Structure and functional properties of the arterial system of the frog submandibular muscle as an object for studying working hyperemia

Architectonics and ultrastructure of the arterial blood vessels of the frog submaxillary muscle are described. Intramuscular arterial vessels 100 divided by 8 micron in diameter have a single layer of smooth muscle cells (SMC), while SMC themselves look simplified and undifferentiated. The contacts between SMC in arterial vessels of all the sizes and myoendothelial contacts in the vessels 80-8 microns in diameter are noted. In the resting muscle, the arterial vessels of all the sizes show spontaneous changes in the diameter. During muscular contraction, the time course of the dilatation of different vessels is different, which is likely to be caused by vasomotion phase differences seen immediately before the contraction.     

Pattern of arteries in the hindlimbs of hybrid mice

The pattern of the arterial system has been studied in the hindlimbs of adult male and female mice in a hybrid strain. A technique was developed to inspect the distribution pattern after the vessels were injected with a blue polymer, the bone was stained with alizarin red S, and the soft tissue was cleared to transparency. Substantial variations were identified in the point of origin of 6 of 41 arterial branches; extra vessels and absence of vessels were uncommon. The types of arterial differences identified in normal adult mice were different from those identified in mice with absence of the tibia, which have absence of major arteries, including the popliteal and posterior tibial arteries.     

Endothelin-1 and U46619 potentiate selectively the venous responses to nerve stimulation within the perfused superior mesenteric vascular bed of the rat

The effects were examined of endothelin-1 and U46619 on the responses to perivascular nerve stimulation of the simultaneously perfused arterial and venous vessels of the superior mesenteric arterial bed of the rat. Stimulation of the nerves at 4-16 Hz for 30 s caused frequency dependent constrictions of both the arterial and venous vessels similar to those produced by bolus doses of exogenous noradrenaline (0.1-10 nmol). Infusion of either endothelin-1 (0.1 nM) or U46619 (1-3 nM) caused small (less than or equal to 5 mmHg) increases in arterial and venous perfusion pressures and selectively potentiated the venous, but not arterial, responses to nerve stimulation. Conversely, endothelin-1 and U46619 potentiated the responses of both the arterial and venous vessels to exogenous noradrenaline. Thus, as reported previously for the arterial vessels of the rat mesentery, the isolated venous vessels constrict to perivascular nerve stimulation in a frequency dependent manner. In addition, endothelin-1 and U46619 potentiate selectively the effects of nerve stimulation on the veins.     

Age-related characteristics of the structure of renal arteries

The investigation has been performed on 337 preparations of human kidneys and on 129 clinical angiograms of kidneys at different age without renal and cardiovascular system pathology. A complex of morphological techniques, mathematical method including, has been used. Peculiarities in architectonics of the intraorganic renal arterial vessels have been described during various age periods of postnatal ontogenesis; essential variations of the renal artery index have been revealed in newborns and adolescents. They reflect functional rearrangement of the vessels during these age periods. Six periods in formation of the renal arterial intraorganic vessels have been determined, when probability of decrease and failure of their compensatory potentialities is especially great.     

Blood vasculature of the lymph node in the dog: anatomical evidence for participation of extrahilar arterial vessels in the blood supply of the cortex.

The organization of the arterial vessels of dog lymph nodes (LN) was studied using methods of visualization of the vasculature by systemic injection of different tracers (colloidal carbon, Micropaque resin and methylmethacrylate) followed by observation of the samples by light microscopy (after clearing of the thick sections of LN) or scanning electron microscopy (corrosion casts). LN from all of the three groups of nodes studied (tracheobronchial, paratracheal and popliteal) showed an extensive network of arterial vessels encircling the capsule of the organ. We found that branches of these capsular arteries penetrated deeply into the cortical domain of LN. The capsule-originating vessels appeared to have a significant participation in the blood supply of the LN parenchyma at the cortical domains of the organs. Our findings are in contrast with current views on the angiology of the LN that consider that virtually all of the arterial capillaries of the LN parenchyma come from hilar arteries. We propose, therefore, that important segments of the LN cortex receive their blood supply from capsular arteries rather than from hilar vessels.     

