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PubMed1980

Development of adrenergic innervation in rat peripheral vessels: a fluorescence microscopic study.

The postnatal development of adrenergic innervation was followed in peripheral blood vessels of Wistar rats. The femoral vessels and their branches, the superficial epigastric and saphenous vessels, and the tail artery, were investigated from birth to maturity. The proximal ends of the vessels were studied with fluorescence microscopy after the catecholamine was converted to a fluorophore by hot formaldehyde vapour, and ultrastructural morphology confirmed that the nerve varicosities mainly contained small vesicles with dense cores, typical of adrenergic innervation. Further confirmation was obtained with reserpine pre-pretreatment, the sodium borohydride specificity test, and experiments to alter the non-specific fluorescence of elastin. The nerves in the arteries were immediately adjacent to the external elastic lamina, and they retained this position throughout postnatal development. Of the three muscular arteries, the development of innervation was earlier and more intense in the saphenous and superficial epigastric arteries than in the tail artery. However, the tail artery surpassed the other two both in the total number of nerves and in the density of innervation per unit area beyond 12 days of age, and maintained this lead to maturity. The superficial epigastric artery had the smallest total number of nerves but had a greater density of innervation than the saphenous. The femoral artery did not develop any appreciable innervation. The femoral vein demonstrated the greatest amount of fluorescence of any of the veins, the others having considerably less innervation than their companion arteries.

Aging↗

PubMed1990

[Immunohistochemical localization of the chondroitin sulfate proteoglycan in demineralized rat periodontal tissue].

We investigated the immunohistochemical localization of the chondroitin sulfates (chondroitin-4 sulfate, -6 sulfate and dermatan sulfate) in demineralized rat periodontal tissue using monoclonal antibodies (2-B-6, 3-B-3). Also, fixative and demineralized methods were established using these monoclonal antibodies. The result showed that the most effective combination of fixative and demineralized methods was 2% glutaraldehyde 1% para-formaldehyde and 5% EDTA. Chondroitin-4 sulfate and dermatan sulfate were widespread in gingival connective tissue and periodontal membrane, with an especially strong response of dermatan sulfate shown along collagen fiber bundles. Chondroitin-6 sulfate was located in peripheral blood vessels. In alveolar bone, chondroitin-4 sulfate and dermatan sulfate were found inside Hareversion canals, Volkman's canals and lacunae. Chondroitin-6 sulfate was localized at peripheral blood in alveolar bone. In cementum, chondroitin-4 sulfate and dermatan sulfate were found at lacunae of cellular cementum and a part of embedding Sharpey's fiber.

Animals↗

PubMed2000

Inhibitory effects of glibenclamide on the contraction of human arterial conduits used in coronary artery bypass surgery.

Glibenclamide has been shown to inhibit prostanoid-induced contraction in a number of blood vessel types. In this study, the effects of glibenclamide on the contraction of human peripheral arteries in response to both prostanoid and non-prostanoid agonists were compared and possible mechanisms of action were investigated. Segments of left internal mammary artery (LIMA) and radial artery, taken from patients undergoing coronary artery bypass graft (CABG) surgery, were mounted in organ baths containing physiological saline solution aerated with 95% O2/5% CO2 at 37 degrees C. Contractions were obtained by either the use of a thromboxane analogue (U46619), L-phenylephrine, KCl or CaCl2. The effects of glibenclamide on these contractions were observed and pEC50 values were determined after manipulation of a logistic curve-fitting equation. Concentration-dependent relaxation of U46619-contracted LIMA and radial artery was observed in the presence of glibenclamide, with calculated pEC50 values of 4.2+/-0.17 (n = 7) for LIMA and 3.26+/-0.48 (n = 5) for radial artery. Incubation of both LIMA and radial artery with glibenclamide (50 microM) caused the concentration-response curves for U46619 and L-phenylephrine to shift significantly to the right. Similarly the KCl tension relationship was caused to shift to the right. Finally, glibenclamide (100 microM) also had an inhibitory effect on Ca2+-induced tension in radial artery. These results show that the inhibitory effects of glibenclamide on human peripheral blood vessels are not restricted to prostanoid-induced contractions. Furthermore, evidence has been provided to suggest that these effects might be mediated through an interaction with voltage-sensitive Ca2+ channels.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1980

Another look at the Sparks-Mandril arterial graft precursor for vascular repair. - Pathology by scanning electron microscopy.

