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

The potential role of adrenaline, both circulating and in the central nervous system, in the maintenance of high blood pressure was examined in stroke-prone spontaneously hypertensive rats (SHRSP). alpha-Monofluoromethyldopa, a long-lasting inhibitor of dopa decarboxylase, was used to induce rapid depletion of central and peripheral catecholamine stores. Subsequent inhibition of phenylethanolamine-N-methyltransferase (PNMT) allowed the gradual restoration of dopamine and noradrenaline but not adrenaline, resulting in a greater relative depletion of adrenaline. Adrenaline was almost totally depleted in the circulation and peripheral tissues. The resting level of blood pressure, however, was unaffected, excepting after administration of a vasopressin (AVP) antagonist. Moreover, there was no reduction in the magnitude of acute pressor responses to electrical stimulation of the rostral ventrolateral medulla oblongata (C1 area), despite extensive loss of adrenaline from the brainstem and spinal cord. The results suggest that adrenaline contributes to the resting level of blood pressure but that its loss can be offset by the pressor activity of AVP. Thus neither central nor peripheral adrenaline stores appear to be essential for the maintenance of hypertension or for centrally-evoked vasoconstriction in adult SHRSP.
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PMID:Effects of depleting central and peripheral adrenaline stores on blood pressure in stroke-prone spontaneously hypertensive rats. 194 21

Haemodynamic and neurohumoral responses to head-up tilt were measured in 28 elderly patients with postural hypotension (EPPH) and 12 healthy elderly subjects (HE). There were no differences in catecholamines between the groups and only noradrenaline increased on tilt (P less than 0.001). Plasma renin activity and aldosterone were similar in HE and EPPH in the supine and tilt positions. In both groups vasopressin increases (P = 0.032), and plasma volume decreases were the same (P = 0.673). Supine EPPH had higher heart rates (P = 0.019) but similar cardiac indices (P = 0.621). Both had similar changes on tilting (P = 0.975 and P = 0.341). Stroke volume decrease was higher in HE (35%) than EPPH (23%; P less than 0.001). HE showed an increase in peripheral resistance on tilting with no change in EPPH (P = 0.005). EPPH had larger coefficients of variation for all variables. The differences in haemodynamic responses and the similarity of neurohumoral responses during tilting suggest end-organ failure in EPPH with individual variations. Postural hypotension in old age is not a single entity.
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PMID:Haemodynamic and neurohumoral responses in elderly patients with postural hypotension. 196 49

The haemodynamic and autonomic nervous system effects of the DA2 agonist, SK & F 101468, have been studied in anaesthetised cats. SK & F 101468 inhibited the tachycardia response to cardiac accelerans nerve stimulation. The inhibition, reversed by L-sulpiride a selective DA2 receptor antagonist, was dose-dependent over the dose range 10-50 micrograms.kg-1 and there was proportionally greater inhibition of the responses to low rather than high frequency stimulation. There was evidence that SK & F 101468-A inhibited sympathetically mediated reflexes, but even at high doses, of up to 500 micrograms.kg-1, there was no inhibition of end-organ responsiveness to noradrenaline, isoprenaline or acetylcholine nor of the bradycardia caused by vagus nerve stimulation. SK & F 101468-A produced falls in blood pressure and heart rate at 50 and 500 micrograms.kg-1, but stroke volume, aortic blood flow and total peripheral resistance, were only slightly affected. These effects of SK & F 101468 in the intact cardiovascular system are consistent with an action on presynaptic receptors at sympathetic nerve endings to reduce transmitter release and thereby selectively reduce responses to sympathetic nerve stimulation.
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PMID:Autonomic and haemodynamic responses to SK & F 101468 (ropinirole), a DA2 agonist, in anaesthetised cats. 196 2