Dynamic viscous flow in distensible vessels of skeletal muscle microcirculation: application to pressure and flow transients

Blood flow in the microcirculation of the rat skeletal muscle during transient changes of arterial pressure is analyzed theoretically. Although flow in such small vessels is quasi-steady and has a very low Reynolds number, time-dependent nonuniform flows along the length of the blood vessels can be observed due to vessel distensibility. The governing equations for a single microvessel are derived using previously measured microvessel elasticity, and several solutions to different inflow and outflow pressures and flow conditions are investigated. The results indicate that when such distensible microvessels are subjected to a step increase of arterial pressure, the arterial flow shows a rapid overshoot followed by a progressive decay to steady-state. An arterial step flow induces a different response which takes the form of a monotonically increasing pressure. Pressure and flows are nonuniform along the vessel length during such transients. In-vitro whole organ pressure-flow data are presented in the dilated rat gracilis muscle which qualitatively agree with the theoretical predictions.     

Ephrin-B2 selectively marks arterial vessels and neovascularization sites in the adult, with expression in both endothelial and smooth-muscle cells

The Eph receptor tyrosine kinases and their membrane-tethered ephrin ligands provide critical guidance cues at points of cell-to-cell contact. It has recently been reported that the ephrin-B2 ligand is a molecular marker for the arterial endothelium at the earliest stages of embryonic angiogenesis, while its receptor EphB4 reciprocally marks the venous endothelium. These findings suggested that ephrin-B2 and EphB4 are involved in establishing arterial versus venous identity and perhaps in anastamosing arterial and venous vessels at their junctions. By using a genetically engineered mouse in which the lacZ coding region substitutes and reports for the ephrin-B2 coding region, we demonstrate that ephrin-B2 expression continues to selectively mark arteries during later embryonic development as well as in the adult. However, as development proceeds, we find that ephrin-B2 expression progressively extends from the arterial endothelium to surrounding smooth muscle cells and to pericytes, suggesting that ephrin-B2 may play an important role during formation of the arterial muscle wall. Furthermore, although ephrin-B2 expression patterns vary in different vascular beds, it can extend into capillaries about midway between terminal arterioles and postcapillary venules, challenging the classical conception that capillaries have neither arterial nor venous identity. In adult settings of angiogenesis, as in tumors or in the female reproductive system, the endothelium of a subset of new vessels strongly expresses ephrin-B2, once again contrary to earlier views that such new vessels lack arterial/venous characteristics and derive from postcapillary venules. While earlier studies had focused on a role for ephrin-B2 during the earliest embryonic stages of arterial/venous determination, our current findings using ephrin-B2 as an arterial marker in the adult challenge prevailing views of the arterial/venous identity of quiescent as well as remodeling adult microvessels and also highlight a possible role for ephrin-B2 in the formation of the arterial muscle wall.     

A new fundamental bioheat equation for muscle tissue--part II: Temperature of SAV vessels

In this study, a new theoretical framework was developed to investigate temperature variations along countercurrent SAV blood vessels from 300 to 1000 microm diameter in skeletal muscle. Vessels of this size lie outside the range of validity of the Weinbaum-Jiji bioheat equation and, heretofore, have been treated using discrete numerical methods. A new tissue cylinder surrounding these vessel pairs is defined based on vascular anatomy, Murray's law, and the assumption of uniform perfusion. The thermal interaction between the blood vessel pair and surrounding tissue is investigated for two vascular branching patterns, pure branching and pure perfusion. It is shown that temperature variations along these large vessel pairs strongly depend on the branching pattern and the local blood perfusion rate. The arterial supply temperature in different vessel generations was evaluated to estimate the arterial inlet temperature in the modified perfusion source term for the s vessels in Part I of this study. In addition, results from the current research enable one to explore the relative contribution of the SAV vessels and the s vessels to the overall thermal equilibration between blood and tissue.     

