Effects of wall distensibility in hemodynamic simulations of an arteriovenous fistula

Arteriovenous fistulae are created surgically to provide adequate access for dialysis patients suffering from end-stage renal disease. It has long been hypothesized that the rapid blood vessel remodeling occurring after fistula creation is in part a process to restore the mechanical stresses to some preferred level, i.e., mechanical homeostasis. The current study presents fluid–structure interaction (FSI) simulations of a patient-specific model of a mature arteriovenous fistula reconstructed from 3D ultrasound scans. The FSI results are compared with previously published data of the same model but with rigid walls. Ultrasound-derived wall motion measurements are also used to validate the FSI simulations of the wall motion. Very large time-averaged shear stresses, 10–15 Pa, are calculated at the fistula anastomosis in the FSI simulations, values which are much larger than what is typically thought to be the normal homeostatic shear stress in the peripheral vasculature. Although this result is systematically lower by as much as 50 % compared to the analogous rigid-walled simulations, the inclusion of distensible vessel walls in hemodynamic simulations does not reduce the high anastomotic shear stresses to “normal” values. Therefore, rigid-walled analyses may be acceptable for identifying high shear regions of arteriovenous fistulae.     

Breakdown of End Walls in Differentiating Vessels of Secondary Xylem in Quercus rubra L.

Formation and breakdown of end walls were studied in the vesselsof the secondary xylem of Quercus rubra L. The end walls inradially expanding vessel members were very thin but showeda three-layered structure— two peripheral layers and adarker central layer. When longitudinal walls of vessel membersformed secon dary walls, the end walls had thickened considerablyand acquired secondary walls on their periphery. The disintegrationof end walls occurred at about the same time as the disintegrationof the vessel proto plasm. Frequent observations of intermediatestages in the disintegrating end walls indicate that breakdownis a gradual process brought about by the activity of vesselmembers' protoplasm.     

Hereditary hemorrhagic telangiectasia or Rendu-Osler-Weber syndrome in the same family

The authors present the case of three patients from the same family in whom hereditary hemorrhagic telangiectasia (HHT) or Rendu-Osler-Weber syndrome was diagnosed. The disease is rare and occurs with multiple telangiectases of the skin and mucosa, and pulmonary arteriovenous fistulae. The clinical status of our patients included multiple telangiectases of the skin and mucosa, recurrent epistaxis, exertion dyspnea and cyanosis. Polycythemia and hypoxemia were observed in the blood. The clinical status and conventional radiological examination of the thoracic region, with the suspicion of arteriovenous (A-V) fistulae, pointed to HHT. A-V fistulae were confirmed by pulmonary angiography. The pulmonary A-V fistulae were operated in all three patients and diagnosis was confirmed by histopathological examination of the operated samples. Clinical improvement was observed after the operation and cyanosis, dyspnea, hypoxemia and polycythemia disappeared.     

Use of Internal Arteriovenous Fistula in Home Haemodialysis

Five patients with previous experience of home haemodialysis (lasting one to two years) had internal arteriovenous fistulae created in a previously non-cannulated limb. After training of the spouses or patients to insert the needles, the arteriovenous cannulas were removed and the patients maintained on fistula dialysis in the home, unattended, overnight, for periods of 1 to 11 months (total patient experience of 30 months). All patients expressed a preference for the arteriovenous fistula, and no significant medical complications have been noted to date.The safe use of a blood pump in the home, overnight, was achieved by the addition of an extra monitor on the outflow (arterial) blood line.     

Importance of the functional activity of thrombocytes and the antiaggregation activity of the vascular walls in regulating blood aggregation

It was established in dog experiments that aggregation activity of platelets and the rate of aggregation were higher in arterial than in venous blood, with the platelet content being identical. Antiaggregation activity of vascular walls of the arterial system. The data obtained indicate the presence of the arteriovenous difference of the function of the vascular-platelet hemostasis, which is of a role in the processes of regulating the state of blood aggregation in the body.     

A simple model of a vessel with a wall sensitive to mechanical stimuli

Smooth muscles in the walls of small blood vessels under normal conditions are always moderately active, so that there is a certain reserve for blood flow adaptation to changed conditions by either narrowing or expanding of the vessel lumen. The previous studies of small vessel hydrodynamics have shown that the activity can cause specific instability of vessel steady states. In order to trace qualitatively the influence of numerous factors on the active state of the vessel, a simplified model of the vessel was proposed, which is reduced to a nonlinear ordinary equation of the first order with delayed argument.     