To study the haemodynamic and neurohumoral effects of nisoldipine (2 X 10 mg) vs captopril (3 X 25 mg), 24 patients with heart failure (New York Heart Association class II and III) due to coronary artery disease were treated in a randomized double-blind trial over 3 months. Both drugs were well tolerated. Clinical status was similarly improved in both groups, nisoldipine exerted an additional antiischaemic effect. Nisoldipine lowered the mean arterial pressure and capillary wedge pressure acutely and also after long-term treatment. The increase in cardiac index and stroke volume index, however, which was pronounced after acute administration, was no longer present after 3 months of therapy at rest and was abolished during exercise. Norepinephrine plasma concentration increased after the first dose, plasma renin activity did not change, and aldosterone plasma concentration showed a small insignificant decrease. Urine concentrations of norepinephrine and vasopressin were slightly elevated after the 3-month therapy. After captopril, mean arterial pressure and pulmonary capillary wedge pressure decreased acutely and at follow up. Cardiac index and stroke volume index increased significantly only during exercise at follow-up. Plasma renin activity was significantly elevated and aldosterone plasma concentration only slightly lowered. In contrast to what was seen with nisoldipine, plasma norepinephrine concentration and urine catecholamine and vasopressin concentrations remained unchanged. In conclusion, the pronounced haemodynamic effects seen after the first dose of nisoldipine are mostly abolished after long-term treatment, probably due to neurohumoral counterregulation. The haemodynamic response to captopril is complete only after long-term treatment, without evidence of activation of the neurohumoral systems.
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PMID:Acute and long-term haemodynamic and neurohumoral response to nisoldipine vs captopril in patients with heart failure: a randomized double-blind study. 168 8

By subcutaneous insertion of osmotic minipumps leading to continuous infusion of l-adrenaline, we were able to induce hypertension in normotensive Wistar-Kyoto strain (WKY) rats which was shown to be completely reversible by application of the non-selective beta-adrenoceptor antagonist carvedilol. No consistent effect of adrenaline on heart rate could be observed. At least in rat heart, adrenaline replaced the original neurotransmitter noradrenaline in amine storage sites, the sum of all catecholamines remaining unchanged. By comparing tissue concentrations of endogenous amines of spontaneously hypertensive rats (SHR) and stroke-prone-SHR (SHR-SP) to the corresponding levels of their normotensive controls of the Wistar-Kyoto strain, we detected various differences in amine handling during the development of high blood pressure. Significant increases of adrenal gland catecholamines at the ages of 8 and 14 weeks are accompanied by striking alterations of catecholamine (CA) storage in other peripheral organs like the heart and kidneys. Most prominent increases, as compared to controls, were found in adrenaline concentrations in heart and kidney at all ages studied, with levels two to four times higher than the respective WKY concentrations. The results are compatible with a permissive role of adrenaline as a cotransmitter in the initiation and/or maintenance of hypertension. After incorporation into endogenous amine storage vesicles, e.g., of the heart, adrenaline is probably released, together with noradrenaline, upon nerve stimulation. By stimulating presynaptic beta 2-adrenoceptors, adrenaline is able to facilitate noradrenaline release and to enhance noradrenergic vasoconstriction. The resulting increase of peripheral sympathetic tone may be responsible for the pathogenesis of rat genetic and human essential hypertension, as well as for the triggering of myocardial infarction. The blockade of presynaptic beta-receptors is supposed to represent an important mechanism of action of non-selective beta-blocking agents. In the case of carvedilol, this effect is supported by additional antagonism at vascular alpha-adrenoceptors, leading to vasodilation.
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PMID:Adrenaline in cardiovascular diseases--effect of beta-adrenoceptor antagonists. 198 53

