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)

The time course of changes in monoamine metabolism in ischemic striatum was assessed by measurement of levels of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-HT) and 5-hydroxy-indole-acetic acid (5-HIAA) 2, 4, 7 and 16 hours after irreversible unilateral carotid ligation in Mongolian gerbils with stroke. DA was reduced to 30% of the level in the contralateral non-ischemic striata by 2 hours after stroke, but DOPAC was significantly elevated (p less than 0.01) to 227%, while HVA remained equal to control. At 4 hours after stroke, DOPAC was 86% of the contralateral non-ischemic striata but HVA had risen to 130%. At 7 hours after stroke, DOPAC in the ischemic striata was 148% of control, while HVA remained at 133%. By 16 hours after stroke, DA, DOPAC and HVA were depleted from the ischemic striata, corresponding to the time course for irreversible damage to the neurotransmitter uptake function of nerve terminals. 5-HT levels in the ischemic striata were 30% of control at 2 hours, 46% at 4 hours, 30% at 7 hours and 21% at 16 hours, while 5-HIAA remained equal to control throughout the time course. These studies indicate that monoamine metabolism continues in ischemic striatum for up to 8 hours after the onset of stroke following irreversible unilateral carotid ligation in the Mongolian gerbil, but metabolism of DA is disrupted by 16 hours after stroke while metabolism of 5-HT continues.
 ...
PMID:Metabolism of monoamine neurotransmitters in the evolution of infarction in ischemic striatum. 244 1

Blood serotonin levels have been measured by spectrofluorometry in 145 patients with various manifestations of acute disorders of the cerebral circulation (ADCC): with ischemic stroke, cerebral hypertensive crises, transient impairments of the cerebral circulation, and with circulatory encephalopathy (DE) in the presence of arterial hypertension combined with atherosclerosis. In ADCC patients the blood serotonin has been measured 7 times, in DE ones 3 times. This level has been found changed in the patients with ischemic stroke and with cerebral hypertensive crises for a long time after the cerebral circulation impairment. Serotonin levels correlated with the condition severity and course in ADCC and DE. The vestibulocerebellar syndrome in DE has been treated more effectively, particularly with trental. The blood serotonin level may be regarded as a prognostic criterion of the disease outcome and of the treatment efficacy.
 ...
PMID:[Dynamics of blood serotonin contents in acute disorders of cerebral circulation and circulatory encephalopathy]. 279 19

Behavioral, physiologic and exertional fatigue is differently defined, though symptoms are similar. The beneficial effect of amantadine on fatiguability in multiple sclerosis is accompanied by neuropeptide and lactate changes in the circulation. Exercise sometimes overwhelms temperature regulating mechanisms and may be associated with heat stroke. Endogenous opioids are markedly increased in the circulation during heat stroke and the use of specific opioid antagonists therapeutically has been proposed for heat stroke. Sympathetic activity changes in endurance trained subjects and vasoconstrictor responses are markedly attenuated. Similar changes occur in parasympathetic function which can be abnormal in up to 90% of endurance trained subjects. Hormonal secretion during prolonged exertion is altered and the normal signals (inhibiting or activating feedback mechanisms) are different in endurance trained subjects. Altitude, associated with acute mountain sickness, is also accompanied by an increase in cranial bloodflow. Circadian and temporal variation in autonomic function are manifest by changes in mast cell numbers and 5-HT containing nerve fibers in temple skin of patients with cluster headache. The remission rate induced by vagal stimulation in subjects with intractable hiccups is also affected by circadian hormonal or neurogenic influences.
 ...
PMID:The autonomic nervous system and fatigue. 296 78

The goal of this study was to determine whether endothelium-dependent responses are impaired in the cerebral microcirculation of stroke-prone spontaneously hypertensive rats (SHRSP). We measured diameters of cerebral arterioles using intravital microscopy in normotensive rats (WKY) and SHRSP (6-8 mo old). Cerebral vasodilator responses to superfusion with adenosine, which is an endothelium-independent agonist, were similar in WKY and SHRSP. In contrast, cerebral vasodilator responses to superfusion with endothelium-dependent agonists were profoundly impaired in SHRSP. Acetylcholine (10(-4) M) increased pial arteriolar diameter 23 +/- 2% (means +/- SE) in WKY and did not change arteriolar diameter in SHRSP (-2 +/- 3%, P less than 0.05 vs. WKY). Serotonin (10(-5) M) increased pial arteriolar diameter 23 +/- 1% in WKY and, in contrast, reduced diameter 11 +/- 1% in SHRSP (P less than 0.05 vs. WKY). Nitroglycerin and acetylcholine produce vasodilatation by activation of guanosine 3',5'-cyclic monophosphate (cGMP). Nitroglycerin was used to determine whether impaired responses of cerebral arterioles in SHRSP were related to altered cGMP activity. We found similar dilatation of cerebral arterioles in WKY and SHRSP in response to nitroglycerin. Thus impaired endothelium-dependent dilatation in SHRSP is not related to alteration of cGMP activity. We speculate that impairment of cerebral vasodilator responses to endothelium-dependent agonists, including vasoactive substances released by platelets, may predispose SHRSP to cerebral ischemia.
 ...
PMID:Impairment of endothelium-dependent responses of cerebral arterioles in chronic hypertension. 312 90

