Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenosine and adenine compounds (AMP, cyclic AMP, ADP and ATP) markedly dilated feline and human pial arteries in vitro, the effect being more prominent with increasing tone of the vessel (active tonic contraction induced by prostaglandin F 2 alpha or serotonin). In contrast, the various adenine compounds were unable to produce any dilation of extracranial arteries tested (branches of lingual, external maxillary, and superficial temporal arteries). The degree of dilatation depended upon the perivascular potassium concentration, so that low potassium increased Emax and reduced ED50 values. Possible involvement of adenine compounds in the vasodilatory phase of the migraine attack is discussed.
Stroke
PMID:Adenine compounds: cerebrovascular effects in vitro with reference to their possible involvement in migraine. 21 63

The cervicovaginal epithelium of neonatal mice produces a material with specific antigenic properties (CVA) and this material is produced in increased amounts after estradiol treatment. Using a cytochemical method, estradiol treatment was shown to result in an increase of adenylate cyclase activity in the same epithelium. When d-propranolol is injected together with estradiol, the increase in CVA is inhibited, while the hormone-induced proliferation of epithelial cells is not influenced. When adenylate cyclase activity is studied under identical conditions, the estradiol-promoted increase in enzyme activity is largely counteracted by d-propranolol. These findings would suggest that Adenosine 3"5"-cyclic monophosphate (cAMP) has a role in some, but not all, estradiol-mediated effects in the neonatal cervicovaginal epithelium.
 ...
PMID:Effects of d-propranolol and estradiol on the cervicovaginal epithelium. 99 Dec 44

Adenosine diphosphate (8 mg per minute for five minutes) was infused into the carotid artery of 63 rabbits. The effects were twofold: systemic hypotension and platelet aggregation in the cerebral circulation. As a consequence of the last effect, platelet emboli were produced which occluded cerebral arteries in a number and size sufficient to cause cerebral ischemia. Areas of focal ischemia were observed through a cranial window, and documented with antipyrine autoradiography. Platelet thrombi were almost entirely transient, being fragmented and removed within a very short time of cessation of ADP infusion. Consequently, no permanent tissue damage ensued. This experimental model approaches the spontaneous transient ischemia attacks (TIAs) in man, demonstrating that these can be caused by pure platelet emboli. A high cholesterol diet administered for two months prior to ADP infusion did not enhance the effect of the procedure or make the platelet aggregation and the following ischemia longer in duration or more severe.
Stroke
PMID:Animal model of TIA: an experimental study with intracarotid ADP infusion in rabbits. 119 26

The rat hearts were subjected to 60-min ischemia by left coronary artery ligation followed by 60-min reperfusion, involving intravenous adenosine inosine or guanosine given in a dose of 1 mg/kg.min-1 in the first 30 minutes of reperfusion. Ischemia and subsequent reperfusion caused a progressive decrease in cardiac output and coronary blood flow. Adenosine was found to enhance coronary blood flow and increase cardiac and stroke outputs. Inosine produced nearly the same, but less pronounced effect. Guanosine increased cardiac output without changing coronary blood flow.
 ...
PMID:[Hemodynamic effects of purine nucleosides in regional ischemia and reperfusion]. 140 75

Hyperkalaemia-induced hypopolarization of the sarcolemnal membrane during standard crystalloid cardioplegic arrest potentiates calcium influx during reperfusion and is associated with depletion of high-energy phosphate reserves. Adenosine has been shown to induce fast cardiac arrest whilst preserving membrane hyperpolarization in an isolated rat heart model. In this study we compared the efficacy of adenosine, both as an arresting agent and as an ultrastructural, haemodynamic and high-energy phosphate preserving agent, in an in situ global ischemia model in the baboon with St. Thomas' Hospital solution No. 2 (ST2; n = 8) and with Krebs-Henseleit buffer (KHB; n = 7). The addition of 10 mM adenosine to the non-cardioplegic KHB (ADO; n = 8) improved haemodynamic recovery significantly in terms of cardiac index (91.6% +/- 7.2 vs 59.9% +/- 9.9) and stroke volume index (101.6% +/- 8.9 vs 55.6 +/- 10.0) and was not statistically distinguishable from the ST2 with regard to cardiac index (91.6% +/- 7.2 vs 94.8% +/- 5.8), stroke volume index (101.6% +/- 8.9 vs 114.0% +/- 8.3) or left ventricular dP/dt (73.1% +/- 9.9 vs 87.0% +/- 12.4). Adenosine triphosphate was best preserved with ADO (103.5% +/- 21.1 vs 67.9% +/- 9.3 and 48.5% +/- 8.7) although this was not statistically significant. This suggests therefore that the mechanism of cardioprotection by adenosine occurs by means other than its role as high-energy phosphate precursor.
 ...
PMID:Adenosine cardioplegia: reducing reperfusion injury of the ischaemic myocardium? 175 47

Possible enhancement of myocardial protection during ischemia and reperfusion by administration of adenosine was evaluated in a pig heart model. Adenosine (100 micrograms/kg/min) was infused into the aortic root during ischemia in group AI (n = 5) and into the right atrium during reperfusion in group AR (n = 6). Group C (n = 6) served as controls. During cardiopulmonary bypass the hearts were subjected to 30 min of normothermic ischemia and 15 min of reperfusion before weaning. In group AI the stroke work index 30 and 90 min after ischemia and the mean arterial pressure 30 min after ischemia were significantly higher than in group C. These parameters did not differ significantly between groups AR and C. All groups showed decrease in myocardial adenosine triphosphate (ATP) and adenylate charge potential (ACP) during ischemia and partial (ATP) or complete (ACP) restoration after ischemia. Adenosine infusion into the aortic root during ischemia (adenosine cardioplegia) thus resulted in improved postischemic heart function, although biochemical correlates in ATP and ACP were not apparent.
 ...
PMID:Effects of adenosine infusion on the pig heart during normothermic ischemia and reperfusion. 178 Jul 37

