Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with end-stage renal disease had a flaccid hemiparesis in conjunction with severe hyperkalemia. The hemiparesis resolved with treatment of the hyperkalemia. The patient was later found to have extracranial vascular disease, and we propose that a severe metabolic abnormality associated with an area of relative cerebral ischemia caused the reversible neurologic deficit.
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PMID:Focal neurologic signs associated with hyperkalemia. 672 65

A number of drugs used in the pharmacotherapy of cerebral metabolic and vascular disease have been studied for their effects on the respiration of mitochondria isolated from the rat brain. Some of these agents increased the respiratory control ratio by more than 5% from base-line values (at p less than 0.05), namely, aminophylline, dihydroergotoxine, ifenprodil, nicergoline, raubasine, and vincamine. The ability of these agents to increase the efficiency of mitochondrial respiration could be correlated with two other attributes peculiar to these five drugs: their ability to contract cerebrovascular smooth muscle when studied in vitro and their ability to decrease the volume of infarcted brain tissue following experimental occlusion of the middle cerebral artery in the cat. Papaverine and its derivatives (naftidrofuryl, viquidil, YC-93) decreased respiratory control, an effect that might correlate with their capacity to effect a vasodilatation of the cerebral vessels and their inefficacy in models of acute cerebral infarction. There is a considerable body of evidence suggesting that one of the earliest and most fundamental perturbations of cerebral ischaemia is a loss of respiratory control. Ifenprodil, vincamine, and some related "anti-ischaemic" compounds are capable of increasing respiratory control in normal cerebral mitochondria, and this capacity might well help to explain their therapeutic potential in cerebrovascular disorders in which energy supply to the brain is limited.
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PMID:Effects of agents used in the pharmacotherapy of cerebrovascular disease on the oxygen consumption of isolated cerebral mitochondria. 706 2

Female reproductive hormones are considered to be protective agents in atherosclerotic vascular disease and stroke. The present study determined if there are unique cerebrovascular responses in female animals to global cerebral ischemia and if 17 beta-estradiol is important to postischemic outcome in brain. Three groups of anesthetized, sexually mature rabbits were treated with normotensive four-vessel occlusion (6 min) and 3 h of reperfusion: females chronically instrumented with 17 beta-estradiol implants (EFEM; n = 8, plasma estradiol level = 365 +/- 48 pg/ml), untreated females (FEM; n = 8, estradiol = 13 +/- 3 pg/ml), and untreated males (M; n = 8, estradiol < limit of radioimmunoassay). CBF (microspheres) and somatosensory evoked potential (SEP) amplitude were measured during ischemia/reperfusion. Baseline hemispheric blood flow and regional flow distribution were not altered by chronic estradiol treatment. Hemispheric blood flow was equivalently reduced during ischemia in FEM and M (6 +/- 1 and 9 +/- 2 ml min-1 100 g-1, respectively); however postischemic hyperemia was greater in FEM than M (CBF = 257 +/- 27 and 183 +/- 27 ml min-1 100 g-1. However, EFEM experienced higher CBF during ischemia (e.g., 13 +/- 2 ml min-1 100 g-1) and less hyperemia (134 +/- 4 ml min-1 100 g-1 in hemispheres) in numerous brain regions than FEM. CBF at 3 h reperfusion was not different among the groups. Recovery of SEPs was incomplete and similar in all groups. We conclude that chronic exogenous 17 beta-estradiol treatment increases CBF during global incomplete ischemia and ameliorates postischemic hyperemia in the female animal.
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PMID:Postischemic cerebral blood flow recovery in the female: effect of 17 beta-estradiol. 779 Apr 16

41 patients (30 men, 11 women, mean age 65.3 +/- 9.7 years) with probable ischemic vascular dementia diagnosed according to stated clinical criteria at least 3 months after hospital discharge and among a few nonhospitalized subjects with thorough clinical, neurovascular and neuroimaging workup have been followed for the past 7 years with serial measures of neurological and cognitive status and cerebral blood flow using stable xenon-enhanced CT. Cognitive impairments correlated with cerebral ischemia rather than CT measurements of infarcted brain volume. A minimum of one follow-up was required and follow-up intervals ranged from 4 months to 6.6 years (mean 3.4 +/- 1.6 years). 9 patients (22.0%) were lost to follow-up, 4.9% died, 9.8% became incapacitated by additional strokes, 2.4% by cancer and 4.9% moved away. Cross-sequential designs adjust for problems of attrition. Mortality rates of 1.4%/year during 1986-1993 are significantly lower than 2.0%/year between 1983 and 1986. Declines in mortality are attributed to control of risk factors and antiplatelet treatment of atherosclerotic cerebral vascular disease and anticoagulant treatment of patients with cardiogenic embolism.
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PMID:Problems encountered with longitudinal neurological, psychometric and cerebral CT imaging among stroke data bank patients with dementia. 780 Jan 15

