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

The acute haemodynamic effects of intravenous infusion of adenosine, a dilator of most vascular beds, were studied in 16 patients (seven with coronary artery disease, nine with normal coronary arteries) undergoing cardiac catheterization for investigation of chest pain. At the lowest dose used (4.3 mg min-1) adenosine increased minute ventilation by 44% (P less than 0.01, n = 11) and reduced pulmonary vascular resistance by 20% (P less than 0.05) without causing other significant haemodynamic changes. Symptoms, including chest discomfort in 14 patients and dyspnoea in 11, limited the maximum dose to 8.5 +/- 2.3 mg min-1 (mean +/- SD, 108 +/- 24 micrograms kg-1 min-1). At this dose, adenosine reduced pulmonary and systemic vascular resistance (by 38% and 34%, respectively) and increased heart rate (by 34%), stroke index (by 12%) and cardiac index (by 52%). Systemic blood pressure and right atrial pressure did not change. Unexpectedly, adenosine increased left ventricular end-diastolic pressure (LVEDP) (from 5 +/- 6 to 14 +/- 10 mmHg, n = 8), pulmonary capillary wedge pressure (from 3 +/- 2 to 10 +/- 5 mmHg, n = 16) and consequently mean pulmonary artery pressure (from 10 +/- 2 to 16 +/- 5 mmHg). Minute ventilation increased by 84% (n = 11), resulting in hypocapnia (PCO2: 31 +/- 3 mmHg, n = 8) and alkalosis (pH: 7.46 +/- 0.02, n = 8). Oxygen consumption was unchanged during the infusion, but increased by 21% 5 min post infusion. All effects were similar in patients with and without coronary artery disease. Adenosine therefore causes pulmonary and systemic vasodilation and respiratory stimulation. Symptoms and an increase in LVEDP of uncertain cause, which occur with high doses, may limit the use of adenosine as a systemic vasodilator in conscious subjects. However at lower doses adenosine causes selective pulmonary vasodilation which merits further study.
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PMID:Acute haemodynamic effects of intravenous infusion of adenosine in conscious man. 228 21

Adenosine receptor stimulation, such as by adenosine monophosphate (AMP), elicits systemic vasodilation that may be useful to control cardiac afterload during treatment of acute low-output cardiac failure. This study compared the hemodynamic effects of graded doses of sodium nitroprusside (SNP) with those of AMP when infused alone or in combination with the positive inotropic agent dopamine (DA) in anesthetized dogs. Both SNP (2-25 micrograms.kg-1.min-1) and AMP (200-2500 micrograms.kg-1.min-1) were effective vasodilators and reduced systemic vascular resistance and arterial pressure in a dose-dependent manner. Heart rate and cardiac index were increased by both agents. When compared at dosages that caused similar decreases in arterial pressure, cardiac index was increased more by AMP than by SNP. Also, AMP-induced vasodilation was associated with less tachyphylaxis. Sodium nitroprusside and AMP, at the dosages used, did not depress atrioventricular nodal conduction or antagonize DA-induced increases in renal blood flow. At equivalent decreases in mean arterial pressure, the increase from baseline in cardiac and stroke indices observed with AMP alone was further increased by the concomitant administration of DA. These results suggest that AMP and DA-AMP may offer significant advantages over SNP or DA-SNP in situations where elevation of cardiac output and reduction in afterload are required.
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PMID:Comparison of hemodynamic changes induced by adenosine monophosphate and sodium nitroprusside alone and during dopamine infusion in the anesthetized dog. 229 5

Adenosine, a potent vasodilator of both the peripheral and coronary vasculature, is increasingly used to produce controlled hypotension in the clinical and experimental setting. To define the influence of adenosine on left ventricular (LV) performance in conscious closed-chest dogs were studied six chronically instrumented autonomically blocked animals before and after the administration of 0.3, 0.6, and 1.2 microM.kg-1.min-1 infusions of adenosine. Systolic performance was quantified by the end-systolic pressure-volume (Pes-Ves) and stroke work end-diastolic volume (SW-EDV) relations. Active diastolic performance was quantified by the time constant of LV relaxation (T), whereas passive diastolic properties were assessed by comparing LV pressures at a common LV volume. Despite a decrease of mean arterial pressure of 51 mmHg, adenosine did not change the slope of the Pes-Ves relation or the end-systolic volume at a pressure of 100 mmHg. The slope of the SW-EDV relation was also unchanged, and its volume axis intercept was slightly reduced. There were no differences in T or in the diastolic pressure at a common LV volume. Thus adenosine appears to have little influence on systolic or diastolic LV performance aside from its marked affect on afterload, indicating it is a useful agent for producing controlled hypotension.
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PMID:Influence of adenosine on left ventricular performance in conscious dogs. 230 9