Fast blood-flow simulation for large arterial trees containing thousands of vessels

Blood flow modelling has previously been successfully carried out in arterial trees to study pulse wave propagation using nonlinear or linear flow solvers. However, the number of vessels used in the simulations seldom grows over a few hundred. The aim of this work is to present a computationally efficient solver coupled with highly detailed arterial trees containing thousands of vessels. The core of the solver is based on a modified transmission line method, which exploits the analogy between electrical current in finite-length conductors and blood flow in vessels. The viscoelastic behaviour of the arterial-wall is taken into account using a complex elastic modulus. The flow is solved vessel by vessel in the frequency domain and the calculated output pressure is then used as an input boundary condition for daughter vessels. The computational results yield pulsatile blood pressure and flow rate for every segment in the tree. This solver is coupled with large arterial trees generated from a three-dimensional constrained constructive optimisation algorithm. The tree contains thousands of blood vessels with radii spanning ~1 mm in the root artery to ~30 μm in leaf vessels. The computation takes seconds to complete for a vasculature of 2048 vessels and less than 2 min for a vasculature of 4096 vessels on a desktop computer.     

Development of an arterial tree in C6 gliomas but not in A375 melanomas

The microcirculation of tumors is severely disturbed. Tumors are usually supplied by fragile capillaries and do not possess the natural hierarchy of blood vessels. The detection of specific markers for arterial and venous endothelial cells (ECs) now enables us to study the vascular tree in tumors. We have injected rat C6 glioma and human A375 melanoma cells into 3.5- to 4-day-old avian embryos. After 10-12 days of reincubation the tumor cells formed solid tumors vascularized by host ECs. In contrast to the melanomas, the gliomas induced an almost normal vascular tree with arterial and venous vessels. The arterial vessels express the arterial EC marker ephrin-B2, and possess a media of smooth muscle alpha-actin (alphaSMA)-positive cells. Venular vessels in the gliomas are ephrin-B2-negative/alphaSMA-positive. Although the gliomas may represent a rare case of vascular tree induction in tumors, the results underline the heterogeneity of tumor-induced angiogenesis. This has an impact on tumor blood flow and thereby also on the efficacy of chemotherapy and radiotherapy.     

The effect of portal hypertension on the structure of the pancreas in rats during the early periods of the experiment]

The model of Hiari disease obtained by a 50% constriction of the rat's posterior portal vein under the diaphragm was used in order to study the response of different structures of the pancreas on the 1st, 3, 5, 7, 15th days of experiment. The arterial vessels were found to have fairly active responses to venous congestion. The greatest load in sustaining microcirculation falls to large arteries, so they are more subjected to dystrophies, the severeness of which is proportional to the thickness of the vessels walls. In later terms of the experiment smaller arterial vessels are involved. Within a month blood circulation in the organ deteriorates and there appear small hemorrhages. The venous congestion results in a change of the structure and secretion of the acinous and insular cells of the pancreas.     

Resistance and capacitance functions of gastric vessels under the action of noradrenaline

In acute experiments on cats, the gastric vascular bed being perfused under constant blood flow, the actions of gastric vessels was investigated using newly elaborated approach to their humoral isolation. Increased doses of noradrenaline elicited the dose-dependent constrictive response of gastric arterial vessels. Perfusion pressure increase in the gastric vascular bed under action of the minimal dose of noradrenaline was more pronounced, than in the intestinal vessels. The capacity of the gastric vascular bed under action of the drug changed in different manner, mostly increased, but could be decreased as well. In contrast to the small intestine the gastric vessels are characterized by more pronounced action of noradrenaline on blood depoting processes.     