The goal of this study was to determine whether responses of cerebral arterioles to products released by platelets are impaired in stroke-prone spontaneously hypertensive rats (SHRSP). The diameter of pial arterioles was measured during suffusion with adenosine 5'-diphosphate (ADP), serotonin, and the thromboxane analogue U-46619, using intravital microscopy in normotensive Wistar-Kyoto rats (WKY) and SHRSP (7-10 months old). Responses of cerebral arterioles to ADP and serotonin were profoundly impaired in SHRSP. ADP (10(-5) M) increased pial arteriolar diameter 17 +/- 3% (mean +/- SE) in WKY and only 4 +/- 1% in SHRSP. Serotonin (10(-5) M) increased pial arteriolar diameter 15 +/- 2% in WKY and, in contrast, reduced the diameter 13 +/- 1% in SHRSP. Nitroglycerin produced a similar dilatation of cerebral arterioles in WKY and SHRSP, suggesting that impairment of dilatation in SHRSP in response to ADP and serotonin was not related to nonspecific impairment of vasodilatation in SHRSP. The thromboxane analogue U-46619 produced a similar constriction of arterioles in WKY and SHRSP. We also examined the possibility that impaired dilator responses of cerebral arterioles in SHRSP in response to ADP and serotonin may be related to production of a cyclooxygenase vasoconstrictor substance. Indomethacin (10 mg/kg i.v.) partially restored dilator responses to ADP and serotonin in SHRSP, without altering responses in WKY. Thus, we speculate that vasoactive substances released by platelets may release a prostanoid constrictor substance from cerebral vessels of SHRSP and thereby predispose SHRSP to cerebral ischemia and, perhaps, stroke.
 ...
PMID:Responses of cerebral arterioles to adenosine 5'-diphosphate, serotonin, and the thromboxane analogue U-46619 during chronic hypertension. 320 60

The serotonin concentration in the platelet-rich plasma of 32 patients with single and multiple stroke type cerebral infarction was investigated at various stages. Serotonin levels were decreased in the acute period. The incidence of serotonin abnormality was higher in multiple types than in the single type. Serotonin levels were significantly decreased in treated hypertensive patients compared with untreated patients. Serotonin levels, therefore, varied according to the type and stage of cerebral infarction.
 ...
PMID:A follow-up study of platelet-rich plasma serotonin in clinical subtypes of cerebral infarction. 358 17

Serotonin, which is released when platelets aggregate at carotid lesions, may contribute to cerebral ischemia. Our goal was to test the hypothesis that dietary treatment of atherosclerosis reverses the augmented cerebral vasoconstrictor response to serotonin. We studied normal cynomolgus monkeys, atherosclerotic monkeys, and atherosclerotic monkeys that were fed a normal (regression) diet for 18 months. Morphometric studies indicated that the regression diet reduced intimal area in the carotid arteries by about 50-75%. Cerebral blood flow was measured with microspheres, and microvascular pressure was measured with a micropipette in pial arteries that were approximately 300 micron in diameter. Values for cerebral blood flow and arteriolar pressure were used to calculate resistance of large cerebral arteries (greater than 300 micron diameter). Infusion of serotonin produced a modest increase in the resistance of large cerebral arteries in normal monkeys. Vasoconstrictor responses to serotonin were increased more than fivefold in atherosclerotic monkeys. The major finding of the study is that dietary treatment of atherosclerosis abolishes augmented cerebral responses to serotonin.
Stroke
PMID:Cerebral vasoconstrictor responses to serotonin after dietary treatment of atherosclerosis: implications for transient ischemic attacks. 368 79

