The Zero-Stress State of Rat Veins and Vena Cava

1991 ◽  
Vol 113 (1) ◽  
pp. 36-41 ◽  
Author(s):  
J. P. Xie ◽  
S. Q. Liu ◽  
R. F. Yang ◽  
Y. C. Fung

The zero-stress state of a vein is, like that of an artery, not a closed cylindrical tube, but is a series of segments whose cross-sections are open sectors. An opening angle of each sector is defined as the angle subtended between two radii joining the midpoint of the inner wall to the tips of the inner wall. Data on the opening angles (mean ± standard deviation) of the veins and vena cava of the rat are presented. For the superior vena cava and subclavian, jugular, facial, renal, common iliac, saphenous, and plantar veins, the opening angle varies in the range of 25 to 75 deg. The inferior vena cava (below the heart), however, has noncircular, nonaxisymmetric cross-sections, a curved axis, and a rapid longitudinal variation of its “diameter;” its zero-stress state is not circular sectors; but the opening angle is still a useful characterization. The mean opening angle of the interior vena cava varies in the range of 40 to 150 deg in the thoracic portion, and 75 to 130 deg in the abdominal portion, with the larger values occurring about the middle of each portion. There are considerable length, diameter reductions, and wall thickening of the vena cava from the homeostatic state to the no-load state in vitro. Physically, the zero-stress state is the basis of the stress analysis of blood vessels. The change of opening angle is a convenient parameter to characterize any nonuniform remodeling of the vessel wall due to changes in physical stress or chemical environment. Change of zerostress state influences the compliance and collapsibility of the viens, their pressure-volume and pressure-flow relationships, the waterfall phenomenon, and the tone in the vascular smooth muscles if the homeostatic stress is changed.

2014 ◽  
Vol 55 (6) ◽  
pp. 732-736 ◽  
Author(s):  
Jorge E Lopera ◽  
Murray Shapiro ◽  
Darlene Sanchez ◽  
Carolina Maya ◽  
Ghazwan Kroma ◽  
...  

2008 ◽  
Vol 1 ◽  
pp. IDRT.S895
Author(s):  
Vanessa A. Aguiare Lopes ◽  
Alexandre Ordones Lopes ◽  
Orlei Ribeiro De Araújo ◽  
Valeska A. Schauer Aguiare

Objectives To report a case in where a mural endocarditis caused by Candida parapsilosis was successfully treated with the combination of 2 antifungal agents, caspofungin and voriconazole, in an extremely premature infant. Description A female infant born at 30.7 weeks with weight 925 g. The infant had a pneumothorax and respiratory distress syndrome, requiring prolonged mechanical ventilation, 1 venous umbilical and 3 central catheters, and broad-spectrum antibiotics. At 51 days of life, an echocardiogram showed an image compatible with fungal vegetation on the junction of the superior vena cava to the right atrium. Blood cultures grew Candida parapsilosis in various sequential samples, despite treatment with fluconazole and amphotericin-B and in vitro sensitivity to these drugs. A treatment of combined voriconazole and caspofungin was initiated resulting in clinical improvement and no need for surgical removal of vegetation. Comments Combined therapy with newer antifungal agents can be life-saving in premature infants with Candida parapsilosis complicated sepsis.


1992 ◽  
Vol 262 (2) ◽  
pp. H544-H552 ◽  
Author(s):  
Y. C. Fung ◽  
S. Q. Liu

The active and passive deformation of a blood vessel is related to the stress in it. Any analysis of stress and strain must begin with the zero-stress state. Recent reports on large blood vessels such as the aorta, pulmonary arteries, and vena cava have shown that, at zero-stress state, blood vessels are not tubes, but opens sectors. This report presents data on the zero-stress state of small blood vessels with lumen diameters down to approximately 50 microns. Zero-stress state of a vessel was obtained by cutting the vessel into rings and then the rings into sectors; each sector is characterized by an opening angle, alpha. In rat ileal and plantar arterioles, the opening angles are in the order of 100-250 degrees; those in the venules are in the order of 50-100 degrees. The effect of norepinephrine on the opening angle alpha is minor; it decreases alpha of the superior mesenteric artery, and increases alpha of the ileocecocolic and ileal arteries. EDTA has little effect on alpha of arteries greater than 100 microns in diameter, but decreases alpha of arteries less than 100 microns. The physiological meaning of the opening angle is demonstrated in terms of the residual strains in a vessel at the no-load state and homeostatic strains at normal blood pressure. The strains in real vessels are compared with those in hypothetical vessels having an opening angle of zero. It is shown that ignoring the opening angle will cause a large error in strain evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)


2001 ◽  
Vol 123 (6) ◽  
pp. 558-564 ◽  
Author(s):  
Peter G. Walker ◽  
Ghanem F. Oweis ◽  
Kevin G. Watterson

