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PubMed1997

Cerebrovascular endothelial dysfunction mediated by beta-amyloid.

beta-Amyloid (A beta) toxicity has a critical role in the pathology of Alzheimer's disease (AD) but its function in the neurodegenerative process is not clearly established. Recently, we demonstrated a novel action of beta-amyloid on peripheral blood vessels: endothelial dysfunction through reactive oxygen species. Here we report the direct effect of A beta on cerebrovascular endothelium. Following treatment with A beta 1-40, bovine cerebral arteries showed characteristic features of endothelial dysfunction such as increased contraction to vasoconstrictor and diminished relaxation to endothelium-dependent vasodilators. Electron microscopy revealed significant damage to the endothelium by A beta. Pretreatment with the antioxidant superoxide dismutase (SOD) and PBN (n-tert-butyl-alpha-phenylnitrone) antagonized the effects of A beta. Endothelial damage induced by A beta could produce ischemic and inflammatory changes contributing to the pathology of AD.

Amyloid beta-Peptides↗

PubMed1982

New developments in alpha-adrenoreceptor drugs for the treatment of hypertension.

The alpha 1- and alpha 2-adrenoreceptor types are defined in terms of the selective binding of radioligands and their displacement from membrane preparations by a range of agonists and antagonists. Their distribution is described in brain, kidney, heart, and peripheral blood vessels. A group of centrally acting clonidine-like drugs are classified in terms of their selectivity for the alpha 2-adrenoreceptors, and it is suggested that differences between alpha-adrenoreceptors in various tissues may allow development of highly selective alpha 2-adrenoreceptor agonists for specific tissue sites such as the juxtaglomerular cells and brainstem nuclei controlling blood pressure. It is further suggested that the aim of treatment with such compounds is to modulate adrenergic activity while retaining normal homeostatic mechanisms. For this purpose, competitive agonists and antagonists are preferable to compounds which bind irreversibly to the receptor.

Adrenergic alpha-Antagonists↗

PubMed2000

Effects of MCI-154, a calcium sensitizer, on cardiac dysfunction in endotoxic shock in rabbits.

This study was designed to observe the effects of MCI-154, a calcium sensitizer, on cardiac dysfunction after endotoxic shock in rabbits. Ten hours after the rabbits were given injection of 1.0 mg/kg endotoxin (Escherichia coli, O111:B4) via marginal ear veins, 0.1 mg/kg MCI-154 was injected intravenously and then 50 mL/kg normal saline (NS) + 0.1 mg/kg MCI-154 was infused continuously at a rate of 0.7 mL/min. During this process, the parameters of cardiac function were measured. It was found that 10 h after the endotoxin injection, heart rate (HR) was increased significantly while the mean arterial blood pressure (MAP), left ventricular systolic pressure (LVSP), isovolumetric pressure (IP), myocardial contractility (MC), and the area of p-dp/dt(max) vector loop (Lo) all were markedly decreased. Treatment with 50 mL/kg NS alone had slight effects on these parameters. On the contrary, LVSP, IP, MC, and Lo all were increased significantly while HR was not obviously changed and left ventricular end-diastolic pressure (LVEDP) was reduced remarkably following MCI-154 administration in endotoxic shock rabbits. The parameters of myocardial contractility were improved nearly to the values in sham shock group and were markedly higher than that in NS alone-treated group. It can be concluded that MCI-154 can exert significant therapeutic effects on cardiac dysfunction after endotoxic shock, for it improves cardiac function, dilates peripheral blood vessels, and slightly affects HR.

Animals↗

PubMed2006

Cardiovascular disease in rheumatoid arthritis.