The Sparks-Mandril blood vessel precursor system, an autogenous tissue growth-promoting device, in spite of its ingenuity and its surgical elegance, has received only limited usage. At technique for peripheral blood vessels by several authors. In the latter period, this laboratory also undertook similar work. The results of seven implantations in dogs and two in patients are reported here in the context of a program on the evaluation of blood vessel substitutes, their mode of operation and their long term performance. The clinical status and the pathology of the grafts at time of failure were investigated using techniques of scanning electron microscopy. This work confirms the findings of other centres regarding the generally unsatisfactory performance of the Sparks-Mandril system. Possible causes for failure in mandril-formed blood vessels are discussed.

Adult↗

PubMed1978

[Experience in the treatment of peripheral vascular injuries].

The authors report the results of the treatment of injuries to the peripheral blood vessels that were observed at the Semmelweis OTE in 16 years. As a result of primary operative treatment the peripheral pulse returned to the injured limb in 10 cases. A quick diagnosis and instant reconstructive surgery is absolutely necessary. Mistakes and complications in the treatment are listed in this paper, based on the own experiences of the authors. The authors stress that these complications should be recognized in time and be treated properly.

Arm↗

PubMed1975

Pharmacological effects of alpha-methyldopa, alpha-methylnorepinephrine, and octopamine on rat arteriolar, arterial, and terminal vascular smooth.

Experiments on rat mesenteric arterioles, metarterioles, and aortae demonstrate that although alpha-methylnorepinephrine is much less potent in inducing contraction than epinephrine on all three blood vessel types, it is either equivalent or only one and a half to two times less potent than the natural postganglionic neurotransmitter, norepinephrine, on these blood vessels. Furthermore, alpha-methylnorepinephrine is equivalent to norepinephrine in its ability to induce maximal contractile responses on rat arterioles, metarterioles, and aortae. Systemic administration of alpha-methyldopa to rats for 15 days shifted the log dose-response curves for all three catecholamines, but not vasopressin or potassium chloride, to the right of all three blood vessel types; the maximal contractile responses to these amines were, however, not affected by chronic treatment with alpha-methyldopa. In addition, acute, intra-arterial administration of 500 mg/kg of alpha-methyldopa was found not only to induce mesenteric arteriolar vasodilatation gradually but also to depress arteriolar reponsiveness to catecholamines. In view of these direct findings, it is difficult to accept the hypothesis that alpha-methyldopa induces hypotension via formation of a "false" postganglionic neurotransmitter substance, namely, alpha-methylnorepinephrine. The present findings suggest that alpha-methyldopa may exert some of its anti-hypertensive action, at least in the rat, by (1) depressing arteriolar responsiveness to circulating and released catecholamines and (2) some unknown direct action on peripheral vascular muscle. In addition, the present study indicates that octopamine is (1) between 60 and 15,000 times less potent than norepinephrine on rat arterioles and metarterioles and (2) incapable of eliciting more than a 40% occlusion of these terminal vessels. It is suggested that such data support the concept that octopamine, in contrast to alpha-methylnorepinephrine, could serve as a false adrenergic neurotransmitter agent and thus account for part or all of the hypotensive action of monoamine oxidase inhibitors like pargyline. The use of complete dose-response curves, several different adrenergic compounds (i.e., epinephrine, norepinephrine, alpha-methylnorepinephrine, octopamine, phenylephrine, and dopamine), and different rat blood vessels supports the concept that adrenergic molecules containing a catecholamine nucleus and a beta-hydroxyl group elicit the most potent constrictor responses from peripheral blood vessels. In addition, the data suggest that the structure-activity relationships for catecholamines and their analogs on terminal vascular smooth muscle are probably different from those for arterial smooth muscle.

Administration, Topical↗

PubMed1978

Monoamine oxidase activity in tissues of spontaneously hypertensive rats.

Monoamine oxidase (MAO) activity was assayed both in central and peripheral blood vessels of spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar Kyoto rats (WKR). The activity of MAO in the brain and peripheral vasculature was essentially the same in both SHR and WKR. It can therefore be concluded that central and peripheral vascular MAO activity is not altered in the genetically hypertensive animals.

Animals↗

PubMed1987

[Peripheral vascular leiomyosarcomas. Apropos of 2 cases].

