Effect of a Surgically Created Side-to-Side Arteriovenous Fistula on Heat Elimination from the Human Hand and Forearm: Evidence for a Critical Role of Venous Resistance in Determining Fistular Flow

1978 ◽  
Vol 55 (4) ◽  
pp. 349-353
Author(s):  
W. F. M. Wallace ◽  
J. P. Jamison

1. In eight patients with a unilateral fistula between the radial artery and a nearby superficial vein, heat elimination from both hand and forearm, as measured by calorimetry, was always substantially greater on the side of the fistula (mean excess from hand-plus-forearm 889 J/min). 2. Fistular blood flow measured by hand-plus-forearm plethysmography in these patients averaged 431 ml/min. Correlation between fistular blood flow and heat elimination was poor (r = 0.70, P < 0.06), probably because heat elimination due to the fistula takes place mainly from veins, whose pattern varies from patient to patient. 3. Approximately half of the total increased heat elimination due to the fistula is from the hand. Occlusion of the circulation to the hand caused fistular flow rate to be reduced by about half. This suggests that the main resistance to fistular flow is venous, proximal veins offering a similar resistance to distal veins. 4. The obligatory heat loss due to the fistula is unlikely to embarrass temperature regulation, except in severe cold stress.

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Takeki Hata ◽  
Masafumi Takahashi ◽  
Masanori Kawaguchi ◽  
Yuichiro Kashima ◽  
Yuji Shiba ◽  
...  

Background: Accumulating evidence indicates that CD4 + T cells contribute to the development of collateral vesssels in ischemic tissue; however, little is known about the responsible subset of CD4 + T cells in the induction of angiogenesis. Th17 cells are recently identified as a new subset of CD4 + T cells and have been associated with the pathogenesis of certain autoimmune diseases. Th17 cells specifically secrete interleukin-17 (IL-17) and regulate various biological functions. The purpose of this study is to investigate the role of CD4 + T and Th17 cells in angiogenic response to hindlimb ischemia. Methods and Results: Unilateral hindlimb ischemia was produced in wild-type (WT: C57BL/6, 8- to 10-week-old) mice treated with or without a neutralizing antibody against CD4. Blood flow perfusion and capillary formation were assessed by using a laser Doppler perfusion imaging (LDPI) and CD31 immunostaining, respectively. Well-developed collateral vessels and capillary formation were observed in WT mice in response to hindlimb ischemia. Treatment with a neutralizing anti-CD4 antibody resulted in almost complete CD4 + T cell depletion (flow cytometry analysis, control: 45.4% vs. antibody: 1.0%) and a significant decrease in angiogenesis after the induction of hindlimb ischemia (LDPI, 21 days, control: 0.61 ± 0.1 vs. antibody: 0.41 ± 0.1, p<0.05). IL-17-deficient (IL-17 −/− ) mice also showed a significant reduction of blood flow perfusion, compared with WT mice (LDPI, day 14: 0.56 ± 0.3 vs. 0.31 ± 0.2, p<0.05; day 21: 0.66 ± 0.3 vs. 0.37 ± 0.3, p=0.05). IL-17 −/− mice had severe ischemic damage of the limb and resulted in a 25% incidence of autoamputation by day 21 (no limb loss in WT mice). Furthermore, capillary formation was also decreased significantly in IL-17 −/− mice (692.9 ± 165.6/mm 2 vs. 1223.3 ± 267.3/mm 2 , p<0.01). Conclusion : These findings demonstrate that Th17 cells, a new subset of CD4 + T cells, contribute to the angiogenic response to hindlimb ischemia and provide new insights into the mechanism by which T cells promote collateral development and angiogenesis.


2019 ◽  
Vol 43 (1) ◽  
pp. 58-61
Author(s):  
Savino Occhionorelli ◽  
Fabio Fabbian ◽  
Yuri Battaglia ◽  
Tommaso Miccoli ◽  
Dario Andreotti ◽  
...  