Adenosine has been proposed as a metabolic factor involved in the regulation of cerebral blood flow. The evidence in support of this hypothesis, presented in this review, includes information on the adenosine receptors associated with cerebral blood vessels, the synthesis and metabolism of adenosine, and the release of adenosine from the brain. Adenosine dilates cerebral blood vessels, acting at an A2 receptor. The critical evidence implicating an involvement of adenosine in cerebrovascular regulation is derived from experiments with adenosine antagonists and potentiators. The antagonists include methylxanthine adenosine receptor antagonists and the enzyme adenosine deaminase. Potentiators include transport inhibitors, enzyme inhibitors, and adenosine precursors. Adenosine has been implicated in vascular regulation during hypoxia/ischemia, hypercapnia, seizures, severe hypotension, and hypoglycemia. Adenosine possesses a number of properties that can be used to minimize neuronal degeneration during cerebral insults, such as ischemia, including vasodilatation, reduction of excitatory transmitter release, reduction of membrane calcium permeability, inhibition of platelets, and neutrophil aggregation. Several recent studies have demonstrated that manipulation of central adenosine tone can alter the extent of cerebral ischemic damage, indicating a potential new therapeutic approach for the treatment of stroke.
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PMID:Adenosine in the control of the cerebral circulation. 270 69

We investigated the effect of adenosine on neurogenic contraction of the canine cavernous carotid artery, using an isometric tension recording device and transmural nerve stimulation. Adenosine, in concentrations under 10(-5)M, had no relaxing effect on the contractions produced by high [K]o solution or 10(-5)M norepinephrine. Transmural nerve stimulation (stimulus: 1 msec duration, 100V intensity) evoked a frequency-dependent contraction, which was abolished by 3 X 10(-7)M tetrodotoxin. Adenosine in concentrations of 10(-6)M and 10(-5)M, inhibited the neurogenic contraction at each frequency, more so in the low frequency range. This inhibitory effect of adenosine was significantly antagonized by 10(-5)M theophylline. Pretreatment with 2 X 10(-8)M dipyridamole had no effect on neurogenic contractions, but augmented the inhibitory effect of adenosine. 10(-5)M theophylline did not augment the neurogenic contractions. The findings that both dipyridamole and theophylline failed to affect the neurogenic contractions in the absence of adenosine suggests that the presynaptic autoinhibition mechanism of adenosine may not be involved in neuromuscular transmission in this tissue. These results suggest that there is a presynaptic adenosine receptor in the nerve terminal which inhibits the release of neurotransmitter in canine cavernous carotid artery. It is also probable that the vasodilating effect of adenosine in the cavernous carotid artery is mainly due to its inhibitory effect on neurotransmission rather than to a direct relaxing effect on smooth muscle.
Stroke
PMID:Presynaptic inhibitory action of adenosine on neuromuscular transmission in the canine cavernous carotid artery. 300 84

Adenosine, administered intravenously (0.25 mg/kg-1/min-1) to rabbits with experimental myocardial infarction, produced a drop in arterial pressure and total peripheral resistance, normalized stroke volume, increased ATP content at the margin of the infarcted area, and reduced LDG activity and increased SDG activity in the ischemized region.
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PMID:[Hemodynamic and metabolic effects of adenosine in experimental myocardial infarction]. 323 Jul 62

