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

Concentrations of various lipids and glycosaminoglycans (GAG) in the intima of the grossly normal and atherosclerotic cerebral arteries were compared with those of the aorta and coronary arteries. The lowest percentage of esterified cholesterol (EC) in total cholesterol, and of chondroitin sulfate-4/6 (CS-4/6) in total glycosaminoglycans and the highest percentage of heparin sulfate (HS) in total GAG are the characteristic features of the normal intima of normal cerebral arteries when compared with those in the aorta and coronary artery. In the cerebral arterial intimas, but not in the aorta or coronary arteries, there was a significant positive correlation between contents of EC and percentage and total content of CS-4/6. Atherogenesis in cerebral arteries is discussed in comparison to that of the aorta and coronary vessels.
Stroke
PMID:Cerebral atherosclerosis in Japanese. Part 5: relationship between cholesterol deposition and glycosaminoglycans. 100 35

The interrelationships between cerebral edema, intracranial pressure (ICP), and cerebral blood flow (CBF) were studied in acute and chronic triethyl tin sulfate treated rats. Prior to pentobarbital anesthesia behavioral observations were made. ICP and regional CBF were measured under steady state conditions and brain water content was determined by vacuum drying of the right cerebral hemisphere. Control and chronic animals were neurologically normal. There were two distinct acute groups: (1) acute low pressure (ALP) animals - alert but tetraperetic, and (2) acute high pressure (AHP) animals - deeply stuporous, with minimal pain response and gross EEG slowing. ICP was significantly elevated only in AHP animals. Hemispheric CBF was significantly reduced in AHP and chronic animals. The interaction of increased pressure and edema (AHP) produced the greatest decrease in CBF, although deep white flows were significantly affected in all experimental groups. Chronic animals had significantly lower flow in four of seven regions compared to ALP animals despite no significant difference in ICP. Water content was significantly increased in all experimental groups with the greatest increase in the chronic animals. In the absence of any significant increase in ICP, cerebral edema appears to cause a significant reduction in cerebral blood flow and this reduction corresponds with the magnitude and location of the edema.
Stroke
PMID:Alterations in behavior, brain electrical activity, cerebral blood flow, and intracranial pressure produced by triethyl tin sulfate induced cerebral edema. 125 1

Plasma crosslinked fibrin polymers (XLFP) are formed as a result of in vivo hemostatic activation and are elevated in thrombotic disease. We have investigated the plasmic degradation of plasma XLFP in vitro to provide information regarding the pattern of crosslinking and the composition of degradation products. Plasma XLFP were identified by sodium dodecyl sulfate (SDS)-agarose electrophoresis and Western blotting and quantitated by gel scanning. D-dimer was measured by enzyme-linked immunosorbent assay and the results were verified by SDS-polyacrylamide gel electrophoresis and Western blotting of the digests. Complete degradation of XLFP occurred only after supplementation of plasma with plasminogen (5 U/mL) and incubation with recombinant tissue plasminogen activator (rt-PA), indicating that the normal plasma plasminogen concentration limits plasmic degradation in vitro. Gel electrophoresis showed that the principal terminal degradation products of XLDP were fragments D, DD, and E, indicating that crosslinking occurred primarily through gamma chain dimers. After adding a low concentration of thrombin to plasma in vitro, XLFP increased progressively before clotting, and the concentration correlated with the increase in the D-dimer concentration after degradation (r = .98). Plasma XLFP and D-dimer concentrations in plasmic digests were significantly elevated in patients with stroke (150 +/- 83 micrograms/mL and 88 +/- 32 micrograms/mL), myocardial infarction (217 +/- 110 micrograms/mL and 84 +/- 30 micrograms/mL), and venous thrombosis (187 +/- 80 micrograms/mL and 86 +/- 19 micrograms/mL) compared with normals (28 +/- 12 micrograms/mL and 25 +/- 7 micrograms/mL). There was a strong correlation between the plasma concentration of XLFP and the D-dimer immunoreactivity of plasma after plasmic degradation (r = .87). The results indicate that XLFP in plasma are crosslinked primarily through gamma chains and degrade to fragment DD with plasminogen activation. Also, the immunoreactivity of in vitro plasmic digests of plasma reflects the concentration of XLFP and may provide a useful indirect measure of in vivo hemostatic activation in patients with thrombotic disease.
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PMID:Plasma crosslinked fibrin polymers: quantitation based on tissue plasminogen activator conversion to D-dimer and measurement in normal and patients with acute thrombotic disorders. 138 60