PURPOSE OF REVIEW: Individuals with rheumatoid arthritis are at increased risk for morbidity and mortality from cardiovascular disease (CVD). The purpose of this review is to discuss recent advances in our understanding of the pathogenesis, prevalence, treatment, and prevention of accelerated atherosclerotic disease in rheumatoid arthritis. RECENT FINDINGS: Recent reports have highlighted the increased risk for silent myocardial infarction and sudden death in rheumatoid arthritis, and the potential roles of traditional and nontraditional risk factors for CVD, including abnormal revascularization of damaged peripheral blood vessels and genetic polymorphisms. Several studies have also added important information on the possible role of anti-tumor necrosis factor-alpha therapy, other disease modifying antirheumatic drugs, and nonsteroidal anti-inflammatory drugs in decreasing CVD risk. SUMMARY: The pathogenic mechanisms involved in accelerated cardiovascular complications in rheumatoid arthritis appear to be complex and multifactorial. Both traditional and nontraditional risk factors potentially contribute to the increased cardiovascular risk. Good control of the inflammation, immunologic disturbances, and metabolic changes seen in rheumatoid arthritis are crucial in the prevention of this potentially lethal complication. There is a need for heightened awareness of the increased risk for silent ischemia, early myocardial infarction, and sudden death. Further exploration of the mechanisms of vascular repair and their potential role in premature atherosclerosis is needed.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1976

The cardiovascular effects of ketamine in man.

The arterial hypertension of ketamine is prevented by verapamil, a calcium ion antagonist. This indicates that ketamine is a direct myocardial stimulant acting by increasing the availability of calcium across the cell membranes of the myocardial and the Purkinjé systems. The positive chronotropic action of ketamine is not reversed by verapamil. Both the chronotropic and the inotropic effects of ketamine are prevented by halothane which acts partly by increased vagal tone and partly by what appears to be a verapamil-like depression of calcium availability. Ketamine blocks the reflex sympathetic response of the peripheral blood vessels to surgical stimuli. The site of the block within the sympathetic reflex arc has not been identified. It is not at the alpha adrenoceptor level. The clinical implications of the findings have been discussed.

Adult↗

PubMedDate not supplied

Responses of human arterial muscle to stable vasoactive substances released from human platelets by collagen and heat aggregated IgG.

The supernatant solutions obtained after aggregation or sonication of washed human platelets were superfused over preparations of human isolated digital arteries using a small volume bioassay method. The agents released from the platelets caused strong contractions of the artery strips. Platelet aggregation induced by 10 micrograms/ml collagen or by 100 micrograms/ml heat aggregated IgG, released 31.5% and 38.5% respectively, of the contractile activity produced by sonication of the platelets. The quantitative contractile effect of supernatants from platelets aggregated by 50 micrograms/ml IgG was significantly less than that for 100 micrograms/ml HA IgG. Similarly, the maximum contractile effect of supernatants from platelets aggregated by 300 ng/ml collagen was significantly less than that for 1 microgram/ml collagen. This suggests that the concentration of contractile agents released from platelets depends on the concentration of aggregating stimulus. Comparison with concentration-effect curves for exogenous serotonin suggests that if the contractility of the platelet supernatant occurring after sonication of platelets is solely due to serotonin, then it is present in a concentration of approximately 3.3 X 10(-6) mol/l (6.6 nmol per 10(9) platelets). It is suggested from this study that in certain clinical situations characterized by hypertension, and in which circulating immune complexes have been found, in vivo platelet activation by immune complexes may be releasing sufficient concentrations of serotonin to constrict peripheral blood vessels and contribute to the hypertension.

Antigen-Antibody Complex↗

PubMed1994

Comparative haemodynamic effects of verapamil, flecainide, amiodarone and sotalol in the conscious rabbit.