One of the major causes of arteriovenous fistula failure is the venous stenosis due to aggressive neointimal hyperplasia. The aim of the study was to assess the arteriovenous fistula maturation comparing absorbable sutures and non-absorbable ones in native vessels. Surgeries performed during a period of 24 months by a single team of expert surgeons were evaluated. Surgeries that met the inclusion criteria, namely, age ⩾ 18 years and radio-cephalic arteriovenous fistula, were considered. According to type of suture, patients were classified as Max group (absorbable suture) and Prol group (non-absorbable). Data pertaining to 70 patients were collected; 51% were men and the mean age was 73 ± 12 years. In Max group, an increasing blood flow was observed during the first 4 weeks without post-operative complications. In Prol group, six patients had thrombosis that resulted in vascular access failure. After the first week, the duplex Doppler ultrasound of both groups showed a regular arteriovenous fistula maturation, with an increase of blood flow rate. Although pre-operative post-tourniquet mean vein diameters of Max group were not adequate, the mean vein diameter and mean blood flow rate increased after 4 weeks, respectively. On the contrary, in Prol group, mean vein diameters and blood flow rate decreased. The maturation of arteriovenous fistula and its functional performance were not altered by the type of suture (absorbable/non-absorbable). Absorbable sutures were associated with good results considering arteriovenous fistula maturation.


1994 ◽  
Vol 77 (4) ◽  
pp. 1834-1839 ◽  
Author(s):  
Y. Nagasaka ◽  
M. Ishigaki ◽  
H. Okazaki ◽  
J. Huang ◽  
M. Matsuda ◽  
...  

To clarify the role of the pulmonary microvasculature in adjusting to increased pulmonary blood flow, we measured arteriolar and venular pressure by the servo-null micropuncture method while changing the pulmonary blood flow in isolated perfused cat lungs. We divided the lung vasculature into three longitudinal segments: 1) arterial (pulmonary artery to 30- to 50-microns arteriole), 2) microvascular (between 30- to 50-microns arteriole and venule), and 3) venous (30- to 50-microns venule to left atrium). The vascular resistance was calculated by dividing the pressure gradient by the flow. The pressure gradient of the microvascular segment did not increase, whereas the pressure gradient of the arterial and venous segments increased simultaneously with flow rate. Total and microvascular resistance decreased with increase of flow rate. Resistances of the arterial and venous segments did not change with increase in flow. We conclude that the microvasculature plays a crucial role in preventing pulmonary hypertension with increases in flow by decreasing microvascular resistance.


Nanomaterials ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1699
Author(s):  
Tomohiro Akiyama ◽  
Takamichi Hirata ◽  
Takahiro Fujimoto ◽  
Shinnosuke Hatakeyama ◽  
Ryuhei Yamazaki ◽  
...  

There are currently no promising therapy strategies for either the treatment or prevention of novel coronavirus disease 2019 (COVID-19), despite the urgent need. In addition to respiratory diseases, vascular complications are rapidly emerging as a key threat of COVID-19. Existing nitric oxide (NO) therapies have been shown to improve the vascular system; however, they have different limitations in terms of safety, usability and availability. In light of this, we hypothesise that a natural-mineral-based novel nanomaterial, which was developed based on NO therapy, might be a viable strategy for the treatment and prevention of COVID-19. The present study examined if it could induce an increase of intravascular NO, vasodilation and the consequent increase of blood flow rate and temperature in a living body. The intravascular NO concentration in the hepatic portal of rats was increased by 0.17 nM over 35.2 s on average after its application. An ultrasonic Doppler flow meter showed significant increases in the blood flow rate and vessel diameter, but no difference in the blood flow velocity. These were corroborated by measurements of human hand surface temperature. To our knowledge, this result is the first evidence where an increase of intravascular NO and vasodilation were induced by bringing a natural-mineral-based nanomaterial into contact with or close to a living body. The precise mechanisms remain a matter for further investigation; however, we may assume that endothelial NO synthase, haemoglobin and endothelium-derived hyperpolarising factor are deeply involved in the increase of intravascular NO.


2009 ◽  
Vol 179 (6) ◽  
pp. 701-710 ◽  
Author(s):  
Mingming Zhu ◽  
Joseph J. H. Ackerman ◽  
Dmitriy A. Yablonskiy

2016 ◽  
Vol 125 (4) ◽  
pp. 898-908 ◽  
Author(s):  
Christina Iosif ◽  
Philipp Berg ◽  
Sebastien Ponsonnard ◽  
Pierre Carles ◽  
Suzana Saleme ◽  
...  