The authors report here two observations of leiomyosarcomas arising from peripheral blood vessels. The first case occurred in the pedious vein and infiltrated into tarsal bones. The second case was localized into leg muscles' tendons, near the knee. The topographical and histological characteristics of peripheral vascular leiomyosarcomas are noted, and compared, according to the review of literature, with those of the great central blood vessels, and of other classical leiomyosarcomas.

Foot↗

PubMedDate not supplied

Pentoxifylline inhibits perforin-dependent natural cytotoxicity in vitro.

Pentoxifylline (PTX) is commonly used in peripheral blood vessel diseases, however it has also been found to decrease the level of proinflammatory cytokines such as IL-12, TNF-alpha and IFN-gamma. Moreover, some authors reported that PTX suppresses spontaneous cytotoxicity of peripheral blood mononuclear cells (PBMC) in vitro. It could influence the mechanism of killing target cells by PBMC. For this reason we evaluated the influence of PTX on spontaneous cytotoxicity of PBMC against K562 and CaSki cell lines. Subsequently, we compared this effect to that evoked by dexamethasone, one of the most effective anti-inflammatory drugs. Our study revealed that PTX inhibits natural cytotoxicity preferentially through inhibition of perforin-mediated cell membrane damage, without a statistically significant influence on apoptosis induction. Furthermore, pentoxifylline inhibits natural cytotoxicity as effectively as dexamethasone. However, the result of PTX inhibitory influence is observed much earlier than that of dexamethasone. Currently PTX is commonly used in diseases that occur more frequently in elderly patients. We suggest that PTX, inhibiting perforin-dependent PBMC cytotoxic activity, could weaken anti-cancer action of immune system thus accelerating the progress of neoplasm formation in these patients.

Anti-Inflammatory Agents↗

PubMed1984

Actions of vasopressin, oxytocin, and synthetic analogs on vascular smooth muscle.

A variety of physiological, pharmacological, and experimental factors are needed to explain why different authors have recorded often confusing and contradictory results of studying blood pressure and blood flow with vasopressin, oxytocin, and their analogs. Vasopressin and a number of synthetic analogs can produce potent constriction of numerous regional arteries and arterioles (e.g., splanchnic, renal, skeletal muscle, carotid, hepatic) in near physiological (i.e., 10(-12) - 10(-10)M) concentrations. Oxytocin appears to be able to elicit much weaker constriction (threshold = 10(-7) - 10(-5)M) and can produce relaxation (i.e., vasodilatation) in the presence of high degrees of tone in skeletal muscle, hepatic, renal, and splanchnic vasculatures; this may account for its blood pressure-lowering actions. With respect to the cerebral, coronary, and pulmonary vasculatures, there appears to be no good direct evidence indicating that either vasopressin or oxytocin can elicit much in the way of constrictor actions. Oxytocin, in contrast to vasopressin, is a potent constrictor of the umbilical-placental vasculature in concentrations found at term pregnancy and during parturition. Blood vessels from animals genetically lacking vasopressin appear to be supersensitive to the contractile actions of neurohypophyseal hormones. The contractile potencies and structure-activity relationships of neurohypophyseal peptides appears to vary with the type of blood vessel; i.v. rat pressor assays do not reflect the latter and cannot be utilized to determine structure-activity relationships of these peptides on vascular smooth muscle. Either a heterogeneity of the vasopressin receptor exists in peripheral blood vessels or there are vasopressin receptor subtypes on vascular muscles. Oxytocin analogs can be designed that are extremely potent splanchnic vasoconstrictors. Further insight into these areas should provide basic information on the role of these peptides in circulatory homeostasis.

Animals↗

PubMed1982

Cerebrovascular effects of the calcium antagonistic dihydropyridine derivative nimodipine in animal experiments.

Isopropyl(2-methoxy-ethyl) 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate (Bay e 9736, nimodipine) is a calcium antagonistic dihydropyridine derivative with a preferential effect on cerebral vessels. It dilates cerebral vessels in several species after intraarterial, intravenous, perlingual, and oral administration in low dosage. Its effect on the peripheral blood vessels is less pronounced so that nimodipine increases cerebral blood flow without substantial decrease of blood pressure. Nimodipine does not inhibit carbonic anhydrase and does not stimulate the oxygen consumption of brain tissue in vitro. Its effect is not influenced by propranolol. Therefore its cerebral vasodilating effect is due to its direct relaxing effect on vascular smooth muscle. Nimodipine prevents the postischaemic impaired cerebral reperfusion in cats. Transient global cerebral ischaemia increases the cerebrovascular resistance to flow by means of the increase in extracellular concentration of potassium ions. Such depolarization produces sustained cerebral vasoconstriction presumably by enhancing transmembrane influx of calcium. Nimodipine does not influence the ischaemic increase in Ko+ ions but effectively prevents the postischaemic cerebrovascular spasm. From its pharmacological properties nimodipine is predicted to be effective in the prevention and therapy of cerebrovascular spasm of various origins and especially in the treatment of postischaemic brain damage.