The effects of adenosine on central and myocardial hemodynamics and metabolism were evaluated during fentanyl anesthesia (100 micrograms.kg-1) in six patients with peripheral vascular disease. Adenosine was intravenously infused, at a rate of 90 +/- 20 (SEM) micrograms.kg-1.min-1, to reduce mean arterial blood pressure by approximately 20% (23 +/- 2% SEM, from 82 +/- 3 to 63 +/- 3 SEM mmHg) during a 20-min period. Systemic and pulmonary vascular resistance indices decreased by 36 +/- 3 and 32 +/- 6% (SEM), and cardiac index increased by 18 +/- 5%. Heart rate, ventricular filling pressures, and whole body oxygen consumption were not affected by adenosine. Despite the reduced mean arterial blood pressure, coronary sinus flow increased by 128 +/- 26% (SEM) in parallel with a 96 +/- 11% (SEM) increase in coronary sinus oxygen content. Left and right ventricular stroke work indices, as well as myocardial oxygen consumption, were maintained. ECG (12-lead) demonstrated signs of ischemia in one subject, while myocardial lactate uptake was unchanged in all subjects. In conclusion, adenosine-induced hypotension in patients with peripheral vascular disease increased cardiac index without affecting myocardial work, whole body, and myocardial oxygen consumptions. The marked increase in coronary sinus blood flow, indicating coronary vasodilation, was not related to increased myocardial work. Further information regarding myocardial effect of adenosine in patients with ischemic heart disease is warranted.
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PMID:Effects of adenosine-induced hypotension on myocardial hemodynamics and metabolism in fentanyl anesthetized patients with peripheral vascular disease. 334 97

We have studied cerebral vascular effects of forskolin, a drug which stimulates adenylate cyclase and potentiates dilator effects of adenosine in other vascular beds. Our goals were to determine whether forskolin is a cerebral vasodilator and whether it potentiates cerebral vasodilator responses to adenosine. We measured cerebral blood flow with microspheres in anesthetized rabbits. Forskolin (10 micrograms/kg per min) increased blood flow (ml/min per 100 gm) from 39 +/- 5 (mean +/- S.E.) to 56 +/- 9 (p less than 0.05) in cerebrum, and increased flow to myocardium and kidney despite a decrease in mean arterial pressure. Forskolin did not alter cerebral oxygen consumption, which indicates that the increase in cerebral blood flow is a direct vasodilator effect and is not secondary to increased metabolism. We also examined effects of forskolin on the response to infusion of adenosine. Cerebral blood flow was measured during infusion of 1-5 microM/min adenosine into one internal carotid artery, under control conditions and during infusion of forskolin at 3 micrograms/kg per min i.v. Adenosine alone increased ipsilateral cerebral blood flow from 32 +/- 3 to 45 +/- 5 (p less than 0.05). Responses to adenosine were not augmented during infusion of forskolin. We conclude that forskolin is a direct cerebral vasodilator and forskolin does not potentiate cerebral vasodilator responses to adenosine.
Stroke
PMID:Effects of forskolin on cerebral blood flow: implications for a role of adenylate cyclase. 381 Jul 33

Adenosine receptors have been identified on brain cortical membranes and microvascular preparations. However, they have not been demonstrated on specific microvascular elements in isolation. 2-3H-chloroadenosine was used as a ligand to investigate the presence of adenosine receptors on isolated mouse cerebral smooth muscle membranes. The binding studies reveal the presence of a high affinity binding site with a Kd value of 33.3 nM and a maximal binding capacity (Bmax) of 283 fmol/mg protein. These findings demonstrate that there is an adenosine receptor on cerebral smooth muscle membranes.
Stroke
PMID:Demonstration of adenosine receptors on mouse cerebral smooth muscle membranes. 608 2

The effect of intra-arterial adenosine on cerebral blood flow was studied in 11 anesthetized dogs. In a first group of 6 dogs, adenosine was infused into a vertebral artery for 40 minutes at a dose of 0.3 to 0.5 mg/kg/min. Blood flow was determined before, during and after the adenosine infusion using the radioactive microsphere technique. In a second group of 5 dogs, adenosine (3 +/- 1 mcg/kg/min) was infused in a similar manner after potentiating its effect with intravenous dipyridamole, and measurements before and after the intravenous dipyridamole and during and after the adenosine infusion were performed. Systemic arterial pressure and blood gases were unchanged throughout the experiment in both groups of dogs. Blood flow to the cerebral hemispheres, cerebellum, brain stem, paraspinous and temporalis muscles remained unchanged during the adenosine infusion in both groups of dogs. Adenosine has been implicated as an active agent in the vasodilatory component of cerebral autoregulation. A controversy exists as to whether intervascular or only interstitial adenosine is of physiologic importance. These findings suggest that intra-arterial adenosine does not play a significant role in the regulation of cerebral blood flow.
Stroke
PMID:Intravertebral artery adenosine fails to alter cerebral blood flow in the dog. 650 17


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