Vascular effects

In addition to the vascular effects, calcium channel blockers (Table 6) such as isradipine, nifedipine (Table 3), and nitrendipine, produce natriuretic... 

Phenylephrine is a fast-acting, short-duration a, agonist. Phenylephrine has primarily vascular effects, and does not impair cardiac or renal function. Phenylephrine is useful when tachycardia limits the use of other vasopressors.24,27-28... 

Vascular Effects of Complement Activation. During complement activation a number of complement fragments (anaphylatoxins), which are polypeptides with inflammatory properties, are released. The anaphylatoxins C3a and C5a induce smooth muscle contraction and enhance vascular permeability (H31). The most pronounced activation of complement with the formation of anaphylatoxins and terminal C5-9 complexes has been observed in septic shock (B29, B30, P2). Studies indicate that there is a relation between high concentrations of anaphylatoxins and C5-9 complexes and the development of ARDS or MODS in patients with sepsis (H10). 

Nowak-Sliwinska, P., Ballini, J. P., Wagnieres, G. 8c van den Bergh, H. Processing of fluorescence angiograms for the quantification of vascular effects induced by anti-angiogenic agents in the CAM model. Microvasc. Res. 79, 21-28 (2010). 

Van Ampting JMA, Hijmering ML, Beutler JJ, van Etten RE, Koomans HA, Rabelink TJ, Stroes ESG. Vascular effects of ACE inhibition independent of the renin-angiotensin system in hypertensive renovascular disease. Hypertension 2001 37 40-45. 

Dobutamine is a /Jj- and / -receptor agonist with some oq-agonist effects. The net vascular effect is usually vasodilation. It has a potent inotropic effect without producing a significant change in heart rate. Initial doses of 2.5 to 5 mcg/kg/min can be increased progressively to 20 mcg/kg/min on the basis of clinical and hemodynamic responses. 

Blum A, Hathaway L, Mincemoyer R, Schenke WH, Casco G, Waclawiw M A, Panza MA, Cannon III RO (2000) Hormonal, lipoprotein, and vascular effects of the selective estrogen receptor modulator raloxifene in hypercholesteronomic men. Am J Cardiol 85 1491-1494... 

Tatchum-Talom R, Martel C, Labrie F, Marette A (2003) Acute vascular effects of the selective estrogen receptor modulator EM-652 (SCH 57068) in the rat mesenteric vascular bed. Cardiovasc Res 57 535-543... 

Is Nitrate Therapy Associated with Adverse Vascular Effects 295... 

Vascular effects Cocaine causes increases in blood pressure and heart rate, which fall to normal levels between doses (Foltin et al. 1995). Tachyphylaxis develops to the cardiovascular effects, even within a single session. Concurrent use of ethanol, cannabis, and cocaine causes even greater cardiovascular effects than those of each drug alone. Interactions can also occur with antidepressant drugs like desipramine. 

Vascular and hematologic effects Ginkgo exerts vascular effects through at least two mechanisms inhibition of platelet-activating factor (PAF) and nitric oxide mechanisms. Ginkgo extract relaxes the porcine basilar artery in a concentration-dependent and partly endothelium-dependent manner (Chen et al. 1997). It also enhances vasorelaxation created by transmural nerve stimulation in arteries with and without the endothelium intact, and is prevented by nitro-L-arginine, indicating that the effect is mediated by nitric oxide. 

Tolonen M Vascular effects of carbon disulfide A review. Scand J Work Environ Health 1 63, 1975... 

Tadepalli AS, Buckley JP Cardiac and peripheral vascular effects of decaborane. Toxicol Appl Pharmacol 29-.IKl-lll, 1974... 

Cardiovascular Effects. Myocardial infarction, severe coronary luminal narrowing, and internal alteration of the carotid artery were found in two patients injected 21 -30 years before with an unreported amount of Thorotrast (Isner et al. 1978). The authors concluded that the vascular effects were the result of chronic alpha irradiation. The patients were injected in the carotid artery, and thorotrastoma (see Other Systemic Effects, below) was found in both patients. 

