Effect of taurine on the microvessel exchange function and adrenergic response of veins and arteries in the cat skeletal muscle

In cats anesthetized with Uretan and perfused with a constant blood volume, Taurine induced responses of neither arterial nor venous vessels of the skeletal muscle but increased the capillary filtration coefficient without any significant change of the capillary pressure in the skeletal muscle's microvessels. Taurine also increased both the constrictor and the dilatory responses of the arterial and venous vessels. The mechanism of the Taurine effects upon the smooth muscle elements of arteries and veins as well as upon proper mechanisms of capillary pressure control and capillary filtration coefficient, seems to be calcium-dependent.     

Effect of Gravity on Blood Distribution and Flow in Large Vessels of Healthy Humans

Ultrasound imaging of vessels and flow Doppler ultrasonography were used to study the hemodynamic responses of large arteries and veins to orthostasis in 230 healthy human subjects of both sexes. The arterial system was shown to respond to orthostasis by differentially reducing the blood flow capacity and velocity, especially the blood supply to the lower extremities. During one-leg upright standing, the blood flow in the arterial bed of the weight-bearing leg was redistributed in favor of antigravity calf muscles. No blood flow redistribution was observed in the vertically oriented non-weight-bearing leg. A single voluntary contraction of the triceps surae muscles caused a transient increase in the volume blood flow in the femoral vein (by 2.5- to 5.0-fold in the recumbent position of the body and by 4- to 10-fold in the upright position).     

Venous return in systemic haemodynamics

The paper generalizes unclear problems of venous return to the heart under different conditions. Data are presented on the venous return/cardiac output ratio, general peripheral resistance, arterial pressure and vascular bed capacity. A concept of double wave nature of formation of the circulation pressor systemic responses is advanced.     

Adrenoceptor function in the bovine pulmonary circulation

The bovine pulmonary vascular response to alpha- and beta-agonists was studied using an awake intact calf model. Pulmonary arterial pressure, pulmonary arterial wedge pressure, left atrial pressure, systemic arterial pressure, and cardiac output were measured in response to 3 min infusions of isoproterenol (beta-agonist; 0.12, 0.24, 0.48, 0.9, and 1.8 micrograms X kg-1 X min-1) and phenylephrine (alpha-agonist, 0.15, 0.30, 0.60, 1.15, and 2.30 micrograms X kg-1 X min-1). Phenylephrine caused an increase in vascular resistance in the pulmonary arterial and venous compartments. The slope of the resistance in response to phenylephrine was greater in the pulmonary arterial than pulmonary venous circulation. Isoproterenol resulted in a dose-dependent decrease in vascular resistance in the pulmonary arteries and veins. The vascular resistance was decreased to the same level in the pulmonary arteries and veins although the arteries showed a greater percent change. In addition, isoproterenol infusion resulted in a transient decrease in arterial pH and increase in values for packed cell volume and haemoglobin.     

Relations between disorders of the intestinal-hepatic basin hemodynamics and absorption function in hemorrhage]

Chronic dog experiments showed that blood loss of 30 ml/kg or an intravenous injection of 1 microgram/kg norepinephrine did not markedly change small intestinal absorption. Blood supply to the liver was maintained at the expense of restricted portal circulation. Adaptation in blood loss seems to support arterial blood supply to the liver and absorbing epithelium of the small intestine to warrant their resistance to circulatory hypoxia and to promote their functional activity.     

Angiostrongylus costaricensis: complete redescription of the migratory pathways based on experimental Sigmodon hispidus infection

Angiostrongylus costaricensis lives in the cecal and mesenteric arteries of its vertebrate hosts, and causes an inflammatory disease in humans. To investigate unknown aspects of the abdominal angiostrogyliasis pathogenesis, infected Sigmodon hispidus were sequentially studied in different times of infection. The study revealed that L3 goes alternatively through two migratory courses during its development into an adult worm: lymphatic/venous-arterial and venous portal pathways. The former is considered the principal one, because it is used by most of the larvae. Like other metastrongylides, A. costaricensis passes over the pulmonary circulation to migrate from the lymphatic system to the arterial circulation, where they circulate during some days before reaching their definitive habitat. The oviposition by mature females began on 15th day. Eggs and L1 were detected mainly in the intestine and stomach, surrounded by inflammatory reaction constituted by macrophages, monocytes, and eosinophils. They were also spread to the lungs, mesenteric lymph nodes, pancreas, spleen, and kidneys. The larvae (L1) exhibited the centripetal capacity to invade the lymphatic and venous vessels of the intestine and mesentery. Adult worms that developed in the venous intrahepatic pathway migrated downstream to reach the mesenteric veins and laid eggs that embolized in the portal hepatic vessels.     