The total cavo pulmonary connection, or TCPC, is a surgical correction to congenital heart defects. The geometry of this connection has been shown to determine the fluid power loss as well as the distribution of hepatic fluid that enters through the inferior vena cava. In vitro studies were performed to measure the power loss and hepatic fluid distribution in models of the TCPC with four different geometries. It was found that a zero offset straight geometry provided good hepatic fluid distribution but large power loss. A zero offset flared geometry provided low power loss but poor hepatic fluid distribution. The optimal geometry from those tested was found to be the zero offset cowl geometry whereby an enlargement was made on one side of the inferior and superior vena cava. So long as the cowl was directed toward the pulmonary artery of lowest flow rate, low power loss and relatively good distribution of hepatic flow could be obtained.


2018 ◽  
Vol 56 (3) ◽  
pp. 173-181
Author(s):  
Elisna Syahruddin ◽  
Aida Lufti Huswatun ◽  
Ari Prabowo ◽  
Jamal Zaini ◽  
Fariz Nurwidya ◽  
...  

Abstract Introduction. Combinations of gefitinib and radiotherapy have been observed to have synergistic and anti-proliferative effects on lung cancer in vitro. In the clinical setting, patients who presented with respiratory difficulties such as superior vena cava syndrome (SVCS), radiotherapy should be given immediately to address the emergency while waiting for the results of epidermal growth factor receptor (EGFR) mutation test. However, there has been no study that described the role of radio-therapy in Indonesian patients with EGFR-mutant lung adenocarcinoma. Methods. This preliminary study aimed to evaluate the efficacy and toxicities of gefitinib and radiotherapy combination in lung adenocarcinoma patients in Persahabatan National Respiratory Referral Hospital, Jakarta, Indonesia. Subjects were consecutively recruited between January 2013 and December 2016. Results. Thirty-one lung adenocarcinoma with EGFR mutations were enrolled. Most of them were male (51.61%) with a median age of 54.5 years old (range 38-70 years old). EGFR mutation characteristics were on exon 21 L858R point mutation (61.30%), exon 21 L861Q point mutation (16.12%) and exon 19 deletion (22.58%). Radiotherapy was given at doses between 30-60 Gy. Among these subjects, median progression-free survival (PFS) was 185 days (95%CI; 123.69 – 246.30), 1-year survival rate (1-yr) was 45.2%, and median overall survival (OS) was 300 days (95%CI; 130.94 – 469.06). There were no grade 3/4 hematological and nonhematological toxicities recorded. The most frequent grade 1 and 2 non-hematological toxicities were skin rash, diarrhea, and paronychia that might be related to tyrosine kinase inhibitor (TKI). Conclusion. The combination of TKI with radiation may be considered in EGFR-mutant lung adenocarcinoma subjects.


2013 ◽  
Vol 2013 ◽  
pp. 1-16 ◽  
Author(s):  
Amr Al Abed ◽  
Tianruo Guo ◽  
Nigel H. Lovell ◽  
Socrates Dokos

A 3D model of atrial electrical activity has been developed with spatially heterogeneous electrophysiological properties. The atrial geometry, reconstructed from the male Visible Human dataset, included gross anatomical features such as the central and peripheral sinoatrial node (SAN), intra-atrial connections, pulmonary veins, inferior and superior vena cava, and the coronary sinus. Membrane potentials of myocytes from spontaneously active or electrically pacedin vitrorabbit cardiac tissue preparations were recorded using intracellular glass microelectrodes. Action potentials of central and peripheral SAN, right and left atrial, and pulmonary vein myocytes were each fitted using a generic ionic model having three phenomenological ionic current components: one time-dependent inward, one time-dependent outward, and one leakage current. To bridge the gap between the single-cell ionic models and the gross electrical behaviour of the 3D whole-atrial model, a simplified 2D tissue disc with heterogeneous regions was optimised to arrive at parameters for each cell type under electrotonic load. Parameters were then incorporated into the 3D atrial model, which as a result exhibited a spontaneously active SAN able to rhythmically excite the atria. The tissue-based optimisation of ionic models and the modelling process outlined are generic and applicable to image-based computer reconstruction and simulation of excitable tissue.


1993 ◽  
Vol 265 (4) ◽  
pp. R772-R780 ◽  
Author(s):  
G. Losonczy ◽  
I. Mucha ◽  
J. DiPirro ◽  
J. Sweeney ◽  
G. Brown ◽  
...  

