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At least 649 records · Page 36Linked to original sources
PubMed1984

[Venous tonus-modifying effect, pharmacokinetics and undesired effects of dihydroergotamine].

In the present review the clinical pharmacology of dihyroergotamine (DHE) is described. The decisive pharmacodynamic effect of DHE, i.e. the tonicization of the capacitance vessels leading to the acceleration of the venous backflow is described by the methods suitable for the detection of this activity in man. In the paragraph on pharmacokinetics the kinetic parameters of DHE at present known are discussed with regard to the usual forms of application. Emphasis is placed on the poor oral bioavailability of DHE as a result of a distinct first-pass metabolism in the liver. Taking into consideration several recently published cases of ergotism after prophylactic use of DHE, the ability of DHE is discussed to raise the peripheral resistance. The symptoms and the incidence of ergotism are reported on and reference is given to particular conditions which favour its occurrence. Among the measures of a medicamentous therapy of ergotism the use of drugs such as sodium nitroprusside and nitroglycerin which exert a direct spasmolytic effect on the vascular muscles is of special importance. Since DHE is at present the only medicament that possesses a reliable constrictor effect on the capacitance vessels, its clinical application demands special caution due to the narrow therapeutic margin of safety.

Administration, Oral↗
PubMed2000

Pulse waveform analysis of arterial compliance: relation to other techniques, age, and metabolic variables.

To assess the physiologic and clinical relevance of newer noninvasive measures of vascular compliance, computerized arterial pulse waveform analysis (CAPWA) of the radial pulse was used to calculate two components of compliance, C1 (capacitive) and C2 (oscillatory or reflective), in 87 normotensive (N1BP, n = 20), untreated hypertensive (HiBP, n = 21), and treated hypertensive (HiBP-Rx, n = 46) subjects. These values were compared with two other indices of compliance, the ratio of stroke volume to pulse pressure (SV/PP) and magnetic resonance imaging (MRI)-based aortic distensibility; and were also correlated with demographic and biochemical values. The HiBP subjects displayed lower C1 (1.34 +/- 0.09 v. 1.70 +/- 0.11 mL/mm Hg, significance [sig] = .05) and C2 (0.031 +/- 0.003 v 0.073 +/- 0.02 mL/mm Hg, sig = .005) than N1BP subjects. This was not true for C1 (1.64 +/- 0.08 mL/mm Hg) and C2 (0.052 +/- 0.005 mL/mm Hg) values in HiBP-Rx subjects. The C1 (r = 0.917, P < .0001) and C2 (r = 0.677, P < .0001) were both closely related to SV/PP, whereas C1 (r = 0.748, P = .002), but not C2, was significantly related to MRI-determined aortic distensibility. Among other factors measured, age exerted a strong negative influence on both C1 (r = -0.696, P < .0001) and C2 (r = -0.611, P < .0001) compliance components. Positive correlations were observed between C1 (r = 0.863, P = .006), aortic distensibility (r = 0.597, P = .19) and 24-h urinary sodium excretion, and between C1- and MR spectroscopy-determined in situ skeletal muscle intracellular free magnesium (r = 0.827, P = .006), whereas C2 was inversely related to MRI-determined abdominal visceral fat area (r = -0.512, P = .042) and fasting blood glucose (r = -0.846, P = .001). Altogether, the close correspondence between CAPWA, other compliance techniques, and known cardiovascular risk factors suggests the clinical relevance of CAPWA in the assessment of altered vascular function in hypertension.

Adipose Tissue↗
PubMed1990

[Evaluation of increasing digital blood flow during early period of air-cooled cold test].