Ten cases of cerebral hemorrhage and one of intraspinal subdural hematoma after thrombolytic therapy are reported. Six patients were treated with streptokinase, four with rt-PA and one with a combination of both drugs. The incidence was 0.5 to 2% and was higher in case of rt-PA therapy (3.7%). In all cases, CT scan showed primary hemorrhage rather than hemorrhagic infarction. Four patients died of stroke. Among the survivors, residual disability was severe in one and mild in five. Only one patient recovered completely. In patients treated with streptokinase, the hemorrhage was probably due to a more than 80% decrease in plasma fibrinogen. In those receiving rt-PA, either excessive dosage (2 cases in our series) or lysis of cerebral microthrombi are thought to be responsible for the hemorrhagic complications. Treatment consists of infection of aprotinin (an anti-fibrinolytic drug), cryoprecipitates with factors V and VIII and protamine sulfate.
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PMID:[Hemorrhage of the brain after therapeutic fibrinolysis. 11 cases]. 143 52

The N-methyl-D-aspartate (NMDA) receptor is believed to play a major role in learning and in excitotoxic neuronal damage associated with stroke and epilepsy. Pregnenolone sulfate, a neurosteroid, specifically enhances NMDA-gated currents in spinal cord neurons, while inhibiting receptors for the inhibitory amino acids glycine and gamma-aminobutyric acid, as well as non-NMDA glutamate receptors. This observation is consistent with the hypothesis that neurosteroids such as pregnenolone sulfate are involved in regulating the balance between excitation and inhibition in the central nervous system.
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PMID:Pregnenolone sulfate: a positive allosteric modulator at the N-methyl-D-aspartate receptor. 165 10

Polycythemia in CAPD patients has been rarely described. Over an eight year period, 4 out of 123 CAPD patients (3%) were identified as having Hct values exceeding 50% for 1 month or longer. All of the 4 patients were insulin dependent diabetics (4/47 diabetic patients, 8.5%). Charts were reviewed on 3 of these 4 patients. Polycythemia developed after a mean of 21 +/- 7 months on peritoneal dialysis. Prior to the development of polycythemia, ferritin levels were low and ferrous sulfate therapy was begun at a time the Hct values were 36 to 40%. Erythropoietin levels were obtained in 2 patients, and were 22 U/L (Hct 51%) and less than 5 U/L (Hct 55%). Renal ultrasound failed to show renal masses or cysts. One patient had a plasma volume of 2.1 L (normal 2.4-3.2 L); another patient was clinically volume depleted. Complications during the period of polycythemia included gangrenous feet requiring amputation in 2 patients, CVA in 2 patients, and splenic infarct in 1 patient. One patient died of cerebral thrombosis. We conclude that polycythemia is uncommon in CAPD patients and occurs most often in diabetic patients. Volume depletion and iron therapy may play a role in its etiology. In this high risk group of patients polycythemia may contribute to vascular complications and should be avoided.
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PMID:Polycythemia in diabetic patients on CAPD. 168 Apr 62