We compared the hemodynamic actions of U-46619, a stable thromboxane A2 (TxA2) prostaglandin H2 (PGH2) analogue, in nonpregnant (NP) rabbits with those observed in late pregnant (P) rabbits. An intravenous injection of U-46619 (10 micrograms) to each of eight NP chronically instrumented rabbits (mean body weight 3.4 kg) induced an immediate (1 min) and reversible fall of cardiac output (CO, 66%) and mean arterial pressure (MAP, 41%, both P < 0.01). P rabbits (n = 6, mean body weight 3.8 kg), however, responded with an elevation of MAP (5%, P < 0.02) upon intravenous injection of the drug (10 micrograms), while CO remained unchanged. The fall of CO in NP rabbits was associated with the temporary disappearance of a fraction of circulating platelets between the superior vena cava and the aortic arch. The number of platelets at 30 and 60 s after U-46619 was reduced (P < 0.05) by 14 and 20% respectively in the aortic blood, whereas caval platelet counts were unchanged until 90 s (-6%, P < 0.05). In contrast, intraaortic administration of this drug (10 micrograms) to NP rabbits resulted in neither thrombocytopenia nor hypotension. U-46619 (10-30 micrograms i.v.) caused no decrease in platelet count in the aorta of P rabbits. In vitro, U-46619-induced aggregation of platelets harvested from P rabbits was also blunted (P < 0.001). This could not be attributed to reduced affinity or number of platelet thromboxane receptors. The data indicate that U-46619 induces a fall of arterial pressure simultaneous with intravascular platelet aggregation.(ABSTRACT TRUNCATED AT 250 WORDS)


2000 ◽  
Vol 14 (3) ◽  
pp. 283-285 ◽  
Author(s):  
David Lamon ◽  
C.K. Chang ◽  
Lindy Hruska ◽  
George Kerlakian ◽  
J. Michael Smith

1995 ◽  
Vol 117 (4) ◽  
pp. 423-428 ◽  
Author(s):  
Young H. Kim ◽  
P. G. Walker ◽  
A. A. Fontaine ◽  
S. Panchal ◽  
A. E. Ensley ◽  
...  

The Fontan operation is one in which the right heart is bypassed leaving the left ventricle to drive the blood through both the capillaries and the lungs, making it important to design an operation which is hemodynamically efficient. The object here was to relate the pressure in Fontan connections to its geometry with the aim of increasing the hemodynamically efficiency. From CT or magnetic resonance images, glass models were made of realistic atrio-pulmonary (AP) and cavo-pulmonary (CP) connections in which the right atrium and/or ventricle are bypassed. The glass models were connected to a steady flow loop and flow visualization, pressure and 3 component LDA measurements made. In the AP model the large atrium and curvature of the conduit created swirling patterns, the magnitude of which was similar to the axial velocity. This led to an inefficient flow and a subsequent large pressure loss (780 Pa). In contrast, the CP connection with a small intra-atrial chamber had reduced swirling and a significantly smaller pressure loss (400 Pa at 8 l.min) and was therefore a more efficient connection. There were, however, still pressure losses and it was found that these occurred where there was a large bending of the flow, such as from the superior vena cava to the MPA and from the MPA to the right pulmonary artery.


2021 ◽  
Vol 9 ◽  
Author(s):  
Andrew D. Spearman ◽  
Ankan Gupta ◽  
Amy Y. Pan ◽  
Todd M. Gudausky ◽  
Susan R. Foerster ◽  
...  

Background: Pulmonary arteriovenous malformations (PAVMs) are common sequelae of palliated univentricular congenital heart disease, yet their pathogenesis remain poorly defined. In this preliminary study, we used paired patient blood samples to identify potential hepatic factor candidates enriched in hepatic vein blood.Methods: Paired venous blood samples were collected from the hepatic vein (HV) and superior vena cava (SVC) from children 0 to 10 years with univentricular and biventricular congenital heart disease (n = 40). We used three independent protein analyses to identify proteomic differences between HV and SVC blood. Subsequently, we investigated the relevance of our quantified protein differences with human lung microvascular endothelial assays.Results: Two independent protein arrays (semi-quantitative immunoblot and quantitative array) identified that soluble vascular endothelial growth factor receptor 1 (sVEGFR1) is significantly elevated in HV serum compared to SVC serum. Using ELISA, we confirmed the previous findings that sVEGFR1 is enriched in HV serum (n = 24, p &lt; 0.0001). Finally, we studied the quantified HV and SVC serum levels of sVEGFR1 in vitro. HV levels of sVEGFR1 decreased tip cell selection (p = 0.0482) and tube formation (fewer tubes [p = 0.0246], shorter tube length [p = 0.0300]) in vitro compared to SVC levels of sVEGFR1.Conclusions: Based on a small heterogenous cohort, sVEGFR1 is elevated in HV serum compared to paired SVC samples, and the mean sVEGFR1 concentrations in these two systemic veins cause pulmonary endothelial phenotypic differences in vitro. Further research is needed to determine whether sVEGFR1 has a direct role in pulmonary microvascular remodeling and PAVMs in patients with palliated univentricular congenital heart disease.


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