Monoaminergic and cholinergic nerve fibres in the human dental pulp

Summary Distribution of cholinesterase-containing nerve fibres was studied in 15 human dental pulps by the thiocholine method. Falk's fluorescent method was used to demonstrate catecholamines (8 dental pulps).Cholinesterases were localized partly in the subodontoblastic plexus sending out fine branches towards odontoblasts, and partly in the nerve fibres attached to the blood vessel walls. These fibres in contrast to those of the subodontoblastic plexus were finer and showed fine varicosities.Monoaminergic terminals were localized mainly along blood vessel walls, however, some fibres having no relation to the blood vessels were also found.Cholinesterase-containing nerve fibres in the periphery of the pulp are considered to be sensitive nerve fibres originating from n.V. Distribution of cholinesterase-containing nerve fibres and monoaminergic terminals along the blood vessel walls indicates that the blood vessels in the human dental pulp might be under both parasympathetic and sympathetic control.     

Congenital coronary artery-cardiac chamber fistulae: Report of two cases

Two cases of coronary arteriovenous fistulae are reported. In the first case, the right coronary artery (RCA) drained into the right ventricular outflow tract, and the distal RCA filled through a branch of the left anterior descending coronary artery. In the second case, the RCA drained into the right atrium and filled through a branch of the left circumflex artery. The fistulae were closed with subcoronary mattress sutures that preserved the continuity of the native circulation.     

Microcirculatory bed of the heart during peripheral arteriovenous shunting

In the experiment performed on 108 test and 28 control dogs, by means of injection and histological methods, the effect of arteriovenous fistula on the cardiac microcirculatory bed has been studied. The arteriovenous blood shunting results in plethora and stasis in the cardiac microcirculatory bed, in dilatation of all its links, in aggregation and adhesion of the blood formed elements, in increased permeability of microvessels, in diapedesis of erythrocytes and in myocardial edema, in winding microvessels, in development of the venoarterial reaction, in hypertrophy of myocytes, recalibration and sclerosis of the microvascular walls.     

Coexistence of intradural spinal arteriovenous malformation and associated developmental anomalies - report of two cases

Spinal arteriovenous malformations (AVM) have been devided into dural (Type I), intramedullary glomus (Type II), juvenile (Type III), and perimedullary direct arteriovenous fistulae (Type IV). AVMs are usually associated with subacute myelopathy in what has been known as Foix-Alajouanine syndrome. We presented two patients with two intradural spinal arteriovenous malformations associated in what we call Foix-Alajouanine syndrome. The both patient developed acute back pain and paresthesias, followed by paraplegia and incontinence. The clinical status of one patient has been improved after particle embolization for a 17 years when he deteriorated up to paraplegia after spinal angiography for follow up. Clinical status in another patient deteriorated, because particle emoblisation cannot be performed due to very descrete presentation of the feeding artery. Extensive neuroradiological examination in both patients revealed coexistence of numerous associated developmental anomalies in both patients. We conclude that arteriovenous malformations occasionally are associated with other vascular and nonvascular developmental anomalies elsewhere in the body. These findings rise attention about keep in mind the suspicion of mutual etiopathogenesis and congenital origin of these anomalies. Early timing of the diagnostic and therapeutic interventiosn are stressed to prevent or delay irreversible ishaemic myellopathy or haemorrhage. For the definitive diagnosis of spinal arteriovenous malformations and evaluation of its occlusion grade after the therapy spinal angiography is needed     

Studies on families with Osler's disease]

The authors examined 143 members of a family, where they found 37 (= 25.87%) of Osler patients. It was only in 30% of these patients that the symptoms occurred before the tenth year of age. As in one patient the symptoms did not appear until the age of 58 years, the possibility cannot be excluded that symptoms of the disease will become manifest even in other, sill younger members of the family in the course of time. Epistaxis was observed in 93% of the cases, nephrorrhagia in no case, hepatopathy and gastrorhagy were found only once in each case. The X-ray examination revealed arteriovenous pulmonary aneurysm in 5 cases. As a rule, oestrogen treatment led to good results. A case of death occurred during an influenza epidemic in a severe anaemic patient. Clinical main symptoms of Osler's disease were epistaxis and arteriovenous fistulae which could be roentgenologically identified in the lung. Teleangiectasia could be detected during the autopsy besides vessel anomalies on the surface even in the bronchi, oesophagus, trachea, stomach, kidneys, small intestine and particularly in the large intestines. Conditions of iron deficiency may very often occur in osler Patients; they require a substituting treatment.     

Cyclic GMP-dependent and cyclic AMP-dependent protein kinases, protein kinase modulators and phosphodiesterases in arteries and veins of dogs. Distribution and effects of arteriovenous fistula and arterial occlusion.