Administration, Oral↗

PubMed2005

Activin induces tactile allodynia and increases calcitonin gene-related peptide after peripheral inflammation.

Calcitonin gene-related peptide (CGRP) is a sensory neuropeptide important in inflammatory pain that conveys pain information centrally and dilates blood vessels peripherally. Previous studies indicate that activin A increases CGRP-immunoreactive (IR) sensory neurons in vitro, and following wound, activin A protein increases in the skin and more neurons have detectable CGRP expression in the innervating dorsal root ganglion (DRG). These data suggest some adult sensory neurons respond to activin A or other target-derived factors with increased neuropeptide expression. This study was undertaken to test whether activin contributes to inflammatory pain and increased CGRP and to learn which neurons retained plasticity. After adjuvant-induced inflammation, activin mRNA, but not NGF or glial cell line-derived neurotrophic factor, increased in the skin. To examine which DRG neurons increased CGRP immunoreactivity, retrograde tracer-labeled cutaneous neurons were characterized after inflammation. The proportion and size of tracer-labeled DRG neurons with detectable CGRP increased after inflammation. One-third of CGRP-IR neurons that appear after inflammation also had isolectin B4 binding, suggesting that some mechanoreceptors became CGRP-IR. In contrast, the increased proportion of CGRP-IR neurons did not appear to come from RT97-IR neurons. To learn whether central projections were altered after inflammation, CGRP immunoreactivity in the protein kinase Cgamma-IR lamina IIi was quantified and found to increase. Injection of activin A protein alone caused robust tactile allodynia and increased CGRP in the DRG. Together, these data support the hypothesis that inflammation and skin changes involving activin A cause some sensory neurons to increase CGRP expression and pain responses.

Activins↗

PubMed1989

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.

Animals↗

PubMed1982

Microvascular and vascular smooth muscle actions of ethanol, acetaldehyde, and acetate.

Data are reviewed that suggest that the peripheral vasodilation and hypotension that often result from ingestion (or administration) of ethanol may, in large part, be a consequence of its direct actions on vascular smooth muscle cells, at both the macro- and microcirculatory levels. At lest two mechanisms appear to contribute to this vasodilator effect: 1) inhibition of the normal rhythm or vasomotion (spontaneous mechanical activity) of vascular smooth muscle; and 2) depression of the contractile responses to endogenous neurohumoral substances that play a role in maintaining vascular tone and regulation of blood flow. The information acquired so far suggests that these dilator actions are related causally to interference with movement and/or translocation of Ca2+ across the vascular membranes. Although acetaldehyde and acetate can evoke some actions on isolated blood vessels that somewhat resemble the actions of ethanol, in situ studies on the splanchnic microcirculation reveal that neither acetaldehyde nor acetate can mimic the dilator actions of ethanol on the microvessels. Evidence is also reviewed that indicates that certain concentrations of ethanol, acting on certain peripheral blood vessels (e.g., cerebral and coronary arteries), can induce direct contractile responses (dose-dependent) and potentiate certain hormones, the effects of which are dependent on free, ionized Ca2+ ions. Lastly, data are reviewed in experimental animals, maintained on liquid diets of ethanol, which may provide insights into why a high incidence of hypertensive vascular disease has been noted in alcoholics.

Acetaldehyde↗

PubMed2000

Effects of menstrual cycle and race on peripheral vascular alpha-adrenergic responsiveness.

