SEARCH · PubMed Health

Results for “BLOOD VESSELS, PERIPHERAL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

PubMed1983

Spectral analysis of Doppler ultrasonic flow signals by a personal computer.

This paper describes a method of performing spectral analysis on Doppler acoustical signals from peripheral blood vessels with the use of an Apple II plus personal computer. Digitization is accomplished with a commercially available analog-to-digital converter. The data are transformed with a fast Fourier technique, and the resultant information is plotted by an inexpensive X-Y plotter and/or on a television receiver.

Blood Vessels↗

PubMed1990

Amitriptyline-induced morphological alterations of the rat blood-brain barrier.

Amitriptyline is known to increase the permeability of the blood-brain barrier but the morphological basis of this increase has not been studied. As catecholamines can influence pinocytosis in dog peripheral blood vessels, the effect of amitriptyline on the pinocytotic activity of blood brain microvessels was studied. Amitriptyline, 34 mg.kg-1 i.p., was injected to rats and the parietal cortex of control and treated animals was prepared for ultrastructural study. Pinocytotic vesicles in endothelial cells were quantified. Amitriptyline significantly increased the density of pinocytotic vesicles in capillary endothelial cells. No other morphological changes occurred after amitriptyline treatment. We conclude that the increase in blood-brain barrier permeability due to amitriptyline may be ascribed at least in part to an increase of pinocytotic activity in brain capillary endothelial cells.

Amitriptyline↗

PubMed1984

Serotonin-S2 receptor binding sites and functional correlates.

Serotonin-S2 receptor binding sites have been labelled with several ligands such as [3H]spiperone, [3H]lysergic acid diethylamide (LSD), [3H]mianserin and [3H]ketanserin, the latter being the most selective ligand. The greatest concentration of the sites occurs in frontal cortical tissue, but they were also detected in striatum, nucleus accumbens and tuberculum olfactorium as well as on membranes of cat and human platelets. The serotonin-S2 sites, labelled with different ligands in different tissues, revealed similar binding properties for drugs, but careful definition of specific binding is necessary because of marked variation in the non-specific binding of drugs in different tissues. Serotonin-S2 sites were demonstrated to have a role in serotonin-induced behavioural excitation in rodents and they probably mediate perception of subjective feelings elicited by serotonin mimetics. In vivo studies revealed involvement of the serotonin-S2 sites in impairment of microcirculation by serotonin and in inflammation provoked by serotonin. On isolated tissues, serotonin-S2 sites mediate serotonin-induced vasoconstriction in peripheral blood vessels (e.g. superficial, coronary, splanchnic vessels) and cerebral blood vessels from various species including man. Serotonin-S2 sites also have a role in serotonin-induced contractions in tracheal smooth muscle and serotonin-induced bronchoconstriction in vivo, but the sites are unrelated to "M"- and "D"-serotonin receptor subtypes, which have been functionally characterized in gastrointestinal smooth muscle. Platelets proved to be an integral model for studying serotonin-S2 sites. Binding, measured on platelet membranes, was shown to be directly related to serotonin-induced platelet aggregation or changes in shape.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

The role of phosphodiesterase inhibitors in heart failure.

Myocardial contractility is dependent on available intracellular calcium and this can be enhanced by increasing intracellular cyclic adenosine monophosphate. One way of achieving this is by inhibiting the phosphodiesterase III enzyme. Over the last 15 years, a number of new drugs with this mechanism of action have been studied in man and have been found not only to have a positive inotropic action on the heart but also a vasodilating action on peripheral blood vessels. This combination of effects produces favourable haemodynamic improvement in patients with chronic heart failure. While some smaller studies showed that this did translate into an improvement in symptoms and functional capacity, a large well-designed and controlled clinical trial showed that survival was decreased when milrinone was used in target daily doses of 40 mg. For this reason, chronic long-term oral therapy with phosphodiesterase III inhibitors is not currently being actively pursued. They may still have a role as acute short-term therapy in severely ill patients who do not respond adequately to optimal standard drug therapy. Milrinone has been one of the most widely studied drugs in this regard. Even during short-term administration, its use should be closely monitored for any evidence of an increase in ventricular arrhythmias or decrease in ventricular function.