Arterial Levels of Oxygen Stimulate Intimal Hyperplasia in Human Saphenous Veins via a ROS-Dependent Mechanism

Saphenous veins used as arterial grafts are exposed to arterial levels of oxygen partial pressure (pO₂), which are much greater than what they experience in their native environment. The object of this study is to determine the impact of exposing human saphenous veins to arterial pO₂. Saphenous veins and left internal mammary arteries from consenting patients undergoing coronary artery bypass grafting were cultured ex vivo for 2 weeks in the presence of arterial or venous pO₂ using an established organ culture model. Saphenous veins cultured with arterial pO₂ developed intimal hyperplasia as evidenced by 2.8-fold greater intimal area and 5.8-fold increase in cell proliferation compared to those freshly isolated. Saphenous veins cultured at venous pO₂ or internal mammary arteries cultured at arterial pO₂ did not develop intimal hyperplasia. Intimal hyperplasia was accompanied by two markers of elevated reactive oxygen species (ROS): increased dihydroethidium associated fluorescence (4-fold, p<0.05) and increased levels of the lipid peroxidation product, 4-hydroxynonenal (10-fold, p<0.05). A functional role of the increased ROS saphenous veins exposed to arterial pO₂ is suggested by the observation that chronic exposure to tiron, a ROS scavenger, during the two-week culture period, blocked intimal hyperplasia. Electron paramagnetic resonance based oximetry revealed that the pO₂ in the wall of the vessel tracked that of the atmosphere with a ~30 mmHg offset, thus the cells in the vessel wall were directly exposed to variations in pO₂. Monolayer cultures of smooth muscle cells isolated from saphenous veins exhibited increased proliferation when exposed to arterial pO₂ relative to those cultured at venous pO₂. This increased proliferation was blocked by tiron. Taken together, these data suggest that exposure of human SV to arterial pO₂ stimulates IH via a ROS-dependent pathway.     

Bufokinin: immunoreactivity, receptor localization and actions in toad intestine and mesenteric circulation

In this study, we have mapped the immunoreactivity and the binding sites for bufokinin, a tachykinin peptide from the toad intestine. Dense bufokinin-immunoreactive fibers were present at the myenteric plexus, but no cell bodies were stained, suggesting an extrinsic origin. Bufokinin nerve fibers were also associated with submucosal blood vessels and mesenteric arteries. Autoradiographic binding sites for [(125)I]Bolton-Hunter-bufokinin were densely localized over the intestinal circular and longitudinal muscle, submucosal blood vessels and the endothelium of mesenteric arteries. Mesenteric veins had minimal immunoreactivity and binding sites. In the anesthetized toad, topical application of bufokinin onto the mesentery caused a 2.7-fold increase in arterial blood flow, observed using intravital microscopy. This study supports a role for bufokinin as an endogenous spasmogen and hemodynamic regulator in the toad intestine.     

Comparative characteristics of systemic and pulmonary hemodynamics during changes in the heart preloading

A greater degree of relative shifts in the systemic arterial pressure in enhancing the right heart pre-load as compared with its diminishing. A primary role of the compensation mechanisms of the enhanced systemic arterial pressure level. The main role in the compensation of integral shifts of the arterial pressure induced by changes in the heart pre-load was shown to belong to the vascular resistance both in the major and the minor circulation circles. An idea of a greater involvement of the capacity function of the vascular bed in the minor circulation circle as compared with that in the major circulation circle in systemic haemodynamic shifts in changes of the heart pre-load, has been advanced.     

Baroreflexes originated in vertebral artery zones upon peripheral vein tonus, systemic arterial blood pressure, and external respiration

The investigation was intended to study the role ofbaroreceptors ofhemodynamically isolated zone of vertebral arteries in regulation of peripheral veins tonus, arterial pressure and external respiration. Pressure decrease in this vascular reflexogenic zone led to reflex responses of increase in femoral vein tonus, elevation of blood pressure level and stimulation of external respiration. The opposite reflex responses of cardio-respiratory functional system to initial pressure activation of vertebral arteries baroreceptors are observed. Basing on generalization of our own findings and similar physiological and morphological researches of other authors, it is established that afferentation from the vertebral artery zone is a reflexogenic factor of somatic muscles' veins tonus regulation. These reflexes of capacity vessels tonic activity changes are part of cardio-respiratory responses of maintaining the tissue gaseous exchange.     

