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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Haemodynamic and metabolic effects of intravenous infusion of adenosine, an endogenous vasodilator, were studied in healthy humans. 2. Catheters were inserted into pulmonary and brachial arteries and into the hepatic and subclavian veins. Cardiac output was determined according to the Fick principle, and splanchnic blood flow was measured by using extraction of Indocyanine Green. Skin blood flow was estimated by a laser Doppler technique, calf blood flow by venous occlusion plethysmography and skeletal muscle and adipose tissue blood flow by a local isotope clearance technique. 3. Adenosine (infused in steps from 40 to 80 micrograms min-1 kg-1 into a central vein) elicited a gradual reduction in the peripheral vascular resistance to less than 50% of the basal level. There was a slight increase in the systemic blood pressure, but the pulmonary arterial and the ventricular filling pressures were unchanged. Cardiac output was doubled, accomplished by a combination of a positive chronotropic effect and an increase in stroke volume, which may be secondary to diminished peripheral resistance. 4. Skin blood flow increased by 100% at 50 micrograms of adenosine min-1 kg-1, whereas splanchnic blood flow rose significantly at 60 micrograms of adenosine min-1 kg-1. Blood flow in the calf, gastrocnemius muscle and adipose tissue did not change significantly. 5. Arterial concentrations of noradrenaline and adrenaline increased by 62 and 43%, respectively, during infusion of adenosine. Arterial levels of glycerol were depressed by more than 50%, but those of glucose and pyruvate were unchanged. 6. In conclusion, exogenous adenosine caused a marked systemic vasodilatation, with different responsiveness in the investigated vascular beds.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemodynamic and metabolic effects of infused adenosine in man. 216 2

Low cardiac output in acute heart failure can result in a functional impairment of organs, when tissue hypoxia occurs and cardiogenic shock develops. To restore cardiac output, various forms of therapy can be considered. Fluid replacement is sometimes beneficial in acute situations where oedema can reduce effective plasma volume. Vasodilators are often contra-indicated in shock, when arterial pressure is usually low. Inotropic therapy consists primarily of the administration of adrenergic agents. Dopamine and noradrenaline can be indicated in severe hypotension, to maintain coronary perfusion. Dobutamine is the catecholamine of choice to increase myocardial contractility. However, decreased responsiveness of the myocardial receptors to adrenergic stimulation rapidly becomes an important limitation. Phosphodiesterase inhibitors represent an interesting option to increase contractility, also by increasing cyclic AMP levels in the myocardium. In this respect, the combination of phosphodiesterase inhibitors with adrenergic agents is attractive. The additional vasodilatory properties of these agents can contribute to the increase in cardiac output with limited risk of further reduction in arterial pressure. In 13 patients with cardiogenic shock persisting despite the use of adrenergic agents, the addition of enoximone, 0.5 mg/kg, resulted in significant increases in cardiac index and stroke volume index and a significant decrease in pulmonary artery balloon occlusion pressure without consistent change in mean arterial pressure. In 8 patients, a second infusion of 0.5 g/kg amplified these effects. All but one of these patients survived the episode of cardiogenic shock, and 5 patients were discharged alive. In some cases, even lower doses of enoximone resulted in dramatic increases in cardiac output and oxygen transport in patients already treated with dobutamine with limited success.
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PMID:The role of enoximone in the treatment of cardiogenic shock. 217 30

In 14 patients with heart failure (New York Heart Association class 2-3) and sinus rhythm the carotid sinus baroreceptors were stimulated to induce a reflex mediated decrease of sympathetic efferent activity and a simultaneous increase in vagal tone. Five patients were in severe heart failure (New York Heart Association class 3) with raised plasma concentrations of noradrenaline at rest (2.99 (0.86) nmol/l (mean (SD)) and nine patients had less severe heart failure (class 2.2 (0.2)) and normal plasma concentrations of noradrenaline at rest. The haemodynamic responses during arterial baroreceptor stimulation were different in both groups. In all five patients with severe heart failure cardiac output increased whereas in the nine patients with less severe heart failure it was unchanged or decreased. The increase of cardiac output in the group with severe heart failure was solely the result of a significant increase of stroke volume index (by 9 (2) ml/m2). In the nine patients with less severe heart failure stroke volume remained unchanged but heart rate decreased significantly by 7 (2) beats/min during baroreceptor stimulation. These data show that an integrated change of autonomic activity consisting of a decrease in sympathetic tone and an increase in vagal activity leads to an increase of stroke volume in patients with severe heart failure and hence to haemodynamic improvement.
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PMID:Haemodynamic changes caused by alteration of autonomic activity in patients with heart failure. 218 68