Possible involvement of cyclic GMP-dependent and cyclic AMP-dependent protein kinases, protein kinase modulators and cyclic nucleotide phosphodiesterases in functions of vascular tissues were investigated in the dog. All of the above activities, localized in the smooth muscle-rich inner layer of the blood vessels, were found to be higher in the arteries than in the veins. The peripheral arteries were disproportionately richer in cyclic GMP-dependent protein kinase (as indicated by high ratios of cyclic GMP-dependent to cyclic AMP-dependent protein kinase) than were the veins, with the exception of the pulmonary artery, an atypical arterial tissue exposed to low blood pressure. Interestingly, the protein kinase ratio for the aorta, an artery with no significant role in blood pressure regulation, was not higher than that for the vena cava. Creation of femoral arteriovenous fistulae in the dogs led to preferential reductions in the cyclic GMP-dependent enzyme activity both in the proximal and distal arteries, whereas it was elevated in the stressed vein distal to the anastomotic site. The cyclic GMP-dependent enzyme was preferentially reduced in the saphenous artery distal to occlusion. Changes in the cyclic GMP-dependent enzyme activity appeared to precede gross atrophy or hypertrophy of the vessels. It is suggested that the vascular cyclic GMP-dependent protein kinase may be closely related to peripheral resistance and its regulation.     

Cyclic GMP-dependent and cyclic AMP-dependent protein kinases,protein kinase modulators and phosphodieterases in arteries and veins of dogs Distribution and effects of arteriovenous fistula and arterial occlusion

Possible involvement of cyclic GMP-dependent and cyclic AMP-dependent protein kinases, protein kinase modulators and cyclic nucleotide phosphodiesterases in functions of vascular tissues were investigated in the dog. All of the above activities, localized in the smooth muscle-rich inner layer of the blood vessels, were found to be higher in the arteries than in the veins. The peripheral arteries were disproportionately richer in cyclic GMP-dependent protein kinase (as indicated by high ratios of cyclic GMP-dependent to cyclic AMP-dependent protein kinase) than were the veins, with the exception of the pulmonary artery, an atypical arterial tissue exposed to low blood pressure. Interestingly, the protein kinase ratio for the aorta, an artery with no significant role in blood pressure regulation, was not higher than that for the vena cava. Creation of femoral arteriovenous fistulae in the dogs led to preferential reductions in the cyclic GMP-dependent enzyme activity both in the proximal and distal arteries, whereas it was elevated in the stressed vein distal to the anastomotic site. The cyclic GMP-dependent enzyme was preferentially reduced in the saphenous artery distal to occlusion. Changes in the cyclic GMP-dependent enzyme activity appeared to precede gross atrophy or hypertrophy of the vessels. It is suggested that the vascular cyclic GMP-dependent protein kinase may be closely related to peripheral resistance and its regulation.     

Vascular NK-1 receptor occurrence in normal and chronic painful Achilles and patellar tendons: studies on chemically unfixed as well as fixed specimens

It is not known as to whether the Achilles and patellar tendons contain neurokinin-1 (NK-1) receptors. This is a drawback when considering the fact that pain symptoms are frequent in these and as recent studies show that the pain symptoms might be cured via interference with blood vessel function. In the present study, the human Achilles and patellar tendons were examined concerning immunohistochemical expression of the NK-1 receptor. Chemically unfixed and fixed specimens, TRITC and PAP stainings and a battery of NK-1 receptor antibodies, including antibodies against the C-terminus and the N-terminal region, were utilized. NK-1 receptor immunoreaction could be detected in inner parts of the walls of large blood vessels and in the walls of small blood vessels. To some extent, NK-1 immunoreaction was also detectable in small nerve fascicles and in tenocytes. It was found to be of utmost importance to apply both chemically unfixed and fixed specimens. The use of chemically unfixed tissue was found advantageous in order to depict the immunoreactions in the blood vessel walls. The observations represent new findings and are of relevance as substance P (SP) is known to be of importance where neurogenic angiogenesis contributes to diseases and as SP on the whole has profound effects concerning blood vessel regulation.     

Pulsatile blood flow, shear force, energy dissipation and Murray's Law

Background  

Murray's Law states that, when a parent blood vessel branches into daughter vessels, the cube of the radius of the parent vessel is equal to the sum of the cubes of the radii of daughter blood vessels. Murray derived this law by defining a cost function that is the sum of the energy cost of the blood in a vessel and the energy cost of pumping blood through the vessel. The cost is minimized when vessel radii are consistent with Murray's Law. This law has also been derived from the hypothesis that the shear force of moving blood on the inner walls of vessels is constant throughout the vascular system. However, this derivation, like Murray's earlier derivation, is based on the assumption of constant blood flow.     