1. The effect of intravenous boluses of verapamil (0.15 mg/kg), flecainide (2 mg/kg), amiodarone (5 mg/kg), and sotalol (1.5 mg/kg) on mean arterial pressure, heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), and peak rate of change of left ventricular pressure (LV dP/dt) were assessed in the conscious rabbit. 2. All four drugs had negative inotropic effects: verapamil reduced peak LV dP/dt by 19 +/- 4% (mean +/- s.e.m.; P < 0.01), flecainide by 27 +/- 9% (P < 0.001), amiodarone by 11 +/- 2% (P < 0.01) and sotalol by 13 +/- 3% (P < 0.01). 3. The drugs had different effects on CO as a result of differences in their actions on peripheral blood vessels: verapamil and amiodarone produced, respectively, a 12 +/- 4% (P < 0.03) and 16 +/- 6% (P < 0.01) increase in CO associated with a substantial vasodilatory effect (TPR reduced 15 +/- 7% [P < 0.05] and 20 +/- 5% [P < 0.01], respectively). Flecainide caused only a small (6 +/- 1%; P < 0.01) increase in CO and sotalol had no effect on either CO or TPR. 4. Bolus intravenous injections of verapamil, flecainide and amiodarone produced an increase in HR, while sotalol reduced HR by 10 +/- 2% (P < 0.01). The increase in HR and cardiac output seen with verapamil, flecainide and amiodarone was in part secondary to reflex increase in sympathetic tone and these changes were abolished after total cardiac autonomic blockade. 5. The modest reduction in cardiac performance associated with sotalol was abolished by cardiac autonomic blockade, suggesting that the predominant effect of sotalol on contractility was mediated through its beta-adrenoceptor blocking effect.

Amiodarone↗

PubMed1964

SOME PHARMACOLOGICAL PROPERTIES OF URIDINE NUCLEOTIDES.

Uridine di-, tri- and monophosphates (UDP, UTP and UMP) contracted the goldfish intestine preparation in that order of decreasing potency. Adenosine triphosphate (ATP) sensitized the gut to UTP and UDP but not to UMP. The fluoro-derivatives of UMP and UTP behaved like the unsubstituted nucleotides on the goldfish intestine but the main effect of 6-azaUDP and large amounts of uracil and uridine was to cause a relaxation. Structure-action relationships are discussed on the basis of these findings. UDPglucose and UDPacetylglucosamine each contracted the goldfish intestine but they were 500-times less active than UDP. Other smooth muscle preparations (tortoise jejunum, rat uterus, guinea-pig ileum and the fowl rectal caecum) contracted to UTP and UDP, but large amounts were needed. The cardiovascular effects in rats of UMP, UDP and UTP were complex and mediated mainly through an action on the peripheral blood vessels. In rats treated with phenoxybenzamine, UMP raised the blood pressure while UDP and UTP first lowered then raised the blood pressure. The fall in blood pressure was not abolished by pronethalol or atropine. The uridine phosphates affected the rat isolated heart only under hypoxic conditions. UTP and UDP dilated the blood vessels of the rabbit ear and UTP was six-times more effective than ATP. UTP and UDP were equiactive in increasing the force of beat of the frog isolated heart. UMP also had an effect if large amounts were given.

Adenosine Triphosphate↗

PubMed1977

Brain and vascular monoamine oxidase activity in the deoxycorticosterone-salt hypertensive rat.

1 The role of monoamine oxidase (MAO) in the maintenance of deoxycorticosterone-sodium chloride (DOCA-salt) hypertension was investigated by assaying the MAO activity both in central as well as peripheral blood vessels and in brain tissue. 2 The results suggest that the activity of MAO in the DOCA-salt hypertensive rat is similar to the activity present in the normotensive rat.

Animals↗

PubMed1981

An investigation into the type of beta-adrenoceptor mediating sympathetically activated renin release in the cat.