Arterial dissection results from bleeding into the vessel wall. Some cases are associated with cervical trauma or have evidence of an underlying vascular disease; many occur without any history of injury or detectable arterial disease. Among the cervical cephalic arteries, the extracranial segment of the internal carotid artery is the vessel most commonly involved; intracranial carotid dissections are much rare. Carotid dissection occurs predominantly in young or middle-aged adults and shows no sex predominance. Although clinical manifestations can be extremely diverse (from isolated headache to rapidly lethal stroke), the most common and suggestive syndrome associates "local" symptoms (such as head or neck pain, Horner's syndrome, pulsatile tinnitus or lower cranial nerves palsy) and delayed (up to several weeks) symptoms of cerebral ischaemia in the territory of the internal carotid artery territory. Dissection can be bilateral or associated with dissection of the vertebral artery. Angiography has long been considered the gold standard for the diagnosis. As this procedure carries a risk of cerebral complications, noninvasive diagnostic approaches such as magnetic resonance imaging and ultrasound have been developed and are increasingly used. The prognosis of carotid dissections depends on the presence and severity of ischaemic brain damage. Recurrent dissections seem extremely rare. Normalization or improvement of the vascular abnormalities during the subsequent weeks is frequent and is an excellent argument in favour of the diagnosis. Although no controlled trial has ever been performed, anticoagulant treatment is often used for a few months when the dissection involves the extracranial segment of the carotid artery. No standard treatment of intracranial carotid dissection has emerged.
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PMID:[Internal carotid artery dissection]. 815 34

A 28-year-old female farmer, without vascular risk factors, developed a limited infarct of the pons, associated with a lymphocytic cerebrospinal fluid (CSF) pleocytosis. Titres of specific antibodies against Borrelia burgdorferi were high in serum and CSF. MRI confirmed an infarct in the territory of the medial pontine arteries, but angiography showed no evidence of cerebral angiopathy. Antibiotic therapy rapidly led to a return to normal of CSF cytology and serology. We suggest that Lyme disease is a possible cause of cerebral ischaemia.
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PMID:Lyme disease presenting as a stroke in the vertebrobasilar territory: MRI. 823 82

The histoblot immunostaining technique for locating and characterizing amyloidogenic proteins was used to obtain information about the relationship of cerebral ischemia/hypoxia to the accumulation of amyloid beta protein (A beta). We investigated brains of 131 subjects (ages 25-94 years, mean 72 years). Three distribution patterns of A beta immunoreactivity were identified: (1) colocalization with diffuse and neuritic plaques of Alzheimer's disease (AD) and aging; (2) diffuse punctuate deposits in the cerebral cortex in association with small vessel cerebral vascular disease ; and (3) cerebral cortical accumulation localized to arterial boundary zones and other regions susceptible to ischemic/hypoxic injury designated "stress-induced deposits" (SID). SID were not identified in tissue sections by immunohistochemical, Congo red or Bielschowsky silver techniques; no histological abnormalities were present in adjacent formalin-fixed tissue sections, SID occurred in subjects with histories of cerebral ischemia, and severe orthostatic hypotension. There was also an association with aging in general and with the incidence of neuritic plaques specifically. These latter findings are consistent with the hypothesis that brain ischemia/hypoxia plays a role in the pathogenesis of AD.
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PMID:Ischemic stress induces deposition of amyloid beta immunoreactivity in human brain. 856 Sep 78

Vascular disease and focal cerebral ischemia still represent the major cause of neurological morbidity and mortality. Mechanisms of hypoxic changes are associated with energy depletion and impairment of biological membranes. Reperfusion after the stroke plays an important role in the development of morphological and functional changes of the nervous tissue. In experiments, different models of focal cerebral ischemia based on the middle cerebral artery occlusion (MCAO) are used. Four main categories of such models are most frequently employed: 1. Temporary intraluminal occlusion of part of the circle of Willis (via internal carotid artery), 2. Abluminal application of the vasoconstrictor peptide (endothelin-1) to the MCA, 3. Tromboembolic models, 4. Microclips. Reliable quantification of morphological changes is also possible. Discussed models are used for testing different types of treatment of the cerebral ischemia, including pharmacological stimulation and blocking of individual membrane receptor systems.
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PMID:[Models of focal hypoxia of the central nervous system]. 863 Oct 55