OBJECTIVE The authors describe herein the creation of an animal model capable of producing quantifiable data regarding blood flow rate and velocity modifications in terminal and anastomotic types of cerebrofacial circulation. They also present the preliminary results of a translational study aimed at investigating the role of terminal and anastomotic types of circulation in arterial branches jailed by flow-diverting stents as factors contributing to arterial patency or occlusion. METHODS Two Large White swine were used to validate a terminal-type arterial model at the level of the right ascending pharyngeal artery (APhA), created exclusively by endovascular means. Subsequently 4 Large White swine, allocated to 2 groups corresponding to the presence (Group B) or absence (Group A) of terminal-type flow modification, underwent placement of flow-diverting stents. Blood flow rates and velocities were quantified using a dedicated time-resolved 3D phase-contrast MRA sequence before and after stenting. Three months after stent placement, the stented arteries were evaluated with digital subtraction angiography (DSA) and scanning electron microscopy (SEM). Patent (circulating) ostia quantification was performed on the SEM images. RESULTS Terminal-type flow modification was feasible; an increase of 75.8% in mean blood velocities was observed in the right APhAs. The mean blood flow rate for Group A was 0.31 ± 0.19 ml/sec (95% CI −1.39 to 2.01) before stenting and 0.21 ± 0.07 ml/sec (95% CI −0.45 to 0.87) after stenting. The mean blood flow rate for Group B was 0.87 ± 0.32 ml/sec (95% CI −1.98 to 3.73) before stenting and 0.76 ± 0.13 ml/sec (95% CI −0.41 to 1.93) after stenting. Mean flow rates after stenting showed a statistically significant difference between Groups A and B (Welch test). Mean and maximal blood velocities were reduced in Group A cases and did not decrease in Group B cases. Control DSA and SEM findings showed near occlusion of the jailed APhAs in both cases of anastomotic circulation (mean patent ostium surface 32,776 μm2) and patency in both cases of terminal-type circulation (mean patent ostium surface 422,334 μm2). CONCLUSIONS Terminal-type arterial modification in swine APhAs is feasible. Sufficient data were acquired to perform an a priori analysis for further research. Flow diversion at the level of the APhA ostium resulted in significant stenosis in cases of anastomotic circulation, while sufficient patency was observed in terminal-type circulation.


Author(s):  
Hannah Northrup ◽  
Maheshika Somarathna ◽  
Savanna Corless ◽  
Isabelle Falzon ◽  
John Totenhagen ◽  
...  

Arteriovenous fistula (AVF) is essential for chronic kidney disease (CKD) patients on hemodialysis, but treatment for AVF maturation failure remains an unmet clinical need. Successful AVF remodeling occurs through sufficient lumen expansion to increase AVF blood flow and lumen area. Aberrant blood flow is thought to impair AVF remodeling, but previous literature has largely focused on hemodynamics averaged over the entire AVF or at a single location. We hypothesized that hemodynamics is heterogeneous, and thus any treatment’s effect size is heterogeneous in the AVF. To test our hypothesis, we used the PDE5A inhibitor sildenafil to treat AVFs in a rat model and performed magnetic resonance imaging (MRI) based computational fluid dynamics (CFD) to generate a detailed spatial profile of hemodynamics in AVFs. 90 mg/kg of sildenafil was administered to rats in their drinking water for 14 days. On day 14 femoral AVFs were created in rats and sildenafil treatment continued for another 21 days. 21 days post-AVF creation, rats underwent non-contrast MRI for CFD and geometrical analysis. Lumen cross-sectional area (CSA) and flow rate were used to quantify AVF remodeling. Parameters used to describe aberrant blood flow include velocity magnitude, wall shear stress (WSS), oscillatory shear index (OSI), and vorticity. Geometrical parameters include arterial-venous (A-V) distance, anastomosis angle, tortuosity, and nonplanarity angle magnitude. When averaged across the entire AVF, sildenafil treated rats had significantly higher CSA, flow rate, velocity, WSS, OSI, and vorticity than control rats. To analyze heterogeneity, the vein was separated into zones: 0–5, 5–10, 10–15, and 15–20 mm from the anastomosis. In both groups: 1) CSA increased from the 0–5 to 15–20 zone; 2) velocity, WSS, and vorticity were highest in the 0–5 zone and dropped significantly thereafter; and 3) OSI increased at the 5–10 zone and then decreased gradually. Thus, the effect size of sildenafil on AVF remodeling and the relationship between hemodynamics and AVF remodeling depend on location. There was no significant difference between control and sildenafil groups for the other geometric parameters. Rats tolerated sildenafil treatment well, and our results suggest that sildenafil may be a safe and effective therapy for AVF maturation.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jun Yu ◽  
Carlos Fernandez-Hernando ◽  
Yajaira Suarez ◽  
Yajaira Suarez ◽  
Michael Schleicher ◽  
...  