Noradrenaline and adrenaline increase blood pressure, although in various organs the perfusion can actually be reduced. Since adrenaline, in contrast to noradrenaline, stimulates a-and jSi-adrenoceptors and the jSi-subtype as well, its vascular effects are more complex than those of noradrenaline. In many vessel beds like the splanchnic area and the skin the O -adrenoceptor-mediated vasoconstriction is dominant. However, in others, like the active skeletal muscles, the jS2-adrenoceptor-mediated vasodilatation increases the blood flow. In the lower concentration range adrenaline induce an increase in blood pressure without elevated diastolic values. Catecholamines reduce the permeability of the vascular endothelium which might be of some importance for their antiallergic properties. 

One important mechanism of serotonin elimination is the (re-) uptake, e.g. by platelets. Furthermore, serotonin is metabolized by monoaminox-idase to 5-hydroxyindoleacetaldehyde and, subsequently, by an aldehyde dehydrogenase to 5-hydroxyindolacetic acid. The vascular effects of serotonin are complex. The direct interaction with vascular smooth muscle induces a vasoconstriction, whereas the stimulation of 5-HT-receptors on the endothelium induces the release of vasorelaxant factors with a dilatation as a result. An intravenous application of serotonin increases the pressure in the pulmonary circulation. A continuous infusion results... 

Cardiovascular effects of Infusion of norepinephrine, epinephrine, Isoproterenol, and dopamine in humans. Infusions were made intravenously during the time indicated by the broken lines. Heart rate is given in beats per minute, blood pressure in millimeters of mercury, and peripheral resistance in arterial blood pressure. (Reprinted with permission from Allwood MJ, Cobbald AF, and Ginsburg J. Peripheral vascular effects of noradrenaline, isopropyl-noradrenaline, and dopamine. Br Med Bull 19 132, 1963. Reproduced by permission of the Medical Department, The British Council. 

This pattern differs from that seen following administration with either a conventional (3- or a-blocker. Acute administration of a (3-blocker produces a decrease in heart rate and cardiac output with little effect on blood pressure, while acute administration of an a-blocker leads to a decrease in peripheral vascular resistance and a reflexively initiated increase in cardiac rate and output. Thus, the pattern of cardiovascular responses observed after labetalol administration combines the features of (3- and a-blockade, that is, a decrease in peripheral vascular resistance (due to a-blockade and direct vascular effects) without an increase in cardiac rate and output (due to (3-blockade). 

Another study of the effects of I on the cardiovascular systemic concluded that, in dogs anesthetized with sodium pentobarbital, the response of blood pressure to intravenous administration of I is a resultant of two separate effects a direct myocardial stimulation that was stopped with dichlorolsoproterenol and a stimulation of vascular smooth muscle that results in a slight increase in renal arterial pressure and a slight decrease in renal arterial flow. Neither atropine nor dichlorolsoproterenol affected these vascular effects. Injections of 1 into a jugular vein or a renal artery had no consistent effect on catecholamine concentrations in plasma taken from a femoral artery or a renal vein. In seven experiments in which I at 21-35 mg/kg was injected into a jugular vein, the mean blood pressure increased from 176/125 + 22/11... 

Barnes, G.E., Bishop, V.S., Kardon, M.E. 1972. Cardiac and peripheral vascular effects of pralidoxlme chloride. Europ. J. Pharmacol. 20 188-194. 

Mirtazapine does not significantly inhibit hepatic cytochrome P450 enzymes. Additive effects may occur when mirtazapine is combined with other drugs with sedative or vascular effects. Mirtazapine should not be used in combination with an MAOI or within 14 days of discontinuing treatment with an MAOI. When it is combined with fluvoxamine, a potent inhibitor of P450 enzymes— including 1A2, 2D6, and 3A4, which metabolizes mirtazapine—the plasma concentration of mirtazapine may be increased by up to fourfold (AnttUa et al. 2001 Demers et al. 2001). 

FDG is readily taken tip by this transport system, although the extent of uptake can be influenced by the concentration of plasma glucose, which competes with FDG for uptake. The efficiency of transport across the blood brain barrier is such that blood flow is generally not limiting for tracer delivery but the potential for a drug to have a direct vascular effect that influences tracer delivery should be considered. 

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