The effects of oxygen and glucose deprivation on vasoactivity were investigated using helical strips of bovine middle cerebral artery. Hypoxia, created by reducing the PO2 of the bath, or oxidative inhibition with 2,4 dinitrophenol (DNP) or sodium azide, significantly reduced contractions induced by serotonin. Normal tonic contractions induced with fresh and aged whole blood, or 5-HT became phasic and quickly relaxed to baseline in a hypoxic environment. Glucose elimination from the Krebs medium, or the inhibition of the glycolytic pathway with iodoacetic acid (IAA), did not significantly reduce serotonin-induced contractions. However, contractions were inhibited more with the combination of oxygen and glucose deprivation, or DNP + IAA, than with oxygen deprivation alone. Efforts to produce rigor in this preparation by oxygen/substrate reduction or metabolic inhibition were unsuccessful. Tonic contractions induced by 70 mM potassium became phasic as the Ca++ concentration was reduced. Contractions resulting from the readdition of Ca++ to arteries exposed to calcium-free high potassium solution were significantly reduced in the presence of oxidative and/or glycolytic inhibitors. The uptake of 45Ca++, as measured by the lanthanum technique, decreased as the bath PO2 was reduced in both serotonin stimulated and unstimulated arteries. Glucose deprivation alone did not affect 45Ca++ uptake. This study suggests that hypoxia has a direct inhibitory affect on cerebral vasoactivity mediated by reductions in sarcoplasmic Ca++ uptake.
Stroke
PMID:Effects of oxygen and glucose deprivation on vasoactivity in isolated bovine middle cerebral arteries. 376 69

In this study hemodynamic and morphometric consequences of atherosclerosis were examined in cynomolgus monkeys. We tested the hypothesis that atherosclerosis augments cerebral vasoconstrictor responses to serotonin. We studied 8 normal and 8 atherosclerotic monkeys, which were fed an atherogenic diet for 17 months. Morphometric studies indicated marked intimal proliferation of extracranial carotid arteries, with only modest reduction in the vascular lumen, as atherosclerotic lesions were displaced outward. Cerebral blood flow was measured with microspheres and microvascular pressure was measured with a micropipette in pial arteries approximately 350 microns diameter. Intracarotid infusion of serotonin reduced microvascular pressure, which indicates constriction of large arteries upstream, but cerebral blood flow did not decrease. Serotonin produced a 2-fold greater reduction in cerebral microvascular pressure in atherosclerotic monkeys than in normal monkeys. Intracarotid histamine increased flow and hypocapnia reduced flow in both normal and atherosclerotic monkeys, without altering cerebral microvascular pressure. We conclude: First, atherosclerosis potentiates constrictor responses to serotonin in large cerebral arteries. Because platelets release serotonin when they aggregate, augmentation of responses by atherosclerosis may have implications for cerebral vascular responses during aggregation of platelets at carotid lesions. Second, despite marked proliferation of intima, atherosclerotic lesions are displaced outward during a prestenotic phase of the disease, so that the lumen is relatively well preserved.
Stroke
PMID:Effects of atherosclerosis on cerebral vessels: hemodynamic and morphometric studies. 381 Jul 23

The effects of changing intraluminal pressure on contractions induced by 70 mM potassium (K+) and 10(-7), 10(-6), and 10(-5) M serotonin (5-HT) were studied in vitro in bovine middle cerebral arteries. Changes in vessel outside diameter in whole-mounted cylindrical sections of artery were detected with a photoelectric infrared device. High K+-or 5-HT (10(-5)M)-induced contractions peaked at 25 mm Hg and were significantly correlated with increasing intraluminal pressure between 25 and 175 mm Hg. Contractions induced with lower concentrations of 5-HT (10(-6), 10(-7) M), norepinephrine, and histamine peaked at 75 mm Hg but were not significantly correlated with rising pressure. Phentolamine (2 X 10(-6) M) added to the extraluminal bath had negligible influence on pressure's ability to affect K+- and 5-HT-induced contractions differently. Reducing bath temperature to 27 degrees C reduced the K+ response at each pressure, but similar temperature changes had little affect on the 5-HT-induced contractions. The K+ response became less sensitive to increasing pressure at low temperatures. Nifedipine (10(-7) M) almost totally eliminated K+-induced contractions, while significantly reducing the responses to all concentrations of 5-HT. The 5-HT responses appeared more sensitive to increasing intraluminal pressure in the presence of nifedipine. Maximum Ca++-induced contractions in the presence of 10(-5) M 5-HT and high K+ occurred at 25 mm Hg, while Ca++-induced contractions and Ca++-induced contractions in the presence of 10(-7) 5-HT or K+ plus 5-HT were maximum at 75 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke
PMID:Evidence that intraluminal pressure affects high potassium- and serotonin-induced contractions differently in the bovine middle cerebral artery: an in vitro study. 381 Jul 76


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>