Influences of endothelium on contractions of aortic ring preparations from 15 to 17 weeks old stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched Wistar-Kyoto rats (WKY) were compared. Noradrenaline-induced contraction was potentiated by endothelium removal; the potentiation was greater in the WKY aorta. Noradrenaline (10(-5) M) induced a biphasic contraction in endothelium-intact WKY aorta, while endothelium-intact SHRSP aorta or endothelium-removed preparations of both strains showed a monophasic sustained contraction. The tension changes in high-K-induced contracture of the endothelium-intact preparation was less pronounced in both WKY and SHRSP aortae. The relaxation by acetylcholine (10(-5) M) of endothelium-intact aortae, precontracted with noradrenaline (5 X 10(-7) M), amounted to 78% in the WKY and to 44% in the SHRSP preparation. In endothelium-removed aortae, sodium nitroprusside induced a comparable relaxation in both WKY and SHRSP preparations. These results indicate that the endothelium plays an important role in controlling the noradrenaline-induced contraction and that the lower influence of endothelium in the SHRSP aorta is most likely due to a decreased activity of this endothelium.
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PMID:Decreased modulation by endothelium of noradrenaline-induced contractions in aorta from stroke-prone spontaneously hypertensive rats. 224 32

We studied the relationships between adrenaline and noradrenaline and factors associated with arteriosclerosis to determine whether catecholamines contribute to the atherogenetic process. We investigated the effects of adrenaline and noradrenaline on cultures of vessel wall cells from rats and analyzed plasma catecholamine levels in humans exposed to atherogenic risk factors, undergoing hemodialysis treatment or following myocardial infarction or stroke. I. Cultured endothelial and smooth muscle cells from vessel walls exhibited enhanced proliferation when exposed to adrenaline or noradrenaline. This indicates that catecholamines trigger the activation of vascular wall cells in vitro. Such activation, the unspecific mesenchymal reaction, is the predominant characteristic change in early atherogenesis. II. In individuals subjected to the atherogenic risk factors smoking, essential hypertension and mental stress, plasma adrenaline concentrations were statistically significantly elevated. Mental stress also caused significantly elevated plasma noradrenaline levels. Plasma noradrenaline concentrations were also elevated in smoking and hypertensive individuals when compared with certain controls, but the differences failed to be statistically significant. III. In dialysis patients, plasma adrenaline and noradrenaline concentrations showed a positive correlation with the activity of the sclerotic process; i.e., plasma catecholamine concentrations increased with the severity of the disease. IV. Patients with persisting arteriosclerotic vascular disease, i.e., patients who had had a myocardial infarction or stroke, had significantly elevated plasma adrenaline and/or noradrenaline levels as late as one year after the event. The results of our investigations suggest that adrenaline and noradrenaline may act as chemical mediators during atherogenesis in man, thus contributing to the development and subsequent complications of arteriosclerosis.
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PMID:Adrenaline and noradrenaline as possible chemical mediators in the pathogenesis of arteriosclerosis. 224 66

The purpose of this work was to study the contractile activity of intracerebral microarterioles and their sensitivity to the calcium antagonist nimodipine. Potassium depolarization evoked contraction and rhythmic activity that was blocked by nimodipine (IC50 0.08 nM). High concentrations of noradrenaline and prostaglandin F2 alpha were needed to elicit a contractile response. Intracerebral microarterioles were very sensitive to endothelin (ED50, 0.2 nM). The contractions evoked by concentrations of endothelin lower than or equal to ED50 were relaxed by nimodipine, which also blocked the amplified response to potassium chloride depolarization occurring with subthreshold concentrations of endothelin. We discuss these observations in relation to brain ischemia.
Stroke 1990 Dec
PMID:Calcium antagonists and vasoconstrictor effects in intracerebral microarterioles. 226 Jan 50

Changes of macro- and microcirculation during haemodialysis and fluid removal are probably dependent on ultimate fluid status and on the efficacy of various regulation mechanisms, especially the catecholamines. This was studied in 20 chronic dialysis patients. Pre- and postdialysis stroke volume, mean arterial pressure, heart rate and systemic vascular resistance were measured. Furthermore, microcirculation was studied by Laser Doppler flow and by intravital microscopy of finger nail fold, measuring red blood cell velocity and capillary density. Pre- and postdialysis noradrenaline and adrenaline were measured. Nine patients proved to be hypovolaemic after dialysis (group I) and 11 patients proved to be normovolaemic or less hypervolaemic (group II) according to vena cava inferior parameters. There was a significant decrease of mean arterial pressure and stroke volume in group I, and an increase of heart rate, whereas in group II there was only a decrease of mean arterial pressure. Systemic vascular resistance did not change in both groups. Noradrenaline decreased although not significantly in both groups, whereas in group I adrenaline increased significantly. There was a significant decrease of skin perfusion in group I, whereas in group II there was a significant increase. Capillary density increased significantly in group II after reaching normovolaemia. Underhydration was leading to a decrease of skin microcirculation on the basis of a decrease of stroke volume and an increase of adrenaline levels. In hypervolaemic patients, who were ultrafiltrated to normovolaemia, skin microcirculation improved on the basis of a decrease of arterial and venous pressure and consequently a decrease of the myogenic response as a local autoregulatory effect.
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PMID:Influence of fluid removal during haemodialysis on macro- and skin microcirculation. Haemodynamic pathophysiologic study of fluid removal during haemodialysis. 231 27