Animals↗

PubMed1993

The development of positive inotropic agents for chronic heart failure: how have we gone astray?

Because cardiac contractility is impaired in chronic heart failure, many pharmacologic agents have been developed to increase the contractile state of the failing heart. These drugs produce impressive hemodynamic effects, but long-term therapy has failed to produce clinical benefits and has increased mortality in treated patients. This experience has led many physicians to suggest that positive inotropic therapy be abandoned as a therapeutic approach for heart failure. However, recent studies suggest that the efficacy and safety of many (if not all) positive inotropic drugs can be greatly enhanced by reducing the dose of these drugs. The importance of dose is dramatically illustrated by the results of trials with vesnarinone, which decreases mortality when used in low doses but increases mortality when administered in doses only twice as large. Although low doses of positive inotropic drugs may be clinically superior to high doses, it is not clear that these low doses exert significant inotropic effects. All positive inotropic drugs exert actions on the circulation in addition to stimulating the heart, and these ancillary properties may be particularly important at low doses of these drugs. Low doses of milrinone and pimobendan may act primarily to dilate peripheral blood vessels; low doses of digitalis may exert only neurohormonal effects, and low doses of vesnarinone may act as an antiarrhythmic agent. If the noninotropic actions of low doses account for the therapeutic benefits of these drugs, then the positive inotropic effects seen at high doses may be primarily responsible for their adverse effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiotonic Agents↗

PubMedDate not supplied

Continuous monitoring of brain ethanol levels by intracerebral microdialysis.

A method is described which allows simultaneous collection of blood and perfusate of discrete brain regions from an individual animal over several hours. This procedure involves catheterization of a peripheral blood vessel (jugular vein) and the insertion of a microdialysis probe into a specified brain area (lateral hypothalamus) for sampling of blood and brain perfusate, respectively. Using this procedure, levels of ethanol in blood and brain perfusates were determined by scintillation counting following administration of [14C]-ethanol (20 mu Ci) to adult male rats at a dose of 0.8 or 2.4 g/kg. Ethanol levels in brain and blood as well as the time-course of disappearance were dependent on the dose administered. Peak blood levels were observed in the first sample taken (i.e., at 10 min), whereas a slight delay was noted in the time to peak level in brain. At subsequent time points, a good correlation was observed between blood and brain perfusate radioactivity levels although perfusate levels were slightly lower. It is concluded that this approach will prove useful for investigating the molecular and cellular mechanisms of action of ethanol by enabling the direct correlation of blood and brain ethanol levels with various behavioral, electrophysiological and/or biochemical measures.

Animals↗

PubMedDate not supplied

Endothelium-dependent relaxation in peripheral vasculature and kidney of non-insulin-dependent diabetes mellitus.

Desmopressin (DDAVP), an AVP.V2-receptor agonist, evokes endothelium-dependent relaxation (EDR) due to nitric oxide (NO), EDR factor (EDRF) in the systemic vasculature, and glomerular afferent arterioles via AVP receptor(s). Glyceryl trinitrate (GTN) causes endothelium-independent (nonreceptor-mediated) vasodilation. We elucidated the possible involvement of EDRF in early non-insulin-dependent diabetes mellitus (NIDDM) and glomerular hyperfiltration (GHF) by DDAVP and GTN infusions. Patients with advanced DM nephropathy (DM.Np) (n = 7) were also examined. DDAVP and GTN decreased the mean blood pressure in DM with GHF (DM + GHF) and without GHF (DM-GHF) greater than that in normal subjects (N), without any difference in the heart rate changes in any group. Plasma levels of cGMP, a cellular messenger of NO, were significantly increased by DDAVP and GTN with a similar increment in each group. DDAVP caused a significant increase in urinary cGMP excretion in each group with a similar increment in each group. However, it caused a transient increase in creatinine clearance only in DM + GHF although GTN did not, and an exaggerated excretion of urinary albumin in early NIDDM, especially in DM+GHF, without a change in beta 2-microglobulin excretion. In contrast, in DM.Np GTN caused a decrease in blood pressure and an increase in plasma cGMP levels, but DDAVP did not. In conclusion, in peripheral vasculature and kidney, an enhanced sensitivity of vascular smooth muscle to NO is present in early NIDDM. The exaggerated dilation of glomerular afferent arterioles by preferentially produced NO in in situ, which causes a rise in PGC, might be partly responsible for the glomerular hyperfiltration and subsequently the increase in the glomerular protein permeation of DM+GHF. However, in peripheral blood vessels of DM.Np EDR is impaired. Thus, EDR seems to change with the development of NIDDM.