The blood circulation inside the spleen. I. The arterial blood vessels general distribution in the rat spleen

As an attempt to investigate the different pathways followed by the blood into the spleen and to analyse their functional significance, a technique was used mainly based on the intraarterial perfusion of a Prussian blue "solution" added of some chemical mediators and vasoactive substances. Such technique provides results which may be analysed taking into account the effect of the anaesthetic used, that may influence the findings. From the anaesthetic used, the sulfuric ether and the barbital sodium produce vasoconstriction of the white pulp blood vessels, whereas the chlorpromazine-promethazine doesn't have this effect, and so the Prussian blue appears inside these vessels. The vasodilator drugs, such as succinonitrile and papaverine hydrochloride, show a general vasodilator effect on the splenic arterial system. Teh arterial vessels of the white and the red pulp, including those placed at the subcapsular areas, become enlarged; into the white pulp, either the central or the peripheral blood vessel plexus of the lymphatic follicle becomes evident. The latter readily constitutes the perifollicular and the pericolumnar plexus. The blood vessels of this plexus become permeable to the Prussian blue "solution" by the heparin sodium effect, and so the dye particles enter the marginal zone and the splenic sinuses. In addition, from the white pulp arteries arise 2 types of anastomotic arterioles which appear enlarged after succinonitrile treatment: The short anastomotic arterioles that crosses the marginal zone entering the red pulp near the white pulp; the long anastomotic arterioles which enter the red pulp and after a long course end up into or around a collector sinus. The addition of histamine dihydrochloride to the perfusion solutions shows a slight vasodilator effect mainly on the subcapsular penicillar arterioles, including the helicine arterioles. The adrenergic stimulation of the splenic blood vessels induces a generalized arterial constriction, except of the anastomotic arterioles, that becomes open; in such way, the blood pathway follows the course of the anastomotic arterioles and the collector arterioles also become constricted. The adrenergic vasoconstrictor effect is inhibited by the phenoxy-benzamine hydrochloride. The addition of acetylcholine chloride, in the dosage, used, induces a generalized arterial vessel constriction, mainly of the perifollicular plexus. This effect is inhibited by atropine sulfate which, on the other hand, produces evident enlargement of the perifollicular and pericolumnar arterial plexus.     

Arterial vascularization of the tail of the pancreas with special reference to the relation of the tail and body vessels

The cauda pancreatis has a characteristic pattern of vascularization. Among the big arterial stems surrounding it, up to 4 arteries, 'caudal arteries', nourish the arterial system of the cauda. These stems originate especially in the Arteria gastroepiploica sinistra and in the lower main splenic branch of the Arteria lienalis. The vascular relations between corpus and cauda can be of different kinds. Five basic types of relations can be identified: type I: the cauda is supplied exclusively by caudal arteries; type II: at least one caudal artery anastomoses with the vessels of the corpus; type III: the cauda is supplied both by the caudal arteries and by vessels of the corpus (non-anastomosing); type IV: combined forms of blood supply by caudal arteries and corpus arteries by way of anastomoses and non-anastomosing vessels are found; type V: the cauda is supplied exclusively be vessels stemming from the corpus. In each of these five types, individual vessels supplying the cauda can assume the function of a terminal vessel.     

Effects of simulated weightlessness on arterial vasculature (an experimental study on vascular deconditioning)

Rats were tail-suspended to simulate microgravity and then studied for changes in arterial vasculature. Parameters investigated included vascular responsiveness at different areas of the body, morphological changes in arteries and vascular endothelium tissue, and the distribution of adrenergic nerve fibers supplying cerebral arteries and arterial vessels. The significance of the results and future research directions are discussed.     

Extra-alveolar veins are contiguous with, and leak fluid into, periarterial cuffs in rabbit lungs.

We previously observed physiological evidence that arterial and venous extra-alveolar vessels shared a common interstitial space. The purpose of the present investigation was to determine the site of this continuity to improve our understanding of interstitial fluid movement in the lung. Orange G and Evans blue dyes were added to the arterial and venous reservoirs, respectively, of excised rabbit lungs as they were placed 20 cmH2O into zone 1 (pulmonary arterial and venous pressures = 5 cmH2O, alveolar pressure = 25 cmH2O). After 10 s or 4 h the lungs were fixed by immersion in liquid N2, freeze-dried, cut into 5-mm serial slices, and examined by light macroscopy. Serial sections of 0.25-0.5 mm were subsequently examined by scanning electron microscopy. In the animals subjected to the zone 1 stress for 4 h, arterial and venous extra-alveolar vessels were surrounded by cuffs of edema. The edema ratio (cuff area divided by vessel lumen area) was greater around arteries than veins and decreased with increasing vessel size. Periarterial cuffs usually contained orange dye and frequently contained both orange and blue dye. Lymphatics containing orange or blue dye were frequently seen in periarterial cuffs. Scanning electron microscopy demonstrated that extra-alveolar veins of approximately 100 microns diameter were anatomically contiguous with arterial extra-alveolar vessel cuffs. In rabbit lungs, both arterial and venous extra-alveolar vessels (and/or alveolar corner vessels) leak fluid into perivascular cuffs surrounding arterial extra-alveolar vessels, and lymphatics located in the periarterial cuff contain fluid that originates from both the arterial and venous extra-alveolar vessels.     

