, James S. Lieberman, and John A. Downey1 May 1998 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 274, No. 5Evaluation of the Early Stage of Carotid Atherosclerosis Using the Vascular Response to Nitroglycerin and High-Resolution UltrasonographyJapanese Circulation Journal, Vol. 62, No. 7Influence of sympathetic stimulation on the mechanical properties of the aorta in humans2 October 2003 | Acta Physiologica Scandinavica, Vol. 159, No. 2 More from this issue > Volume 217Issue 6December 1969Pages 1644-1651 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.217.6.1644PubMed5353039History Published online 1 December 1969 Published in print 1 December 1969 Metrics

Hemodynamic correlates of the various components of the first hear sound.

Previous studies in this laboratory having demonstrated that AV valve closure is not directly responsible for the rapid vibrations of the first heart sound, the mechanism of production of this "sound" was studied further in 30 experiments in dogs. The experiments were performed with multiple pressure catheterization, and intracardiac phonocatheterization, and were compared with external phonocardiograms and electrocardiograms. In 10 experiments, the first derivatives of the left and right ventricular pressures were also recorded. In four experiments, direct epicardial and arterial sound tracings were obtained. These experiments revealed that three groups of vibrations, or components, were often visible in the external phonocardiogram, and in intracardiac and epicardial tracings. The first component follows the onset of left ventricular pressure rise and closure of the mitral valve but coincides with the rapid rise of the first derivative of LV pressure. The second component has no relationship with right heart events, occurs before aortic valve opening, and coincides with the sudden change of course of the first derivative of LV pressure. The third component occurs slightly after aortic valve opening, and seems related to sudden increase of aortic wall tension. It is probably the physiological equivalent of the aortic "ejection sound." Thus, the first two components are both left ventricular in origin while the third is of aortic origin.