Adult↗

PubMed2005

Divergent effects of zinc depletion in brain vs non-brain endothelial cells.

Dietary zinc deficiency is common in developing as well as developed countries. Endothelial cells (EC) lining the inner surface of peripheral blood vessels are sensitive to zinc deficiency and lose structural integrity when exposed to culture media low in zinc or to zinc chelators. In contrast, we demonstrate here that human brain microvascular EC (HBMEC), which constitute the blood-brain barrier (BBB), resist zinc depletion and respond by enhancing their barrier function. This response was specific for HBMEC and did not occur in non-brain EC, such as human umbilical vein endothelial cells, human aortic endothelial cells, and human iliac vein endothelial cells. Our results suggest the presence of specific mechanisms to counteract zinc deficiency at the BBB, likely involving HBMEC junctional complexes. Understanding the mechanisms involved in this unique response might provide means to modulate the BBB dysfunction associated with neurological disorders such as stroke, multiple sclerosis, and Alzheimer's disease.

Aorta↗

PubMed2005

Risk factors of sudden death in the Japanese hot bath in the senior population.

A series of experiments were carried out to clarify the cause of death and the risk factors related to sudden death in the Japanese senior population while bathing in a Japanese style "hot bath." The biodynamic changes while bathing were carefully monitored under actual bathing situations occurring in both the winter and summer seasons. We observed double product (DP), total peripheral blood vessel resistance (TPR), cardiac output (CO), and blood vessel compliance (COMP) by measuring blood pressure, heart rate, pulse wave, and electrocardiogram (ECG). The finding of a high level of DP in the elderly suggests that more myocardial oxygen consumption is needed than for young adults, particularly in subjects with arrhythmia. Although the values for TPR and CO changed somewhat during bathing, the changes were considered normal and to be expected. However, more significant and substantial changes were observed during the winter experiment than during the summer experiment, no doubt owing to lower temperature of the bathing room. The value of COMP did not vary significantly between winter and summer subjects. Twelve subjects in the elderly developed ECG changes while bathing such as supraventricular extrasystole or ventricular tachycardia. No clinical significance was found in the biochemical analyses of the blood obtained before and after bathing. In conclusion, some subjects in the elderly showed risky changes in the above parameters and ECG, factors which may partially explain some of the causes of the many reported cases of lapse of consciousness and unexpected sudden death in the elderly while bathing especially in the winter season. Cold climate, hot water immersion, and hydrostatic pressure may affect their physiological compensation along with existing of coronary stenosis or weakness of respiratory function as a normal consequence of advanced age.

Adult↗

PubMed1993

Comparative hemodynamic effects of amiodarone, sotalol, and d-sotalol.