In 12 patients with primary hypertension (World Health Organization stage 2) inadequately controlled by chronic standard triple therapy, hydralazine was replaced by felodipine, a new vasodilating dihydropyridine derivative, and the acute effects of the drug on central and renal hemodynamics were monitored. Following baseline measurements, an oral solution of felodipine (0.075-0.1 mg/kg) was given. Fifteen minutes after intake of felodipine, a significant hypotensive response was observed, and the maximal response (23% reduction of mean arterial pressure) occurred after 30 min. There was a linear relationship between the changes in mean arterial pressure and log plasma concentration of felodipine. Cardiac output (dye dilution) increased during maximal blood pressure reduction, from 5.3 +/- 1.0 to 6.6 +/- 2.4 L/min (p less than 0.01), partly because of increased heart rate from 57 +/- 4 to 65 +/- 9.1 beats/min (p less than 0.01) and partly because of increased stroke volume from 93 +/- 14 to 104 +/- 33 ml (p less than 0.05). Renal plasma flow (para-aminohippuric acid clearance) increased significantly (p less than 0.05) from 343 +/- 138 to 391 +/- 154 ml/min, while glomerular filtration rate ([51Cr]EDTA clearance) did not change. Arteriovenous noradrenaline difference increased 36% during felodipine therapy, when corrected for blood flow increase. We conclude that felodipine is a calcium inhibitor with potent vasodilating properties.
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PMID:Systemic and renal hemodynamic effects of single oral doses of felodipine in patients with refractory hypertension receiving chronic therapy with beta-blockers and diuretics. 241 Jun 88

Correlation between blood pressure (BP) and total peripheral vascular resistance (TPR), hypotensive mechanisms of calcium antagonists, and cardiovascular responses to norepinephrine with and without administration of calcium antagonists were investigated in normotensive and genetic essential hypertensive humans. Supine resting decreased BP, heart rate (HR), stroke volume (SV), and cardiac output (CO), and, in contrast, it increased TPR. After 1 h supine rest, BP was positively correlated with TPR (r = 0.710; number = 45, p less than 0.001), but it was not correlated with CO. Intravenous infusion of the calcium antagonist diltiazem lowered BP and TPR, without apparently affecting HR, SV, and CO. In contrast, the calcium antagonist nifedipine diminished BP and TPR while increasing HR, SV, and CO. Norepinephrine elevated BP and TPR and decreased HR, SV, and CO. Prior administration of nifedipine inhibited elevation of TPR after treatment with norepinephrine. In contrast, prior administration of propranolol did not inhibit norepinephrine-induced BP and TPR elevation. From the results it may be concluded that elevation of BP is dependent on alteration of TPR, but not CO, in essential hypertensive humans. The arterial vasodilating effects of calcium antagonists induce a fall in both TPR and BP and inhibit norepinephrine-induced TPR increase. This suggests that abnormal contraction and relaxation of systemic arterial smooth muscle is a primary cause of the development and persistence of high BP in genetic (main gene) essential hypertensive humans.
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PMID:Pathophysiological background for the use of calcium antagonists. 241 8

Ketanserin, which preferentially blocks 5-HT2-serotonergic receptors, was injected intravenously (i.v.) to patients with congestive heart failure in a bolus dose of 10 mg, followed by an i.v. infusion of 3 mg/h over a period of 4 h. The drug caused a decrease in total peripheral resistance and, conversely, an increase in stroke volume. Right atrial and pulmonary artery pressures were decreased. Plasma noradrenaline rose twofold over the basal levels shortly after injection, but showed a distinct fall 2 h after beginning of the treatment. The concentrations of ketanserin in plasma after bolus injection approximated 100-150 ng/ml. The sympathoneuronal and sympathoadrenal reaction during tilting were increased after i.v. injection of 10 mg ketanserin in volunteers. The noradrenaline and adrenaline levels in plasma rose significantly more when compared with values before the injection of the drug. In vitro as well as in vivo ketanserin exerts a concentration-dependent inhibitory effect on the active transport of serotonin and catecholamines (dopamine, noradrenaline, adrenaline) into human platelets. Considering platelets as a model of the sympathetic neurons, the inhibition of reuptake of catecholamines by ketanserin could contribute to the observed increase in circulating catecholamines after injection of the drug.
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PMID:Effect of ketanserin on hemodynamics, plasma-catecholamine concentrations, and serotonin uptake by platelets in volunteers and patients with congestive heart failure. 241 24


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