After completion of abdominal aortic graft, 29 patients received an i.v. infusion of placebo (n = 16) or clonidine 7 micrograms kg-1 (n = 13) over 120 min in a double-blind study. Cardiovascular variables were measured and plasma samples obtained up to 5 h after arrival in the recovery room, for assay of noradrenaline, adrenaline, vasopressin and renin concentrations. Noradrenaline, adrenaline and vasopressin concentrations decreased in the clonidine group throughout recovery (P less than 0.001, 0.05 and 0.05, respectively, vs placebo). Heart rate was less in the clonidine group (P less than 0.01). There was no significant difference in mean arterial pressure between groups. Stroke volume was larger (P less than 0.01) and there were fewer episodes of hypertension (P less than 0.05) and tachycardia in the clonidine group. In addition, a reduction in the number of circulatory interventions (P less than 0.05) and episodes of shivering was noted in the clonidine group. Mean (SD) postoperative volume requirements were larger in the clonidine group (total postoperative input: clonidine 1462 (604) ml; placebo 1064 (348) ml (P less than 0.05]. These data are consistent with the observation that clonidine modifies endocrine and circulatory status after major surgery.
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PMID:Effect of clonidine on the circulation and vasoactive hormones after aortic surgery. 199 45

Dopexamine hydrochloride is a novel compound with properties of DA1-dopaminergic and beta 2-adrenergic receptor agonism and neuronal noradrenaline uptake inhibition. It has been shown to produce beneficial renal and haemodynamic effects in patients with severe heart failure. We compared the haemodynamic effects of dopexamine (0.5 to 6 micrograms/kg/min) with those of dobutamine (5 to 25 micrograms/kg/min) in 9 patients with severe congestive heart failure. The two drugs were similar in their effects at peak infusion rates: heart rate increased (dopexamine 87 +/- 17 to 100 +/- 14; dobutamine 91 +/- 18 to 103 +/- 17 min-1), cardiac index increased (dopexamine 1.7 +/- 0.5 to 2.8 +/- 1.1; dobutamine 1.8 +/- 0.5 to 3.0 +/- 1.1 l.min-1.m-2) and systemic vascular resistance decreased (dopexamine 1553 +/- 221 to 1117 +/- 432; dobutamine 1721 +/- 347 to 1280 +/- 433 dyne.s.cm-5). Neither drug affected pulmonary artery wedge pressure (dopexamine 24 +/- 6 to 22 +/- 6; dobutamine 25 +/- 9 to 24 +/- 10 mm Hg). Dopexamine had significantly lower peak effects on left ventricular stroke work index (dopexamine 20 +/- 9, dobutamine 27 +/- 15 g.m.m-2, P less than 0.05) and cardiac power output (dopexamine 0.71 +/- 0.36, dobutamine 0.93 +/- 0.46 W, P less than 0.05). These haemodynamic effects, due largely to vasodilatation but with some contributory positive inotropy, indicate that dopexamine will be useful in the acute treatment of congestive heart failure.
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PMID:Comparison of the haemodynamic effects of dopexamine and dobutamine in patients with severe congestive heart failure. 201 Feb 43

The aim of this study was to investigate the effect of small alterations in the extracellular magnesium concentration on the tone of feline middle cerebral arteries and to examine the role of the endothelium in these responses. We measured the isometric tension of isolated arterial rings placed between two stainless steel wires in a tissue chamber containing Krebs-Henseleit solution aerated with a gas mixture containing 95% O2 and 5% CO2 at 37 degrees C. After precontraction with noradrenaline, a decrease of the extracellular magnesium concentration from 1.2 mM to 1.0 and 0.8 mM resulted in sustained relaxations, whereas elevation of the extracellular magnesium concentration from 0.8 mM to 1.2 mM caused an increase in vascular tone when the endothelium was intact. The magnesium deficiency-related dilations were absent in endothelium-denuded vessels and were inhibited by 5 x 10(-6) M oxyhemoglobin and 10(-5) M methylene blue, suggesting the involvement of an endothelium-derived relaxing factor in this vascular response. However, 5 x 10(-7) M nifedipine or 3 x 10(-5) M dichlorobenzamil did not affect the magnesium deficiency-related relaxations. Therefore, nifedipine-sensitive calcium channels or the sodium/calcium antiport system are not involved in this vascular action of magnesium. We conclude that small alterations in the extracellular magnesium concentration, possibly within the physiological range, are able to modify the basal formation and release of endothelium-derived relaxing factor and thus alter arterial smooth muscle tone in this vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Jun
PMID:Endothelium-dependent influence of small changes in extracellular magnesium concentration on the tone of feline middle cerebral arteries. 205 79