The effects of propranolol, phentolamine, and atropine on canine coronary vascular gradients

The objective of this study was to measure pressure gradients in the coronary circulation following the administration of three receptor-blocking drugs, propranolol, phentolamine, and atropine when administered singly and in sequence. As well, we examined the responses of these gradients to eight interventions: left stellate ganglion or left vagosympathetic trunk stimulation, administration of isoproterenol, acetylcholine, noradrenaline, adenosine, phenylephrine, or adrenaline. Using a multiple linear regression model we examined the actions and interactions of the receptor-blocking agents on hemodynamic variables and vascular gradients. Propranolol reduced heart rate as expected and blocked the responses to isoproterenol administration. As well, it abolished the epicardial coronary artery diastolic gradient. The gradient was restored when propranolol was the second receptor blocker administered but was abolished when it was the third. Phentolamine induced vasodilation with a decrease in coronary small vessel gradients. This effect persisted without regard to the sequence of administration. When it was the second or third agent it decreased the microcirculation and small vein gradients, an action it did not manifest when given singly. Atropine singly did not alter pressures or gradients; but as the second agent it altered the transmural, outflow tract, epicardial diastolic, and microcirculation and small vein diastolic gradients; and as the third agent the changes were in the transmural, epicardial systolic and diastolic, and small artery systolic and diastolic gradients. The pattern of responses was not predictable and that indicates that unique changes occur in the responses of the coronary circulation when multiple receptor-blocking agents are employed. Adrenergic control tends to dominate in the coronary arterial circulation, and muscarinic control in the coronary microcirculation and veins with considerable overlap.     

Comparative characterization of reactions of skeletal muscle arterial and venous vessels to combined adrenergic effects

In experiments with the constant blood flow perfusion of the cat calf muscle and combined actions of adrenalin and noradrenaline were tested as to the blood flow resistance changes of the arterial and venous blood vessels. Separately applied the catecholamines evoked vascular resistance changes practically similar in value; combined effects of catecholamines realized in greater increase of arterial than venous resistance. In contrast to arterial vessels supramaximal stimuli resulted in much lesser constrictive effect as compared with reaction of intramural veins to separately applied catecholamines. Greater doses of catecholamines being combined, stability of effector system of skeletal muscle veins is decreased as compared to arteries.     

Changes in the major circulation vessel capacity and their role in forming the venous return shifts under the effect of catecholamines

The study relates to characteristics of the major circulation vessel capacity and their part in forming the venous return shifts under the effect of catecholamines. In anesthetized cats, using the developed technique of controlled experiment enabling to stabilize the blood flow in the circulation arterial segment, fulfilling of pressor responses to i. v. administration of noradrenaline, adrenaline was found to increase the venous return, on the average, by 40% by means of changes in the major circulation vessel capacity (its venous segment, mainly). About 5% of the blood volume seems to become mobilized in the animal organism.     

Differential effects of prostaglandins A1 and A2 on pulmonary vascular resistance in the dog.

The effects of PGA1 and PGA2 were studied in the canine pulmonary vascular bed. Infusion of PGA1 into the lobar artery decreased lobar arterial and venous pressure but did not change left atrial pressure. In contrast, PGA2 infusion increased lobar arterial and venous pressure and the effects of this substance were similar in experiments in which the lung was perfused with dextran or with blood. These data indicate that under conditions of controlled blood flow PGA1 decreases pulmonary vascular resistance by dilating intrapulmonary veins and to a lesser extent vessels upstream to the small veins, presumably small arteries. The present data show that PGA2 increases pulmonary vascular resistance by constricting intrapulmonary veins and upstream vessels. The predominant effect of PGA2 was on upstream vessels and the pressor effect was not due to interaction with formed elements in the blood or platelet aggregation.     