The effects of adenosine on myocardial blood flow and metabolism, central hemodynamics, and the intrapulmonary shunt fraction were investigated. Fourteen patients with two- or three-vessel coronary artery disease and with an ejection fraction greater than 0.5 were studied in the operating room following sternal closure after elective coronary artery bypass grafting. Systemic and pulmonary hemodynamics and global (coronary sinus), as well as regional myocardial blood flow (great cardiac vein flow), and metabolic variables were measured. Adenosine was given in infusion rates of 15, 30, 60, and 120 micrograms.kg-1.min-1. Infusion rates of 60 and 120 micrograms.kg-1.min-1 decreased mean arterial blood pressure (11% and 16%, respectively), systemic vascular resistance index (30% and 43%), and pulmonary vascular resistance index (24% and 31%), increased cardiac index (25% and 45%), heart rate (14% and 15%), and stroke volume index (9% and 25%), and had no effect on central filling pressures. These infusion rates doubled the intrapulmonary shunt fraction and decreased arterial O2 tension by 26%. Great cardiac vein flow and coronary sinus flow increased 60% with adenosine infusion of 30-60 micrograms.kg-1.min-1 and 120% with 120 micrograms.kg-1.min-1. The ratio of great cardiac vein flow to coronary sinus flow, regional myocardial oxygen consumption, and mean regional lactate extraction and uptake were not significantly altered by adenosine. Adenosine caused a significant depression of the ST segment at infusion rates of 60 and 120 micrograms.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of adenosine on myocardial blood flow and metabolism after coronary artery bypass surgery. 845 98

Basic neuroscience research findings during the past five years have established a clear relationship between the excitatory amino acid (EAA) neurotransmitters (glutamic and aspartic acid) and various pathological states. A major mechanism of neural tissue degeneration following cerebral ischemia, and perhaps other neurodegenerative diseases, seems to involve overactivity of the EAA system in brain. This process is called delayed excitotoxicity and it has become a focal point for the design of new drugs that inhibit its course (EAA receptor blockers). Very recently it has been shown that it is possible to block delayed excitotoxicity using adenosine A1 receptor agonists which inhibit EAA release pre-synaptically. This approach is very effective in reducing post-stroke neurological damage in a number of animal models and has certain advantages when compared to the EAA receptor blocker strategy. Adenosine agonists not only inhibit excitotoxicity but they also block granulocyte activation and the capillary no-reflow phenomenon which results. An additional adenosinergic approach involves brain permeable adenosine uptake blockers which would serve to increase adenosine levels somewhat selectively at ischemic foci thereby inhibiting EAA release. The adenosinergic approach to stroke therapeutics may be a potentially effective strategy for new drug development in neurology, and may have general applicability to other neurodegenerative disease states where excitotoxicity is being implicated.
 ...
PMID:Adenosinergic approaches to stroke therapeutics. 197 12

The effects of adenosine and sodium-nitroprusside (SNP) on central and myocardial haemodynamics and metabolism were evaluated during fentanyl anaesthesia (100 micrograms.kg-1) in six patients with peripheral vascular disease. The investigation was performed during stable anaesthesia, before scheduled abdominal aortic graft surgery. Adenosine and SNP were infused intravenously in random order over 20 min, leaving a 30-min control period in between. The vasodilators were titrated in order to reduce mean arterial pressure by approximately 25%. Adenosine (90 +/- 20 micrograms.kg-1.min-1) reduced mean arterial pressure from 10.9 +/- 0.3 to 8.4 +/- 0.4 kPa (82 +/- 3 to 63 +/- 3 mmHg), and SNP (0.7 +/- 0.1 micrograms.kg-1.min-1) from 11.0 +/- 0.2 to 8.4 +/- 0.3 kPa (83 +/- 3 mmHg to 63 +/- 3 mmHg), during the hypotension period. Cardiac index remained unaffected during induced hypotension with both vasodilators, while heart rate increased during SNP infusion (8 +/- 3%) and remained unaffected with adenosine. Left ventricular stroke work index and myocardial oxygen consumption decreased during SNP infusion (33 +/- 3% and 17 +/- 5%, respectively), while these parameters were unchanged with adenosine. Adenosine hypotension increased coronary sinus flow 1-2 fold (128 +/- 26%), together with increased coronary sinus oxygen content (96 +/- 11%). In contrast, coronary sinus flow decreased during SNP hypotension (-15 +/- 4%) with unaffected coronary sinus oxygen content. It is concluded that adenosine, in contrast to SNP, is associated with a hyperkinetic myocardial circulation.
 ...
PMID:Myocardial effects of adenosine- and sodium nitroprusside-induced hypotension: a comparative study in patients anaesthetized for abdominal aortic aneurysm surgery. 203 28

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)
 ...
PMID:Haemodynamic and metabolic effects of infused adenosine in man. 216 2


1 2 3 4 5 6 7 8 Next >>