We examined the role of the locus coeruleus (LC) in the regulation of the hemodynamics and sympathetic nerve activity in anesthetized rats. Unilateral microinjection into the LC of the excitatory amino acid, L-glutamate (Glu), elicited dose-dependent decreases in arterial pressure (AP) and heart rate (HR). The bradycardic response was partially attenuated after intravenous injection of atropine sulfate, but the greater part of this response still remained. Interruption of the ascending projections of the LC by midbrain transection did not affect the depressor and bradycardic responses elicited by chemical stimulation. The renal sympathetic nerve activity showed transient but strong inhibition with this stimulation. Cardiac output was measured using an electromagnetic flowmeter implanted in the ascending aorta. The stroke volume and total peripheral resistance (TPR) were calculated. Microinjection of Glu elicited a significant decrease in TPR and slight decreases in cardiac output and stroke volume. Microinjection of the inhibitory amino acid, gamma-aminobutyric acid (GABA), or the alpha 2-adrenergic agonist, clonidine, exerted no effect on AP and HR. The present results therefore suggest that: (1) the LC neurons have an inhibitory influence on the sympathetic nervous system, and stimulation of these neurons can elicit depressor and bradycardic responses; (2) the depressor response was produced predominantly as a result of a decrease in vascular resistance, rather than a decrease in cardiac output; (3) these inhibitory responses may be provided not via the ascending projections of the LC; and (4) the LC neurons do not have a tonic influence on the cardiovascular system.
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PMID:Chemical stimulation of the locus coeruleus: inhibitory effects on hemodynamics and renal sympathetic nerve activity. 168 67

Venous thromboembolism is complex with a multifactorial etiology. The Virchow triad (changes in blood flow, changes in vessel wall, and changes in the properties of blood) gives the main factors involved in venous thromboembolism. Venous stasis during immobilization in general anesthesia, stroke with hemiparesis, and heart failure plays a central role. The thromboembolic process can be initiated by a disturbance in the normal "hemostatic balance," with an increased thrombogenic potential, due to release of thromboplastin and collagen exposure during vessel wall injury by stasis and hypoxia, decreased fibrinolysis during surgery, malignancy, among others. Many substances modify these processes, including heparan sulfate, AT III, protein C, t-PA inhibitor, and alpha 2-antiplasmin.
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PMID:Pathophysiology of venous thromboembolism. 175 82

Optimization of the contrast-to-noise ratio (CNR) is described for microcirculation magnetic resonance (MR) imaging techniques based on flow-compensated/flow-dephased sequences, both with and without even-echo rephasing. The authors present the most advantageous manner of applying flow-dephased gradients, such that dephasing is maximal while diffusion losses are minimal. The theoretical considerations include phase, diffusion, echo time, and bandwidth in the determination of the optimal parameters for microcirculation imaging. Studies in phantoms consisting of stationary and flowing copper sulfate in Sephadex columns demonstrate the validity of the calculations. Optimized in vivo images of a rat stroke model demonstrate the potential of the flow-compensated/flow-dephased technique and the importance of optimizing CNR.
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PMID:Maximization of contrast-to-noise ratio to distinguish diffusion and microcirculatory flow. 180 29

We induced experimental delayed cerebral vasospasm by the intracisternal injection of greater than 0.5 ml blood in 30 rats. Seventy-two hours later the basilar artery was exposed via the transclival approach and photographed at high-power magnification through an operating microscope. We then evaluated the effect of topical (n = 30) and intravenous (n = 20) magnesium sulfate on the spastic artery by computerized image analysis. A greater than 50% reduction in baseline diameter of the basilar artery was observed in the rats subjected to subarachnoid hemorrhage compared with the 10 controls (p less than 0.0001). Intravenous magnesium sulfate dilated the spastic artery to approximately 75% of the baseline diameter in control rats (p less than 0.0001). Topical magnesium sulfate caused dramatic dilation of the basilar artery in both the control and the subarachnoid hemorrhage groups to near 150% of the baseline diameter in the controls (p less than 0.001). All rats receiving intravenous magnesium sulfate reached therapeutic plasma levels of the ion. Hemodynamic effects were mild and immediately reversible upon cessation of magnesium sulfate administration. We suggest that magnesium has a role in the treatment of subarachnoid hemorrhage-induced vasospasm in humans.
Stroke 1991 Jul
PMID:Magnesium sulfate reverses experimental delayed cerebral vasospasm after subarachnoid hemorrhage in rats. 185 12


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