The present study was performed to elucidate peripheral hemodynamic changes, especially, digital blood flow, caused by an air-cooled cold test. Experiments were carried out by placing the subject's left hand in a box that was kept at a temperature of about 18 degrees C by air-cooling. At the same time, the digital blood flow, digital blood pressure, compliances of the peripheral resistance and capacitance vessels were measured. These parameters were measured on the left forefinger of the cooled side, and also on the opposite side according to Kato's method at 3 points, 1) at normal condition (before cooling stated). 2) 30 seconds after the cooling began and 3) 10 minutes after the cooling began. The following results were obtained; 1) The systemic blood pressure, digital blood pressure and heart rate showed no statistically significant differences in measurements taken at the above three stages. 2) The mean value of the digital blood flow was found to have increased after 30 seconds, and to have decreased after 10 minutes of cooling. Statistically, significant differences were noted at the above three stages. 3) The mean value of the peripheral vascular resistance was found to have increased after 30 seconds, and to have decreased after 10 minutes. 4) Compliances of the peripheral resistance vessel and capacitance vessel showed no significant changes on either side except between normal condition and after 10 minutes of cooling.

Adult↗
PubMed1992

[Vascular effects of urapidil administrated during extracorporeal circulation].

Urapidil exerts a combined central sympathetic and peripheral alpha-1 adrenergic receptor inhibition. Urapidil induces arterial vasodilation but its effects on venous capacitance are more difficult to assess. During cardiopulmonary bypass with constant perfusion index (2.4 l.min-1 x m-2) total peripheral resistance varies similarly as to arterial pressure and, as the apparatus venous reservoir is filled continuously by simple gravity from the right atrium, a decrease in venous blood reservoir level reflects an increased venous capacitance. Twenty-six patients undergoing cardiac surgery were anaesthetized with fentanyl and midazolam and randomly assigned to one of two groups. During normothermic cardiopulmonary bypass, group 1 was administered i.v. urapidil 12.5 mg and group 2 a placebo. In group 1, arterial pressure decreased by 33 +/- 14% (mean +/- SD) at the second minute while total peripheral resistance decreased from 1,384 +/- 255 to 927 +/- 193 dyn.s.cm-5. Then this two parameters regained group 2 values after the eighth minute. Reservoir blood level was lower in group 1 than in group 2 from the second to the eight minute (p < 0.05) with maximum effect at 7 minutes. It is concluded that urapidil exerts arterial and venous dilation. Its arterial effects seem greater during normothermic cardiopulmonary bypass than in normal conditions and its maximum venous effects seem to occur after its maximum arterial effects. The short duration of action may be due to the small dose administered.

Aged↗
PubMed1978

Effect of diazoxide on capacitance vessels.

Haemodynamic changes after an i.v. bolus of diazoxide 300 mg were studied in 11 hypertensive subjects. A hypotensive effect due to a fall in total peripheral vascular resistance was found in all of them, but changes in the peripheral circulation were less regular. A uniform change in forearm blood volume, blood flow, vascular resistance and venous distensibility was not found after diazoxide. This is interpreted as being due to a reflex increase in sympathetic activity, which counteracts the direct vasodilator action of the drug.

Adult↗
PubMed1975

[Effect of dihydroergotoxin on myocardial capacitance vessels].

Experiments were performed on the isolated cat hearts, coronary vessels being perfused with donor cat blood. Dihydroergotoxin injected into the coronary vessels (0.5 mg) decreased their vascular capacity. This resulted from active constriction of the coronary vessels, since it was seen in experiments with the heart arrested with strophathin as well. Active constriction of the coronary veins under the action of dihydroergotoxin was not related to its specific properties as an alpha-blocking drug, and resulted from a direct action of the drug on the smooth muscle of the coronary veins.

Animals↗
PubMed1985

Extracardiac and coronary vascular effects of digitalis.