Cytidine 5'-diphosphocholine, CDP-choline or citicoline, is an essential intermediate in the biosynthetic pathway of the structural phospholipids of cell membranes, especially in that of phosphatidylcholine. Upon oral or parenteral administration, CDP-choline releases its two principle components, cytidine and choline. When administered orally, it is absorbed almost completely, and its bioavailability is approximately the same as when administered intravenously. Once absorbed, the cytidine and choline disperse widely throughout the organism, cross the blood-brain barrier and reach the central nervous system (CNS), where they are incorporated into the phospholipid fraction of the membrane and microsomes. CDP-choline activates the biosynthesis of structural phospholipids in the neuronal membranes, increases cerebral metabolism and acts on the levels of various neurotransmitters. Thus, it has been experimentally proven that CDP-choline increases noradrenaline and dopamine levels in the CNS. Due to these pharmacological activities, CDP-choline has a neuroprotective effect in situations of hypoxia and ischemia, as well as improved learning and memory performance in animal models of brain aging. Furthermore, it has been demonstrated that CDP-choline restores the activity of mitochondrial ATPase and of membranal Na+/K+ ATPase, inhibits the activation of phospholipase A2 and accelerates the reabsorption of cerebral edema in various experimental models. CDP-choline is a safe drug, as toxicological tests have shown; it has no serious effects on the cholinergic system and it is perfectly tolerated. These pharmacological characteristics, combined with CDP-choline's mechanisms of action, suggest that this drug may be suitable for the treatment of cerebral vascular disease, head trauma of varying severity and cognitive disorders of diverse etiology. In studies carried out on the treatment of patients with head trauma, CDP-choline accelerated the recovery from post-traumatic coma and the recuperation of walking ability, achieved a better final functional result and reduced the hospital stay of these patients, in addition to improving the cognitive and memory disturbances which are observed after a head trauma of lesser severity and which constitute the disorder known as postconcussion syndrome. In the treatment of patients with acute cerebral vascular disease of the ischemic type, CDP-choline accelerated the recovery of consciousness and motor deficit, attaining a better final result and facilitating the rehabilitation of these patients. The other important use for CDP-choline is in the treatment of senile cognitive impairment, which is secondary to degenerative diseases (e.g., Alzheimer's disease) and to chronic cerebral vascular disease. In patients with chronic cerebral ischemia, CDP-choline improves scores on cognitive evaluation scales, while in patients with senile dementia of the Alzheimer's type, it slows the disease's evolution. Beneficial neuroendocrine, neuroimmunomodulatory and neurophysiological effects have been described. CDP-choline has also been shown to be effective as co-therapy for Parkinson's disease. No serious side effects have been found in any of the groups of patients treated with CDP-choline, which demonstrates the safety of the treatment.
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PMID:CDP-choline: pharmacological and clinical review. 870 78

Nonrheumatic atrial fibrillation (AF) frequently coexists with other risk factors for cerebral ischemia. This study was originally designed to determine which combinations of clinical and echocardiographic abnormalities were most closely associated with the risk of cerebral ischemic events. Patients with cerebral ischemic events (n = 214) and community-based control subjects (n = 201) underwent transesophageal echocardiography and carotid artery imaging. Adjusted odds ratios (ORs) were determined using multiple logistic regression analysis. Independent risk factors for cerebral ischemia included diabetes, carotid stenosis, aortic sclerosis, left ventricular dysfunction, left ventricular hypertrophy, left atrial (LA) spontaneous contrast, and proximal aortic atheroma. Nonrheumatic AF in combination with LA spontaneous contrast and LA enlargement showed a strong association with cerebral ischemic events (OR 33.7 [95% confidence interval 4.53 to 251]). In subjects with sinus rhythm or nonrheumatic AF, LA enlargement was not associated with an increased risk of cerebral ischemic events in the absence of LA spontaneous contrast. However, only 2 patients and 1 control subject had nonrheumatic AF without LA spontaneous contrast or LA enlargement. Therefore, study of a larger number of subjects is required to address the issue of whether nonrheumatic AF itself carries increased risk. The combination of nonrheumatic AF with LA spontaneous contrast is a potent risk factor for cerebral ischemia. Ascertaining the risk factor in nonrheumatic AF requires adequate examination for underlying cardiac, aortic, and carotid vascular disease. Transesophageal echocardiography may contribute to this assessment.
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PMID:Atrial fibrillation with left atrial spontaneous contrast detected by transesophageal echocardiography is a potent risk factor for stroke. 875 87


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