Localization of the sites of pulmonary vasomotion by use of arterial and venous occlusion

In this study, we present a new approach for using the pressure vs. time data obtained after various vascular occlusion maneuvers in pump-perfused lungs to gain insight into the longitudinal distribution of vascular resistance with respect to vascular compliance. Occlusion data were obtained from isolated dog lung lobes under normal control conditions, during hypoxia, and during histamine or serotonin infusion. The data used in the analysis include the slope of the arterial pressure curve and the zero time intercept of the extrapolated venous pressure curve after venous occlusion, the equilibrium pressure after simultaneous occlusion of both the arterial inflow and venous outflow, and the area bounded by equilibrium pressure and the arterial pressure curve after arterial occlusion. We analyzed these data by use of a compartmental model in which the vascular bed is represented by three parallel compliances separated by two series resistances, and each of the three compliances and the two resistances can be identified. To interpret the model parameters, we view the large arteries and veins as mainly compliance vessels and the small arteries and veins as mainly resistance vessels. The capillary bed is viewed as having a high compliance, and any capillary resistance is included in the two series resistances. With this view in mind, the results are consistent with the major response to serotonin infusion being constriction of large and small arteries (a decrease in arterial compliance and an increase in arterial resistance), the major response to histamine infusion being constriction of small and large veins (an increase in venous resistance and a decrease in venous compliance), and the major response to hypoxia being constriction of the small arteries (an increase in arterial resistance). The results suggest that this approach may have utility for evaluation of the sites of action of pulmonary vasomotor stimuli.     

Spare alpha adrenoceptors in the peripheral circulation: excitation-contraction coupling

Postsynaptic alpha adrenoceptors in arteries and veins represent a mixed population of alpha 1 and alpha 2 adrenoceptors, with both subtypes mediating vasoconstriction. In the peripheral arterial circulation, postsynaptic vascular alpha 1 adrenoceptors are found in the adrenergic neuroeffector junction, whereas postsynaptic vascular alpha 2 adrenoceptors are located extrajunctionally. In the venous circulation, it appears that alpha 2 adrenoceptors may be predominantly junctional, whereas alpha 1 adrenoceptors may be predominantly extrajunctional. In general, alpha 1 adrenoceptors play a more important functional role in arteries than in veins, with the converse being true for postsynaptic vascular alpha 2 adrenoceptors. The relationship between alpha-adrenoceptor occupancy and vasoconstrictor response is more favorable for postsynaptic vascular alpha 1 adrenoceptors than for alpha 2 adrenoceptors in both arteries and veins, and there is evidence for a receptor reserve in alpha 1 adrenoceptors in both the arterial and venous circulation. No reserve in postsynaptic vascular alpha 2 adrenoceptors is seen in the arterial circulation, but in isolated venous preparations, a reserve in alpha 2 adrenoceptors has been observed. It has been suggested that spare alpha 2 adrenoceptors found in veins, but not arteries, may be responsible, at least in part, for the exaggerated alpha 2-adrenoceptor-mediated response of veins relative to arteries.     

Systemic hemodynamics affecting cardiac output during hypocapnic and hypercapnic hypoxia

Systemic hemodynamic adjustments involved in the control of cardiac output (CO) were examined in chronically instrumented unanesthetized sheep inhaling gas mixtures resulting in hypocapnic hypoxia (H) [arterial pH (pHa) = 7.53, arterial partial pressure of O2 (Pao2) = 30 Torr, arterial partial pressure of CO2 (Paco2) = 29 Torr] or hypercapnic hypoxia (HCH) (pHa = 7.14, Pao2 = 34 Torr, Paco2 = 72 Torr) for 1 h. H (n = 7) and HCH (n = 6) resulted in 26% and 61% increases in CO, respectively, and mean systemic arterial pressure rose to a greater extent during HCH. Both H and HCH resulted in increased blood flow (microsphere method) to the peripheral systemic circulation including the brain, heart, diaphragm, and nonrespiratory skeletal muscle (the latter blood flow increased 120% during H and 380% during HCH). Gastrointestinal and renal blood flow remained unchanged during H and HCH. Transit time of green dye from the pulmonary artery to regional veins in the hindlimb and intestine was 5.0 and 8.2 s, respectively, during base-line conditions and remained unchanged with HCH. During HCH, regional O2 consumption increased 274% for the hindlimb and decreased 39% for the intestine. Total catecholamines rose 250% during H and 3,700% during HCH. During hypocapnic and hypercapnic hypoxia, CO is augmented in part by systemic hemodynamic adjustments that include a redistribution of blood flow and a translocation of blood volume to the fast transit time peripheral systemic circuit. The sympathetic nervous system may play an important role in mediating these systemic hemodynamic adjustments.     