The effects of intravenous boluses of amiodarone (5 mg/kg), racemic sotalol (enantiomeric ratio d/l-sotalol 1:1;1.5 mg/kg), and d-sotalol (0.75 mg/kg) on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), left ventricular end-diastolic pressure (LVEDP), and peak rate of change of left ventricular pressure (LV dp/dt) were assessed in conscious rabbits. Amiodarone and sotalol had a modest negative inotropic effect: amiodarone reduced peak LV dp/dt by 8 +/ 2% (mean +/- SEM) (p < 0.05) and sotalol by 6 +/- 2% (p < 0.05). These two drugs had quite different effects on CO as a result of differences in their actions on peripheral blood vessels: amiodarone caused a 13 +/- 3% (p < 0.05) increase in CO associated with a substantial vasodilatory effect (TPR reduced 25 +/- 3%; p < 0.01); sotalol did not produce any substantial change in either CO or TPR. Bolus intravenous injection of amiodarone was associated with a significant increase in HR (12 +/- 3%; p < 0.01), whereas sotalol reduced HR by 7 +/- 1% (p < 0.05). In contrast, administration of the dextro-rotatory optical isomer, d-sotalol, produced no significant change in peak LV dp/dt, LVEDP, CO, TPR, or HR. These results confirm that amiodarone and racemic sotalol have a comparatively weak cardiodepressant action. The experiments also show that the reduction in cardiac performance associated with racemic sotalol is mediated predominantly through the beta-adrenoreceptor blocking action of the levo-rotatory isomer (l-sotalol) rather than any substantial cardiodepressant effect of the dextro-rotatory isomer.

Amiodarone↗

PubMed1988

Effect of conditioning and deconditioning stimuli on metabolically determined blood flow in humans and implications for congestive heart failure.

Peripheral blood vessels do not dilate normally in congestive heart failure (CHF). The mechanisms responsible for this impairment are not well understood. In this review, a group of studies performed over the past 3 years aimed at examining these mechanisms further are described. These studies suggest that in CHF, fluid retention has a negative effect on vasodilator capacity, thereby limiting peak forearm blood flow. A second mechanism is described that is slowly reversing and not directly dependent on cardiac function; it is believed that this mechanism may be related to the vascular deconditioning associated with severe CHF. This postulate is based on studies that have shown that peak vasodilator capacity is higher in the trained arms of tennis players, that improved vasodilator capacity can be induced by a localized unilateral training program, and that vasodilator capacity is reduced by localized deconditioning. Furthermore, the level of conditioning on vasodilator capacity may be mediated by chronic changes in blood flow. Further studies are necessary to confirm these relations.

Blood Flow Velocity↗

PubMed1994

A quantitative and cartographic study of retinal microvasculopathy in acquired immunodeficiency syndrome.

We quantified the retinal microvascular abnormalities in 57 eyes from autopsy patients with the acquired immunodeficiency syndrome (AIDS) and in 24 eyes from gender- and age-matched control subjects. We related retinal vascular changes to the topography of cytomegalovirus retinitis. Analysis of retinal trypsin digests revealed more vascular attenuation (P = .005), increased ratio of endothelial cells to pericytes (P = .001), and more microaneurysms (P = .02) in eyes of AIDS patients without cytomegalovirus retinitis than in those of control subjects. Cytomegalovirus retinitis was frequently bilateral, extensive, and distributed along blood vessels. Peripheral retinitis was more frequent than macular infection. Lymphocytes aggregated focally in arterioles, venules, and capillaries leading to areas infected with cytomegalovirus. Acquired immunodeficiency syndrome microvasculopathy occurs in the absence of cytomegalovirus retinitis and is not accounted for by immunosuppression alone. The location and character of these vascular changes in AIDS indicate an ischemic pathogenesis. In AIDS patients with cytomegalovirus retinitis, the vascular changes are more profound and include capillary destruction.

AIDS-Related Opportunistic Infections↗

PubMed2000

Activation of cardiac vagal afferents facilitates late vagal inhibition in neurones of the rostral ventrolateral medulla oblongata bilaterally.