The administration of digitalis glycosides causes a variety of extracardiac effects. In both normal human subjects and in other species, digitalis increases smooth muscle tone of resistance and capacitance vessels. The vasoconstriction is mediated, in part, by a direct action of these glycosides on smooth muscle and, in part, by an increase in alpha-adrenergic tone. Constriction of coronary and splanchnic vessels may lead to myocardial or mesenteric ischemia. In contrast to normal subjects, patients with congestive heart failure demonstrate arteriolar and venodilation in response to these glycosides, possibly because the myocardial effect, to increase cardiac output and peripheral blood flow, overcomes the vasoconstrictor properties of these drugs. Other important actions of digitalis glycosides occur in the central and peripheral nervous systems. Their effects on the area postrema of the medulla oblongata are largely responsible for the alpha-adrenergic-mediated peripheral vasoconstriction, as well as the nausea and vomiting that frequently accompany digitalis intoxication. Actions of glycosides on the cerebral cortex are responsible for the wide range of neurotoxic effects that range from visual disturbances and headaches to seizures and coma. Finally, peripheral neurologic effects of digitalis glycosides on baroreceptor and cardiac afferent fibers may: improve the depressed function of these receptors in the situation of heart failure, and reflexly lower peripheral vascular resistance, thereby partially preventing the vascular constrictor action of these glycosides.

Animals↗
PubMed2004

Endothelial venodilator response in carriers of genetic polymorphisms involved in NO synthesis and degradation.

AIMS: Polymorphisms of the NOSIII gene and of the CYBA gene have been associated with a number of pathological conditions such as arterial hypertension, coronary artery disease, and myocardial infarction. Because endothelium-dependent vasodilation is impaired in these disorders, we hypothesized that polymorphisms of NOSIII or CYBA might modulate endothelial function of venous capacitance vessels already before cardiovascular disease becomes overt. METHODS: Endothelium-dependent and -independent venodilation was assessed by measuring local vascular responses to bradykinin and sodium nitroprusside in the dorsal hand vein after preconstriction with phenylephrine in 72 healthy male Caucasians after careful exclusion of cardiovascular risk factors. Genotyping was performed for polymorphisms of the NOSIII gene (T-786C, G894T, (CA)(n)) and the CYBA gene (C242T). RESULTS: Genotype distribution for each polymorphism followed the Hardy-Weinberg equilibrium. In all studied single nucleotide polymorphisms no significant difference between the respective genotypes and the venodilator response to either sodium nitroprusside or bradykinin was observed, and the number of CA repeat copies was not related to the venodilator response to bradykinin. Mean venodilation induced by bradykinin 50 ng min(-1) (+/-SEM) for homozygote carriers of the single nucleotide polymorphisms was 48.9 +/- 8.5% venodilation (G894T; wild type: 49.8 +/- 6.9), 50.3 +/- 11.0% venodilation (T-786C; wild type: 42.6 +/- 5.2), and 30.4 +/- 9.1% venodilation (C242T; wild type: 49.2 +/- 6.0), respectively. CONCLUSIONS: This study suggests that the studied polymorphisms of NOSIII and CYBA do not significantly modulate endothelium-dependent venodilation in individuals without vascular risk factors.

Bradykinin↗
PubMed1984

Effect of platelet activating factor on the human nasal mucosa.

In order to determine the effect of PAF-acether on the vascular bed in the human nose, 11 healthy volunteers were studied. Rhinomanometry was performed to determine the effect on the capacitance vessels, and the 133Xe wash-out method enabled determination of the mucosal blood flow, regulated mainly by the resistance vessels. These measurements were made before and after topical administration of PAF-acether in three different doses; 0.26 micrograms, 2.6 micrograms and 26 micrograms per nostril. The results indicate that PAF-acether induces a dose-dependent vasoconstriction of the capacitance vessels and a reduction in mucosal blood flow. That PAF-acether should be a principal mediator in the allergic reaction in the human nose is not supported by these findings.

Adult↗
PubMed2003

Monovalent cation (MC) current in cardiac and smooth muscle cells: regulation by intracellular Mg2+ and inhibition by polycations.