1 Stimulation of the renal nerves in the cat was previously shown to cause renin release which could be blocked by propranolol. An attempt was made in this study to determine the type of beta-adrenoceptor mediating this response.2 In anaesthetized, unilaterally nephrectomized cats, a comparison was made of the ability of two selective beta-adrenoceptor antagonists to block the tachycardia and hypotension caused by isoprenaline (mediated respectively by beta(1)- and beta(2)-adrenoceptors) and the release of renin caused by renal nerve stimulation.3 Isoprenaline (mean dose of 0.224 +/- 0.022 nmol/kg), increased heart rate by approximately 43 beats/min and decreased mean blood pressure by 47 mmHg. Stimulation of the distal cut ends of the renal nerves, at a rate sufficient to reduce renal blood flow by 30%, resulted in an approximately 150% increase in plasma renin activity.4 Administration of the selective beta(1)-adrenoceptor antagonist, atenolol (0.38 to 11.28 mumol/kg), caused a dose-related inhibition of nerve stimulated renin release and of isoprenaline-induced tachycardia, with no diminution of the vasodepressor response to isoprenaline; in contrast, the selective beta(2)-adrenoceptor antagonist, erythro-DL-(7-methylindan-4-yloxy)-3-isopropylamino-butan-2-ol (ICI 118, 551, 0.03 to 2.86 mumol/kg), caused a dose-related inhibition of the isoprenaline-induced vasodepression without altering the increase in plasma renin activity caused by renal nerve stimulation. Only at the highest dose of ICI 118, 551 was there a reduction of isoprenaline-induced tachycardia, by about 40%.5 The selective inhibition of neurally activated renin release by atenolol but not by ICI, 118, 551 is consistent with the suggestion that the beta-adrenoceptors mediating renin release resemble those in the heart more closely than those in peripheral blood vessels.

Adrenergic beta-Antagonists↗

PubMed1990

A case report of chronic neutropenia: clinical and ultrastructural findings.

This case report of severe periodontitis concerns a young male patient with chronic idiopathic neutropenia seen between 1981 and 1983 by the School of Dental Medicine of Geneva and from 1984 to 1988 by the Eastman Dental Hospital of London. The patient was maintained by intermittent systemic antibiotics, subgingival chlorhexidine irrigation, conventional debridement, brushing, and wire-mesh and composite splinting of loose teeth. After leaving school, at the patient's express wish, the extreme downhill pattern of the periodontitis resulted in removal of affected teeth and overdenture construction. The extracted teeth and associated soft tissues were examined for relevant plaque and host response features. The intact morphotypes associated with the advancing front of the lesion were invariably Gram-negative or positive coccoid cells, or less commonly short rods, as in all documented forms of periodotitis. Connective tissue destruction was associated with a leucocyte accumulation comprising mainly polymorphonuclear neutrophils (PMN) and plasma cells. Both were observed degenerated more deeply than in routine adult periodontitis, including PMN lysosome loss and lymphocyte maturation within peripheral blood vessels. Only in one instance, one part of the superficial connective tissue of one block contained bacteria. It was concluded that the features of plaque and the lesion suggest a typical first line of defence response as in other forms of periodontitis. From the consideration of the 10 years clinical history of the patient, it is clear that non-surgical management is possible even in extreme cases, without any compromise of the patient's oral or systemic health, and in accord with the patient's wishes.

Adolescent↗

PubMed1996

Expression of basic fibroblast growth factor in desmoplastic melanoma.

Basic fibroblast growth factor (bFGF) is an established growth factor for melanocytes and a potent angiogenic factor. The expression of bFGF was investigated in 23 desmoplastic melanomas. (DM) (12 males, median age 64 years, and 11 females, median age 54 years) by immunostaining of formalin-fixed, paraffin-embedded sections with high-affinity purified antibody raised against recombinant human bFGF (Scios Nova, Inc.). The tumors were characterized by level II invasion in 1 case (5%), level IV invasion in 11 cases (48%), level V invasion in 8 cases (35%), and indeterminate in 3 cases. bFGF expression was observed in 22 of 23 tumors (95%), either immune localized to tumor cell nuclei in 17 of 22 tumors (77%), or to the cytoplasm of tumor cells in 5 of 22 tumors (23%). Also in these cases, bFGF was strongly expressed in the nuclei of vascular endothelial cells. Maximal expression was noted in the peripheral blood vessels of 20 tumors (91%) versus intratumoral vessels of 13 DM (59%). In conclusion, the expression of predominantly nuclear bFGF by tumor cells in DM suggests a role in mediating the desmoplastic phenotype. In addition, the localization of bFGF to vascular endothelium, particularly at the periphery of the tumor, may be relevant to tumor angiogenesis.