Vascular effects, formation, clearance and release of endothelin peptides in the pig

The formation, release, clearance and vascular effects of endothelin (ET)-like immunoreactivity (-LI) was studied in the pig in vivo. Intravenous infusion of ET-1, 2 and 3 (20 pmol/kg/min for 20 min) increased vascular resistance in the kidney, spleen and skeletal muscle. The most pronounced effects were evoked by ET-1 which caused increases in renal, splenic and skeletal muscle vascular resistance of 554, 528 and 38%, respectively, and a threshold response was observed at 80 pmol/l ET-LI in arterial plasma. During the infusion a large portion of arterial plasma, ET-LI was cleared over the kidney, spleen and skeletal muscle, whereby the most pronounced clearance was observed for ET-1 (73–93%). The ET-1 precursor Big-ET (1–39) given in a similar dose produced only a slight increase in renal vascular resistance (by 20%) and was cleared only over the kidney and not over the spleen or skeletal muscle. Using an ET-1 specific antiserum it was found that plasma ET-1 levels increased 11-fold during the infusion of Big-ET, indicating formation of ET-1 from Big-ET. The half-lives of circulating ET-1, 2 and 3 were 1.3–2.1 min and of Big-ET 8.9 min. Induction of asphyxia for 2 min increased the overflow of ET-LI from the spleen, suggesting local release, and caused splenic vasoconstriction. During i.v. administration of endotoxin for 4 h, arterial plasma ET-LI increased 7-fold and renal and splenic vasoconstrictor responses developed that correlated significantly with the arterial plasma ET-LI. Furthermore, a local release of ET-LI in the spleen was observed during endotoxin administration. Chromatographic characterization of the ET-LI in plasma during endotoxin administration revealed presence of ET-1 and Big-ET. It is concluded that there exists specificity both concerning the vasoconstrictor effects and removal from the circulation of ET peptides, both mechanisms being most prominent for ET-1 in the kidney. Furthermore ET-1 seems to be formed from circulating Big-ET and release of ET-LI can be detected during situations like asphyxia and sepsis.     

Free transplantation of venous network pattern skin flap

We report a patient treated by transplantation of a venous network pattern skin flap containing two superficial cutaneous veins. Through one of the veins, arterial blood passed into the capillaries, restoring circulation and ensuring survival of the flap.     

Selective type 5 phosphodiesterase inhibition alters pulmonary hemodynamics and lung liquid production in near-term fetal lambs.

Nitric oxide causes dilation of the pulmonary circulation and reduction in net lung liquid production in the fetal lamb, two critical perinatal events. Phosphodiesterase inhibition alone causes similar changes and also enhances the effects of nitric oxide. To better define the cyclic guanosine 5'-monophosphate (GMP) pathway in these events, we studied the effects of a specific phosphodiesterase inhibitor, E4021, on pulmonary arteries and veins isolated from near-term fetal lambs, as well as in intact, chronically instrumented late-gestation fetal lambs. In the in vitro experiments, both pulmonary arteries and veins relaxed to E4021 in a dose-dependent manner, although pulmonary veins were significantly more sensitive to E4021. Pretreatment with N(G)-nitro-l-arginine (L-NNA) abolished this response in arteries but not in veins. In both arteries and veins, pretreatment with beta-phenyl-1,N2-etheno-8-bromoguanosine-3',5'-cyclic monophosphorothionate blunted relaxations to E4021. In the in vivo experiments, E4021 infusion into either the pulmonary artery or central venous circulation increased pulmonary blood flow and decreased pulmonary vascular resistance, and these responses were blunted by pretreatment with L-NNA. Net lung liquid production, measured by a dye-dilution technique using blue dextran, decreased when E4021 was infused directly into the pulmonary artery and this effect was not altered by L-NNA. There was no effect on lung liquid production when E4021 was infused into the central venous circulation. Taken together, these results suggest that the pulmonary hemodynamic effects of E4021 involve the cyclic GMP pathway and are primarily nitric oxide synthase dependent. In contrast, the effects on E4021 on net lung liquid production appear to be independent of nitric oxide synthase, suggesting that these two critical perinatal events might be modulated independently.