1 Previously we have described a monovalent cation (MC) current that could be unmasked by the removal of extracellular divalent cations in vascular smooth muscle cells (SMC) and cardiac myocytes, but specific and potent inhibitors of MC current have not been found, and the mechanism of its intracellular regulation remains obscure. 2 Here we show that small MC current is present in intact cells and could be dramatically up-regulated during cell dialysis. MC current in dialyzed cells strongly resembled monovalent cation current attributed to Ca(2+) release-activated Ca(2+)-selective (CRAC) channels, but its activation did not require depletion of Ca(2+) stores, and was observed when the cells were dialyzed with, or without BAPTA. 3 Intracellular free Mg(2+) inhibits MC current with K(d)=250 microM. 4 Extracellular (but not intracellular) spermine effectively blocked MC current with K(d) =3-10 microM, while store-operated cations (SOC) channels and capacitative Ca(2+) influx were not affected. 5 Spermine effectively inhibited MC current-induced SMC depolarization, and prevented Ca(2+) paradox-induced vascular contracture. 6 Both, MC and SOC currents were inhibited by 2-aminoethoxydiphenyl borate (2-APB). 7 It is concluded that MC current could be regulated by intracellular Mg(2+), and low concentrations of extracellular spermine could be used to discriminate it from SOC current, and to assess its role in cellular function.

Animals↗
PubMed1981

Direct effects of nitroglycerin on the resistance, exchange and capacitance functions of the canine intestinal vasculature.

In the isolated dog ileum perfused with constant flow, nitroglycerin (NTG) produced dose-dependent arteriolar and venous dilatation. Experiments were performed in 22 ileum preparations to advance the study on the pre- and postcapillary resistances, functional capillary pressure, capillary filtration coefficient (CFC) and vascular compliance. At venous pressure (Pv) of 0, 10 and 20 mm Hg, and intra-arterial infusion of NTG in a submaximal dose (30 microgram/min) reduced the total and precapillary resistances, but did not change the postcapillary resistance and functional capillary pressure. This agent slightly increased the CFC calculated from a Pv range of 0 to 10 mm Hg and significantly increased the CFC value calculated from a Pv change of 0 to 20 mm Hg. At Pv = 0 mm Hg, NTG infusion caused a regional volume pooling by 1.2 +/- 0.4 mg/100 g. The vascular compliance in terms of delta blood volume/delta Pv was also significantly increased after NTG. The myogenic responses (reduction in CFC and increase in precapillary resistance) to an elevation of Pv were essentially identical before and after NTG infusion. The results suggest the NTG at the dose used acts primarily on the arterioles, precapillary sphincters and postcapillary capacitance vessels. The postcapillary resistance vessels (mainly the venules) are little affected. Although the resistance and exchange vessels are dilated by NTG, the myogenic constriction of these vessels upon Pv rises is not significantly altered.

Animals↗
PubMed1986

Postsynaptic alpha 1- and alpha 2-adrenergic receptors in adrenergic control of capacitance vessel tone in vivo.

The involvement of postsynaptic alpha 2-adrenergic receptors in the adrenergic constriction of the capacitance vessels was studied in anesthetized, spontaneously breathing dogs under ganglionic blockade (hexamethonium, 10 mg/kg + 10 mg/kg/hr; methylatropine, 0.5 mg/kg). Effective vascular compliance was measured as an indicator of venous tone (blood volume was varied by +/- 4 ml/kg in an 11-minute cycle of infusion, withdrawal, withdrawal, and reinfusion) and was calculated from the correlation between the observed changes in central venous pressure and the changes in blood volume. Sympathetic activity and central venous pressure were lower and effective vascular compliance was higher than values in untreated conscious dogs. The alpha 2-agonist UK 14,304 (5-bromo-6-[imidazolin-2-ylamino]-quinoxaline; 0.04 and 0.12 micrograms/kg/min; n = 6) dose-dependently lowered compliance and increased central venous pressure to levels found in conscious dogs, as did the alpha 1-agonist methoxamine (10 and 30 micrograms/kg; n = 6). Rauwolscine (alpha 2-antagonist), 0.3 mg/kg, significantly attenuated the effects of UK 14,304, but not those of methoxamine, while prazosin (alpha 1-antagonist), 0.12 mg/kg, attenuated the effects of methoxamine, but not those of UK 14,304 (n = 6 each). Under beta-blockade (nadolol, 2 mg/kg; n = 12) venous tone was increased to about physiological levels by norepinephrine, 0.15 micrograms/kg/min i.v., or by neuronal norepinephrine release induced by tyramine, 10 micrograms/kg/min i.v. These increases were significantly attenuated by prazosin as well as by rauwolscine and were abolished by a combination of both. These results indicate that postsynaptic alpha 2-adrenergic receptors (in addition to alpha 1-adrenergic receptors) are functional in the venous system in vivo and contribute substantially to adrenergic sympathetic and humoral regulation of venous tone.