Nogo-B, a member of the reticulon 4 family of proteins, is the dominant isoform expressed in endothelial, vascular smooth muscle and inflammatory cells. We previously have shown Nogo-B plays a critical role in vascular remodeling after injury in vivo . In mice and rabbits, neointimal expansion of injured blood vessels is associated with a marked reduction in Nogo-B, and, in humans, the loss of Nogo-B correlates with stenotic lesions and plaque rupture. However, the role of Nogo-B in regulating arteriogenesis or angiogenesis is not known. In the present study, we investigated the role of Nogo-B in arteriogenesis/angiogenesis using a mouse hindlimb ischemia model in Nogo-A/B KO (NgKO) and wild-type (WT) littermate control mice. Nogo-B mRNA and protein levels increased in the ischemic leg relative to the contralateral leg in WT. Hindlimb ischemia reduces tissue perfusion by 80% followed by a complete recovery of flow to pre-surgical values in WT after 4 weeks. In NgKO, there was a marked decrease in blood flow recovery post-ischemia, which was accompanied by a reduction in capillary density (assessed by isolectin staining), a decrease in smooth muscle/pericyte recruitment and an impaired collateral artery remodeling (assessed by quantitative angiography) compared to WT. Blood vessel formation and remodeling during ischemia requires coordination of the inflammatory response with regulated gene expression that promotes blood vessel assembly. Thus, we assessed the presence of tissue macrophages (F4/80 immunochemistry) 3 days after ischemia and found a 76% reduction of F4/80 positive cells in ischemic tissue in NgKO compared to WT. Mechanistically, the impaired recruitment of tissue macrophages was associated with reduced spreading, impairment of chemotaxis in response to monocyte chemokines compared to WT cells (76±4 vs. 113±8 cells/field in NgKO vs. WT), but not adhesion, of isolated bone marrow derived monocytes from NgKO compared to controls. Moreover, NgKO macrophage demonstrated impaired Rac activation, translocation and cytoskeletal organization upon stimulation of with chemokines. In conclusion, our data suggests that endogenous Nogo coordinates macrophage mediated inflammation with angiogenesis, arteriogenesis and blood flow control.


1994 ◽  
Vol 14 (5) ◽  
pp. 877-881 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson ◽  
Peter L. Lutz

The exceptional ability of the turtle brain to survive prolonged anoxia makes it a unique model for studying anoxic survival mechanisms. We have used epiillumination microscopy to record blood flow rate in venules on the cortical surface of turtles ( Trachemys scripta). During anoxia, blood flow rate increased 1.7 times after 45–75 min, whereupon it fell back, reaching preanoxic values after 115 min of anoxia. Topical super-fusion with adenosine (50 μ M) during normoxia caused a 3.8-fold increase in flow rate. Superfusing the brain with the adenosine receptor blocker aminophylline (250 μ M) totally inhibited the effects of both adenosine and anoxia, while aminophylline had no effect on normoxic flow rate. None of the treatments affected systemic blood pressure. These results indicate an initial adenosine-mediated increase in cerebral blood flow rate during anoxia, probably representing an emergency response before deep metabolic depression sets in.


2019 ◽  
Vol 8 (10) ◽  
pp. 1690 ◽  
Author(s):  
Saranya Veluswamy ◽  
Payal Shah ◽  
Christopher Denton ◽  
Patjanaporn Chalacheva ◽  
Michael Khoo ◽  
...  

Sickle cell disease (SCD) is an inherited hemoglobinopathy characterized by polymerization of hemoglobin S upon deoxygenation that results in the formation of rigid sickled-shaped red blood cells that can occlude the microvasculature, which leads to sudden onsets of pain. The severity of vaso-occlusive crises (VOC) is quite variable among patients, which is not fully explained by their genetic and biological profiles. The mechanism that initiates the transition from steady state to VOC remains unknown, as is the role of clinically reported triggers such as stress, cold and pain. The rate of hemoglobin S polymerization after deoxygenation is an important determinant of vaso-occlusion. Similarly, the microvascular blood flow rate plays a critical role as fast-moving red blood cells are better able to escape the microvasculature before polymerization of deoxy-hemoglobin S causes the red cells to become rigid and lodge in small vessels. The role of the autonomic nervous system (ANS) activity in VOC initiation and propagation has been underestimated considering that the ANS is the major regulator of microvascular blood flow and that most triggers of VOC can alter the autonomic balance. Here, we will briefly review the evidence supporting the presence of ANS dysfunction in SCD, its implications in the onset of VOC, and how differences in autonomic vasoreactivity might potentially contribute to variability in VOC severity.


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