A reduced activity of cardiac vagal afferent fibres is considered as one of the pathophysiological causes of post-infarction complications [A. Head, Baroreflexes and cardiovascular regulation in hypertension. J. Cardiovasc. Pharmacol. 26 (1995) S7-S16]. The mechanism of how a reduction of cardiac vagal activity leads to enhanced sympathetic drive and systemic hypertension is however not yet clear. Experimental data have shown that the rostral ventrolateral medulla oblongata (RVLM) plays an important role in tonic blood pressure regulation, the control of sympathetic vasoconstriction and cardiac performance. The aim of the study was to determine whether activation of cardiac vagal afferents contributes to eliciting the long-lasting late inhibition that we have previously shown to occur in neurones of the RVLM [A. Zagon, K. Ishizuka, I. Rocha, K.M. Spyer, Late vagal inhibition in neurones of the ventrolateral medulla oblongata in the rat. Neurosci. 92 (1999) 877-888]. The experiments were carried out in terminally anaesthetised and artificially ventilated rats using in vivo intracellular recordings. The data confirmed that late vagal inhibition is elicited by cumulative activation of functionally different vagal afferents, including those that originate from cardiac receptors. It was also demonstrated that activation of cardiac afferents could lead to a significant increase in the duration of this long-lasting late response component. Facilitation of late vagal inhibition was observed in RVLM neurones both ipsi- and contralateral to the stimulated nerve. It is suggested that such facilitation of late vagal inhibition may be a mechanism of how pulse-synchronous activation of cardiac afferents leads to a tonic modulation of the activity of RVLM neurones. An attenuation of late vagal inhibition during reduced activity of cardiac vagal afferents could lead to enhanced excitability in these neurones which in turn can lead to an increase in medullary sympathetic outflows towards the heart and peripheral blood vessels.

Animals↗

PubMedDate not supplied

Occurrence of a unique protein toxin from the Indian King Cobra (Ophiophagus hannah) venom.

A unique (lethal-cardiotoxic-hemorrhagic) protein toxin (Toxin CM55) was isolated and purified from Indian King Cobra (Ophiophagus hannah) venom by CM-sephadex ion exchange chromatography and reverse phase HPLC. The purified toxin had an SDS-molecular weight of 22 +/- 0.5 kD. UV absorption spectra of Toxin CM55 showed a peak at 280 nm, whereas when excited at 280 nm fluorescence, Toxin CM55 showed an E(max) at 333.4 nm. Toxin CM55 had an LD(50) of 28.28 microg/20 g (i. v.) in albino mice. The cardiotoxic action of the toxin was established on isolated guinea pig/rabbit heart and guinea pig auricle. In rats, Toxin CM55 caused ECG abnormalities including widened QRS complex and monomorphic ventricular tachycardia suggesting that the possible site of action of Toxin CM55 was the ventricle. Toxin CM55 produced significant vasoconstriction on peripheral blood vessels. It produced significant contraction of isolated guinea pig ileum, rat fundus and rat uterus, which was completely antagonised by methysergide. The toxin was found to release a significant amount of serotonin from rabbit platelets. Toxin CM55 produced cutaneous hemorrhage in albino mice, which was also produced in reserpine and p-chloro phenylalanine pretreated animals. Rabbit antiserum was raised against Toxin CM55, which gave prominent bands in immunogel diffusion and immunoelectrophoresis. The antiserum provided 2 LD(50) protection against Toxin CM55-induced lethality in mice and also neutralised 3 MHD hemorrhagic dose of the toxin.

Animals↗

PubMed2003

Local cryoglobulin deposition in primary central nervous system lymphoma.

Primary central nervous system lymphomas (PCNSLs) represent malignant non-Hodgkin's B-cell lymphomas confined to the central nervous system. Recent years have brought a dramatic increase in the frequency of PCNSL in the immunocompromised and immunocompetent populations. Cryoglobulins are cold-precipitable immunoglobulins associated with a number of infectious, autoimmune, and neoplastic disorders. Although it is known that patients with hematologic malignancies (eg, B-cell lymphomas, chronic lymphocytic leukemia, plasma cell dyscrasias) may have cryoglobulinemias and cryoglobulin deposition in several organs (eg, kidney, liver skin, blood vessels, peripheral nervous system), PCNSL associated with cryoglobulin deposition has not been previously described. This report demonstrates localized cryoglobulin deposition within the tumor bed in an immunocompetent patient with PCNSL.

Adult↗

PubMed1988

Pedal hemangioma (venous malformation) occurring in Turner's syndrome: an additional manifestation of the syndrome.