Experimental measurements of the temperature variation along artery-vein pairs from 200 to 1000 microns diameter in rat hind limb

Theoretical studies have indicated that a significant fraction of all blood-tissue heat transfer occurs in artery-vein pairs whose arterial diameter varies between 200 and 1000 microns. In this study, we have developed a new in vivo technique in which it is possible to make the first direct measurements of the countercurrent thermal equilibration that occurs along thermally significant vessels of this size. Fine wire thermocouples were attached by superglue to the femoral arteries and veins and their subsequent branches in rats and the axial temperature variation in each vessel was measured under different physiological conditions. Unlike the blood vessels < 200 microns in diameter, where the blood rapidly equilibrates with the surrounding tissue, we found that the thermal equilibration length of blood vessels between 200 microns and 1000 microns in diameter is longer than or at least equivalent to the vessel length. It is shown that the axial arterial temperature decays from 44% to 76% of the total core-skin temperature difference along blood vessels of this size, and this decay depends strongly on the local blood perfusion rate and the vascular geometry. Our experimental measurements also showed that the SAV venous blood recaptured up to 41% of the total heat released from its countercurrent artery under normal conditions. The contribution of countercurrent heat exchange is significantly reduced in these larger thermally significant vessels for hyperemic conditions as predicted by previous theoretical analyses. Results from this study, when combined with previous analyses of vessel pairs less than 200 microns diameter, enable one estimate the arterial supply temperature and the correction coefficient in the modified perfusion source term developed by the authors.     

Using hydraulic input impedance in determination of changes in the arteries of different calibre

In anaesthetised cats, the arterial input impedance in combination with seven-element lumped-parameter model was used to estimate the resistance change in arteries of different caliber. The results show that the method gives reasonable estimations of changes in hydraulic resistance of arterial vessels of different caliber. We found that the method of vascular input impedance permits to reveal and assess quantitatively local constrictions and dilations as well as hemodynamically insignificant stenosis of conduit arteries.     

Mechanics of caudal artery relaxation in control and hypertensive rats

Alterations of smooth muscle function can just as easily stem from mechanical alterations in its ability to relax as from alteration in contraction. Since a failure of arterial smooth muscle to relax may contribute to the development of hypertension, we felt it necessary to study the relaxation process in greater depth. The effect of load on the time course of relaxation of rat caudal artery smooth muscle was analyzed either by comparing afterloaded contractions against various loads or by imposing abrupt alterations in load. Unlike mammalian striated muscles in which relaxation was reported sensitive to loading conditions, relaxation in the smooth muscle of the rat caudal artery (n = 17) was found to be largely independent of loading conditions. This type of relaxation has been termed "inactivation-dependent" relaxation; it is typical of muscle tissue in which the calcium sequestering apparatus is poorly developed. Our results suggest that calcium resequestration, or some biochemical process downstream to it, is the rate-limiting step during relaxation in arterial smooth muscle and that this is not qualitatively different for hypertensive arterial smooth muscle. These analytic techniques were used in the study of relaxation of hypertensive vessels. Quantitative analysis of the relaxation curves showed that both isometric and isotonic relaxation time was prolonged in hypertensive arterial smooth muscle. Prolonged isotonic relaxation indicates that hypertensive arteries remain narrowed for prolonged periods compared with normotensive vessels. Such narrowed vessels may be a factor in the increased total peripheral resistance seen in genetic hypertension.