In a randomized double-blind study, the haemodynamic and anti-ischaemic effects of the new dihydropyridine calcium channel blocker isradipine (5 mg and 10 mg thrice daily (t.i.d.) were investigated over 1 week in nine patients with coronary artery disease and chronic effort angina and compared with nifedipine (20 mg t.i.d.) and placebo. In standardized exercise stress tests and exercise radionuclide ventriculography, haemodynamics improved under medication compared with placebo: resting end-diastolic and end-systolic volume index decreased on isradipine 5 mg, 10 mg and on nifedipine, and ejection fraction at rest increased with all medications. Resting mean arterial pressure was reduced compared with placebo accompanied by a decrease in systemic vascular resistance (P less than 0.05) and systolic wall tension (P less than 0.05). Cumulative ST-segment depression was significantly reduced by all three medications (-48%, -23%, -36%), while the increase in work capacity was insignificant. No significant change was found for either heart rate, double product, cardiac index, or stroke work index. Resting plasma levels of noradrenaline, adrenaline and renin activity increased with all three medications (except adrenaline at isradipine 5 mg). Isradipine has favourable effects comparable with those of nifedipine in patients with chronic stable angina and can be safely administered in these patients.
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PMID:Effects of the calcium antagonist, isradipine, and nifedipine on resting and exercise haemodynamics and the neurohumoral system in patients with stable chronic angina. 214 13

To study the hemodynamic characteristics of elderly hypertensives, elderly subjects (greater than or equal to 65 years old) were divided into normotensives (NT, n = 15), borderline hypertensives (BH, n = 10) and established hypertensives (EH, n = 20) and compared each group with similarly divided middle aged subjects (greater than or equal to 35 years old, less than 65 years old), NT (n = 23), BH (n = 112) and EH (n = 79). An attempt was also made to clarify what factor is most important regarding left ventricular hypertrophy (LVH) in elderly hypertensives. The results showed that with advancing age, cardiac output and stroke volume decrease (p less than 0.05), total peripheral resistance and volume-elasticity index increase (p less than 0.05), daily lability of systolic pressure increases and the baroreceptor slope increases. Furthermore, almost all of these tendencies are exacerbated by hypertension (p less than 0.05). With advancing age, pressure response to infused noradrenaline is enhanced (p less than 0.05), but on exercise, there are wide variations in each group and no distinct differences were observed. Echocardiographic examinations revealed LVH in 50% of elderly hypertensives. There were no apparent differences between both groups with or without LVH in their family and personal histories of hypertension, resting hemodynamics, hormonal examinations and hypertensive complications other than the heart. However, on exercise, the pressure response was more enhanced in the group with LVH than in the group without LVH (p less than 0.05). There was no significant correlation between resting systolic pressure (SBP) and left ventricular mass index (LVMi), but, there was relatively good correlation (r = 0.563, p less than 0.05) between SBP at peak exercise and LVMi. Using delta SBP/delta HR as a parameter of pressure responsibility on exercise test, 9 out of 10 patients with LVH showed above 1.0, while all of 10 patients without LVH showed under 1.0. Pressure response to infused noradrenaline seems to be more enhanced in the group with LVH than in the group without LVH. It was concluded that enhanced pressure responsiveness to recurring stress might induce or at least sustain LVH in hypertensives, due to enhanced alpha-adrenoceptor responsiveness.
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PMID:[Hemodynamics of elderly hypertensives]. 214 26


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