Gender differences in the incidence of many cardiovascular diseases may be due to the effects of sex hormones. Both alpha(1)- and alpha(2)-adrenergic receptors produce vasoconstriction in peripheral blood vessels and have demonstrated gender effects in previous studies. In addition, race has been shown to influence the effects of some alpha-adrenergic stimuli. We therefore sought to determine the effects of the menstrual cycle and race on peripheral blood flow responses to the intra-arterial infusion of phenylephrine (alpha(1)-agonist) and clonidine (alpha(2)-agonist). Ten white and 8 black women were studied during the early luteal phase and the follicular phase; these phases were verified in each woman through measurements of plasma estradiol and progesterone. Plasma norepinephrine was measured with HPLC. During phenylephrine infusion, there was significantly greater vasoconstriction in the luteal phase versus the follicular phase (P<0.05). There were no differences (P>0.8) between white and black women. During clonidine infusion, white women showed significantly more vasoconstriction in the follicular phase than during the luteal phase (P<0.006). For black women, the responses for both phases did not differ (P>0.9). Blood pressures were significantly higher in the black women (diastolic P<0.005, systolic P<0.05). The luteal-phase elevation of alpha(1)-adrenergic responses may be due to elevated levels of estradiol, progesterone, or both. The lack of luteal-phase reduction in alpha(2)-adrenergic vasoconstriction in black women may contribute to their increased pressor responses to adrenergic stimuli.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Peripheral vascular actions of ethanol and its interaction with neurohumoral substances.

Data are reviewed which suggest that the peripheral vasodilatation and hypotension which result from ingestion (or administration) of ethanol may, in large part, be a consequence of its direct actions on vascular smooth muscle cells, both at the macro- and microcirculatory levels. At least two mechanisms appear to contribute to this vasodilator effect: (1) inhibition of the normal rhythm or vasomotion (spontaneous mechanical activity) of vascular smooth muscle; and (2) depression of the contractile responses to endogenous neurohumoral substances that play a role in maintaining vascular tone and regulation of blood flow. In addition, data is presented to indicate that human umbilical blood vessels are extremely sensitive to the vasospasmic actions of ethanol. The data acquired so far suggest that the dilator actions are related causally to interference with movement and/or translocation of Ca2+ across the vascular membranes. In addition, these actions appear to resemble the peripheral vascular effects of general anesthetics. Evidence is also reviewed which indicates that certain concentrations of ethanol, acting on specific peripheral blood vessels (e.g., cerebral arteries), can induce direct contractile responses (dose-dependent), and potentiate certain hormones, the effects of which are dependent upon free, ionized Ca2+ ions. None of these actions nor the vasodilator actions can be attenuated, prevented or mimicked by any known pharmacologic antagonist. Lastly, this chapter cites recent findings, in experimental animals, maintained on liquid diets of ethanol, which may provide insights into why a high incidence of hypertensive vascular disease has been noted in alcoholics.

Acetaldehyde↗

PubMed1991

Endothelium-dependent contractions.

The endothelial cells help to control the tone of the underlying vascular smooth muscle by releasing vasoactive factors. In physiological circumstances, the release of relaxing factors (nitric oxide and endothelium-derived hyperpolarizing factor) appears to predominate. However, in certain blood vessels (peripheral veins and large cerebral arteries), the normal endothelium has the propensity to release vasoconstrictor substances, among which are superoxide anion and thromboxane A2; the release of these endothelium-derived vasoconstrictors may contribute to the autoregulatory processes. In most blood vessels, anoxic conditions initiate the release of an unidentified endothelium-dependent contracting factor. Cultured endothelial cells, and blood vessels maintained under culture conditions for prolonged periods of time, release the vasoconstrictor peptide endothelin. A characteristic of vascular diseases is that the ability of the endothelial cells to release relaxing factor(s) is reduced, while the generation of contracting factor is maintained or enhanced.

Animals↗

PubMed2001

Function and clinical significance of platelet-derived microparticles.

Microparticles released from platelets (PMPs) may play a role in the normal hemostatic response to vascular injury because they demonstrate prothrombinase activity. PMPs were first observed as released vesicles from platelets following adhesion to vessel walls, and flow cytometry is now the most widely used method for studying PMPs. PMPs are thought to play a role in clinical disease because they express phospholipids that function as procoagulants. High shear stress can initiate both platelet aggregation and shedding of procoagulant-containing PMP, suggesting that PMP generation by high shear stress occurs in small diseased arteries and arterioles under various clinical conditions. In addition, the possibility that PMPs evoke cellular responses in their immediate microenvironments has recently been suggested. Despite many interesting findings, the significance of PMPs in various clinical conditions remains controversial. For example, it is not known whether PMPs found in peripheral blood vessels cause thrombosis, or if they are the results of thrombosis. There has been some question about whether the PMPs found in thromboses are consumed locally, meaning that PMPs circulating in the peripheral blood are not functionally important. Currently, the number of clinical disorders associated with elevated PMPs is increasing.

Animals↗