Mechanisms to explain the reverse perivascular transport of solutes out of the brain

Experimental studies and observations in the human brain indicate that interstitial fluid and solutes, such as amyloid-beta (Abeta), are eliminated from grey matter of the brain along pericapillary and periarterial pathways. It is unclear, however, what constitutes the motive force for such transport within blood vessel walls, which is in the opposite direction to blood flow. In this paper the potential for global pressure differences to achieve such transport are considered. A mathematical model is constructed in order to test the hypothesis that perivascular drainage of interstitial fluid and solutes out of brain tissue is driven by pulsations of the blood vessel walls. Here it is assumed that drainage occurs through a thin layer between astrocytes and endothelial cells or between smooth muscle cells. The model suggests that, during each pulse cycle, there are periods when fluid and solutes are driven along perivascular spaces in the reverse direction to the flow of blood. It is shown that successful drainage may depend upon some attachment of solutes to the lining of the perivascular space, in order to produce a valve-like effect, although an alternative without this requirement is also postulated. Reduction in pulse amplitude, as in ageing cerebral vessels, would prolong the attachment time, encourage precipitation of Abeta peptides in vessel walls, and impair elimination of Abeta from the brain. These factors may play a role in the pathogenesis of cerebral amyloid angiopathy and in the accumulation of Abeta in the brain in Alzheimer's disease.     

Arteriovenous difference in antithrombin III activity and the antiaggregation properties of the vessel wall

The paper is concerned with the data on the arteriovenous difference in antithrombin III activity and antiaggregation properties of the aortal and inferior vena cava walls in Wistar rats. A correlation between the changes identified and different thromboresistance of the arteries and veins is suggested.     

Modified human umbilical vein graft arteriovenous fistulae as a source of angioaccess in maintenance hemodialysis

Forty-six modified human umbilical vein graft arteriovenous fistulae were used for maintenance hemodialysis in 45 patients with chronic renal failure. Complications were encountered in 15 of the 46 grafts after one to 24 months. In only one case did a graft become infected. The results show a significantly lower complication rate than for any other graft material.     

Aggregation of platelets in damaged vessels

The only certain physiological function of platelets is their aggregation in injured vessel walls as haemostatic plugs. The association of thrombocytopenia with petechial haemorrhages suggests that platelets are somehow required for the functional integrity of small vessels, but no mechanism has yet been established. The pathological aggregation of platelets as thrombi in atherosclerotic arteries is commonly, if not always, initiated by haemorrhage. In artificial vessels, platelets tend to aggregate on the walls wherever blood flow is non-laminar. The mural aggregation of platelets is not prevented by unphysiologically high wall-shear forces. The facts suggest, on the contrary, that the process depends in some way on abnormal haemodynamic conditions. This contribution is mainly concerned with questions about how haemodynamic conditions in and around vascular leaks affect arriving platelets that aggregate there, and about the chemical agents responsible for making the platelets reactive. The effects of these agents are known mainly from in vitro experiments in which aggregation can be quantitatively correlated with biochemical effects by simple and reproducible methods; the relevance to their reactions in haemostasis and thrombosis is uncertain. It is difficult to devise quantitative methods for analysing these processes in vivo because of the very low concentrations at which endogenous agents can activate platelets and haemostasis factors in the plasma; the rapidity with which platelets aggregate in a damaged blood vessel; and the complexity and inconstancy of the haemodynamic situation. All these factors must be accounted for in hypotheses of haemostasis. New experimental approaches towards analysing the haemostatic mechanism in vivo are described.     

Platelet - vessel wall interaction: role of blood clotting

Vascular damage initiates not only the adhesion and aggregation of blood platelets but also coagulation, which is of mixed (intrinsic and extrinsic) origin. Evidence is presented that thrombin, generated as a result of the injury, is a prerequisite for platelet aggregation. Platelets, after activation, in their turn promote coagulation. Prostaglandin I2 (PGI2 or prostacyclin) inhibits coagulation induced by damaged vascular tissue. This effect of PGI2 is mediated by the inhibition of platelets in their participation in the generation of factor Xa and thrombin. Dietary cod liver oil, by changing plasma coagulability, decreases the procoagulation activity of vessel walls, and arterial thrombosis. Another fish oil with similar effects on plasma coagulability and some other haemostatic parameters does not modify vessel wall-induced clotting, nor does it significantly lower arterial thrombosis tendency; this indicates the physiological relevance of vessel wall-induced clotting in arterial thrombus formation. Some evidence is also given for the importance of vessel wall-induced clotting in primary haemostasis.