Two infants with Turner's syndrome and an unusual vascular tumor or malformation of the feet are described. In one child, the lesion developed in the dorsal metacarpal area, whereas in the other, the lesion was located in a bilaterally symmetrical distribution over the dorsum of the feet. Both lesions were characterized by a proliferation of tortuous, thick-walled veins with imperfectly formed muscular walls. Redundancy of the endothelial lining leading to intimal "webs" and intraluminal vascular channels was prominent. The similarity of these two lesions clinically and histologically suggests that they do not represent a fortuitous occurrence, but an additional manifestation of Turner's syndrome. Furthermore, their existence indicates that the vascular abnormality in Turner's syndrome may be more generalized than previously recognized and may include abnormalities of peripheral blood vessels in addition to those of the heart and aorta.

Foot Diseases↗

PubMed1999

Lumbar sympathectomy failed to reverse mechanical allodynia- and hyperalgesia-like behavior in rats with L5 spinal nerve injury.

The L5 spinal nerve ligation model of neuropathic pain in rats has been proposed as a model for sympathetically maintained pain (SMP) based on the effects of surgical or chemical sympathectomy on nerve injury induced behavior. In an attempt to confirm that the lesion produces an animal model of SMP, surgical sympathectomies were independently conducted in two different laboratories (Johns Hopkins and University Kiel) using male Sprague-Dawley (n = 30) or Wistar rats (n = 14). The L5 spinal nerve was ligated or cut and ligated. Using von Frey hairs, paw withdrawal threshold and incidence of paw withdrawal were tested concurrently before and after the sympathectomy. The sympathectomy was either verified by (a) glyoxylic acid staining of peripheral blood vessels of the hindpaw or (b) skin temperature measurements of the hindpaws. To blind the experimenter, surgeries and behavioral tests were performed by two different investigators and a sham sympathectomy was performed at Johns Hopkins. Decreased paw withdrawal thresholds and increased frequencies of paw withdrawal on the lesioned side were observed after the L5 lesion. Thus, the L5 spinal nerve ligation resulted in behavioral signs of allodynia and hyperalgesia to mechanical stimuli. Lumbar surgical sympathectomy 1-3 weeks after the lesion or prior to lesion with bilateral removal of the sympathetic ganglia L2-L4, however, did not reverse or prevent the behavioral changes induced by the nerve injury. The lack of effect of the sympathectomies was independent of the testing paradigm used. Experiments in Wistar and Sprague-Dawley rats yielded the same results. Potential reasons for the discrepancies between the present study and earlier reports are discussed. These results indicate that an L5 spinal nerve injury rat model is not a reliable model for SMP.

Adrenergic Fibers↗

PubMed1998

Endothelial expression of the 5-hydroxytryptamine1B antimigraine drug receptor in rat and human brain microvessels.

In addition to triggering vasoconstriction of peripheral blood vessels, which led to its discovery as a circulating neurohormone 50 years ago, serotonin (5-hydroxytryptamine) acts as a neurotransmitter/ modulator in the central nervous system and regulates local cerebral blood flow and vascular permeability through direct and indirect effects on intraparenchymal microvessels. Among the various 5-hydroxytryptamine receptors which mediate these effects, particular attention has been paid to the 5-hydroxytryptamine1B and 5-hydroxytryptamine1D subtypes, as the preferred targets of modern antimigraine agents. Immunoelectron microscopic labeling of the 5-hydroxytryptamine1B receptor in rat brain parenchyma has revealed a distinct localization to the endothelium of microvessels, which was predominantly cytoplasmic as opposed to membrane-bound, contrary to that on preterminal unmyelinated axons [Riad et al. (1997) Soc. Neurosci. Abstr. 23, 1214]. Similar observations have now been made in human cortical tissue, in which the expected localization of the vascular 5-hydroxytryptamine1B receptor to periarteriolar myocytes was also confirmed. Such a dual localization in human brain microvessels suggests that the 5-hydroxytryptamine1B receptor might mediate opposite effects, vasodilatory and contractile, depending upon its activation by circulating or centrally released 5-hydroxytryptamine. It raises new possibilities as regards 5-hydroxytryptamine effects on human brain microvessels in health and disease, and notably the triggering of migraine headache.

Animals↗