Adrenergic alpha-Antagonists↗
PubMed1987

Graphic analysis of serotonin effects in dog heart-lung preparation.

Graphical analysis of the effects of serotonin on cardiac function and pulmonary circulation was performed, using the dog heart-lung preparation. The equilibrium points, at which the cardiac output (CO)-curve and venous return (VR)-curve cross in the right atrial pressure (RAP) or left atrial pressure (LAP)-CO relations, were directly recorded on two X-Y recorders. CO- and VR-curves were directly depicted by changing the blood level in the reservoir, and by inducing ventricular fibrillation and simultaneously occluding pulmonary arterial trunk, respectively. Single injections of serotonin, 300 micrograms, into the right or left atrium, induced a negative inotropic response. Low rate (less than 30 micrograms/min) of infusion of serotonin had no effect on the CO-curve or on the slope-gradient of VR-curve in the LAP-CO relation. At a rate of 60 or 120 micrograms/min, however, the CO-curve was moved downwards to the right, indicating a negative inotropic effect. Pulmonary mean filling pressure increased and the slope-gradient of pulmonary VR-curve decreased, indicating an increased resistance to venous return from the pulmonary circulation. Pulmonary arterial pressure was markedly elevated. In order to obtain the capacitance ratio between the extracorporeal circuit and the pulmonary circulation, a shift of blood volume to the pulmonary circulation was induced by elevating the aortic pressure, which also decreased the slope-gradient. The calculated capacitance ratio became greater during the infusion of serotonin, indicating that the capacitance in the pulmonary circulation was lowered. It is likely that serotonin has contractile effects on the pulmonary arterial and venous vascular beds, elevating the pulmonary filling pressure and resistance to venous return.

Animals↗
PubMed1988

Exogenous ATP and hepatic hemodynamics in the perfused rat liver.

The actions of exogenous adenosine triphosphate (ATP) on hepatic hemodynamics were analyzed in the isolated perfused rat liver. The effects of ATP (10, 40, and 160 microM) on hepatic circulatory resistances were determined from changes in portal vein flow, portal vein perfusion pressure, hepatic arterial perfusion pressure, and hepatic capacitance. ATP decreased portal vein flow under conditions of constant perfusion pressure, but it increased portal vein perfusion pressure under constant flow perfusion. ATP increased the resistance of the presinusoidal regions and reduced hepatic capacitance. Adenine derivatives including adenosine, adenosine monophosphate (AMP), adenosine diphosphate (ADP), and ATP also decreased portal vein flow; the order of vascular activity of the adenine compounds was ATP greater than ADP greater than AMP = adenosine. The shock-protective actions of ATP may reflect hepatic hemodynamic adjustments.

Adenosine Triphosphate↗
PubMed1982

Calcium-entry blockers and vascular smooth muscle.

Calcium-entry blockers depress the myogenic activity and the responsiveness to vasoconstrictor stimuli of the smooth muscle cells of the precapillary vessels. Thus, they can reduce the afterload of the heart and have antihypertensive properties. Their inhibitory effect on the contractile responses of the vascular smooth muscle cells of large arteries also results in the reduction or the abolition of vasospastic episodes. By inhibiting the constrictor responses of the splanchnic capacitance vessels to the sympathetic nervous outflow, they reduce the preload of the heart. However, different calcium-entry blockers differ in their ability to affect different cardiovascular variables and in the onset and duration of their effect; they also have different degrees of tissue selectivity. This variability must reflect differences in pharmacodynamic and pharmacokinetic properties.

Angina Pectoris↗