Adult↗

PubMed1989

Immunohistochemical localization of chondroitin sulfate and dermatan sulfate proteoglycan in human gingival connective tissue.

This study investigated the immunohistochemical localization of chondroitin sulfate (chondroitin, 4-sulfate and 6-sulfate) and dermatan sulfate proteoglycan (PG) in human gingival connective tissue, using monoclonal antibodies. Dermatan sulfate was found to be widespread in connective tissue, with an especially strong response shown in collagen fiber bundles under the epithelial basement membrane. Chondroitin 4-sulfate occurred widely in connective tissue but showed only a weak response. Chondroitin 6-sulfate was located in peripheral blood vessels. Chondroitin was not detected in gingival connective tissue.

Antibodies, Monoclonal↗

PubMed1971

Cardiovascular changes associated with skeletal muscle spasm in tetraplegic man.

1. A study has been made of the effect of spontaneous and induced muscle spasms on blood pressure, heart rate, hand blood flow, calf blood flow and occluded vein pressure in the hand and foot in non-bedridden patients with chronic, closed, complete, localized transection of the cervical spinal cord.2. Both types of spasm produced a similar response consisting of an increase in blood pressure and occluded vein pressure and a decrease in heart rate and hand and calf blood flow. The changes commenced within 2-3 sec and usually reached maxima in 20-30 sec. On some occasions there was a temporary initial increase in heart rate and calf blood flow.3. The changes occurred independently of changes in bladder pressure.4. It is concluded that the changes in peripheral blood vessels result from a spinal sympathetic reflex to somatic afferents associated with muscular contraction.

Adult↗

PubMed1993

Afferent and efferent components of the cardiovascular reflex responses to acute hypoxia in term fetal sheep.

1. We studied the effects of acute isocapnic hypoxia on arterial and central venous pressures, carotid and femoral blood flows and heart rate in intact and carotid denervated fetal sheep between 118 and 125 days gestation, after pre-treatment with either saline, atropine or phentolamine. Electrocortical activity (ECoG) and the incidence of fetal breathing movements (FBM) were also compared between intact and carotid denervated fetuses. 2. There were no significant differences between intact and denervated fetuses in any variable measured during normoxia. Soon after the onset of hypoxia a marked bradycardia occurred in intact, but not in denervated fetuses. Femoral blood flow and femoral vascular resistance (perfusion pressure/femoral blood flow) increased in intact, but not in denervated fetuses. Carotid blood flow increased in both groups of fetuses during hypoxia, but carotid vascular resistance did not change. During hypoxia, the incidence of FBM and low-voltage ECoG was similarly reduced in both groups of fetuses. 3. Atropine produced a rise in fetal heart rate during the control period in intact but not in denervated fetuses. At the onset of hypoxia atropine prevented the initial bradycardia seen in intact fetuses. In denervated fetuses a further increase in heart rate occurred throughout the hypoxia. 4. All denervated fetuses treated with phentolamine died during the hypoxic challenge, but nine out of fourteen intact fetuses treated with phentolamine survived. 5. In intact fetuses which survived hypoxia after treatment with phentolamine, the increase in arterial blood pressure was smaller and the increase in femoral resistance did not occur. In these fetuses a rise in heart rate occurred in hypoxia. Carotid vascular resistance decreased during hypoxia after administration of phentolamine. 6. Our results indicate that the initial cardiovascular responses of the late gestation sheep fetus to hypoxia are reflex, and that the carotid chemoreceptors provide the afferent limb of this reflex. The bradycardia is mediated through a muscarinic pathway, as it is blocked by atropine. The femoral vasoconstriction is mediated through an alpha-adrenergic mechanism, mediated both neurally by a carotid chemoreflex and via catecholamines released directly from the adrenal medulla. Both these components are blocked by phentolamine. 7. The differences in survival between intact and denervated fetuses during hypoxia after phentolamine suggest that the carotid chemoreflex response to hypoxia involves mechanisms in addition to vagal efferents to the heart and alpha-adrenergic actions at peripheral blood vessels.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗

PubMed1976

Hypoxia and lung mast cells: influence of disodium cromoglycate.

Rats kept in 10% O2 for three or more weeks developed mast cell hyperplasia in the lungs, especially round the alveoli and the small peripheral blood vessels, which became thickened during chronic hypoxia. There was a significant correlation between the degree of right ventricular hypertrophy (RVH) and the numbers of alveolar and small vessel mast cells. However, mast cell hyperplasia developed more slowly than RVH. Daily treatment with disodium cromoglycate failed to prevent RVH in hypoxic conditions but was associated with retardation of growth in both hypoxic and control rats. Neither acute nor chronic hypoxia increased the degree of degranulation in the lung mast cells.

Animals↗

PubMed1994

Distribution of nitric oxide synthase activity in arterioles and venules of rat and human intestine.

NO is produced within peripheral blood vessels through the action of the differentially distributed constitutive and inducible NO synthase isoforms in the vessel wall. As in other sites in the periphery, NO exerts local vasodilatory actions in the gastrointestinal microvasculature and is proposed to play a role in enteric vasomotor regulation. Using NO synthase histochemistry and endothelial cell immunohistochemistry, we provide the first anatomic evidence of NO synthesis in both endothelial and smooth muscle cells of submucosal blood vessels in the rat and human intestine. The findings of this study indicate that 1) as in the periphery, both the endothelial and vascular smooth muscle cells of the microvessels irrigating the rat and human intestinal wall possess NO synthesis potential, 2) NO synthase activity is predominantly localized to discrete subcellular patches, and 3) the source of NO within the vascular wall, either intimal or medial, should be a consideration in future studies in terms of the relative contribution of these sources of vasomotor tone in the rat and human gut wall.

Amino Acid Oxidoreductases↗

PubMed1990

Role of nitric oxide in regulation of basilar artery tone in vivo.

Previous studies have suggested that nitric oxide (NO) may be a major endothelium-derived relaxing factor in peripheral blood vessels. This study tested the hypotheses that 1) formation of NO from L-arginine contributes to basal tone of cerebral arteries in vivo and 2) dilator responses of cerebral arteries to acetylcholine are dependent on formation of NO. Diameter of the basilar artery was measured through a cranial window in anesthetized rats. Under control conditions, topical application of 10 microM NG-monomethyl-L-arginine (L-NMMA, an arginine analogue that inhibits enzymatic formation of NO), constricted the basilar artery by 11 +/- 1% (means +/- SE). L-Arginine (100 microM), which had no effect on baseline diameter, abolished vasoconstriction in response to L-NMMA. L-Arginine did not alter vasodilation during acetylcholine (1 microM) (11 +/- 2 vs. 12 +/- 2%) or vasoconstriction during serotonin (1 nM) (-15 +/- 3 vs. -16 +/- 2%). L-NMMA (5-10 microM) abolished the dilator response of the basilar artery to acetylcholine but did not alter responses to nitroglycerin (0.01 microM) (24 +/- 4 vs. 20 +/- 3%). The inhibitory effect of L-NMMA on the vasodilator response to acetylcholine was prevented by L-arginine. These studies suggest that synthesis of NO from L-arginine influences resting tone of the basilar artery in vivo. Dilatation of the basilar artery to acetylcholine in vivo appears to be dependent on formation of NO from L-arginine.

Acetylcholine↗