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

A study was made of the vascular protein synthesis in young, genetically hypertensive rats, mainly in their renal arteries. Some of the rats were treated either with 3.5 mg/kg of phenoxybenzamine (POB) or with 4 mg/kg of propranolol twice daily, from 6 to 8 weeks of age. 3H-proline was injected intravenously into each rat before sacrifice to analyse the in vivo incorporation rates of tritiated proline into the vascular collagen and vascular non-collagenous proteins. Evidence has been presented that: (1) the rates of incorporation of 3H-proline into collagen and non-collagenous proteins of the renal arteries in spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SHRSP) were greater than those in normotensive Wistar Kyoto rats (WKY); (2) the administration of POB decreased incorporation of 3H-proline into the collagen and non-collagenous proteins of the renal arteries concomitant with a reduction of blood pressure in every rat strain; (3) the administration of propranolol failed to decrease the incorporation of 3H-proline into these connective tissue proteins in the renal arteries and this drug did not reduce blood pressure in every rat strain; (4) the incorporation rates of 3H-proline into these protein fractions in hearts were similar in every rat strain which received any drug treatment. These results indicate that an increased synthesis of collagen and non-collagenous proteins in the renal arteries of young SHR and SHRSP rats participates in the pathogenesis of spontaneous hypertension in the early hypertensive stage.
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PMID:Enhanced protein synthesis in the renal arteries of genetically hypertensive rats: its possible role in causing hypertension. 399 8

This paper presents 3 cases of generalized livedo racemosa and cerebral infarction in female patients ages 27, 39, and 42 years. Livedo racemosa is characterized by a broken, irregular pattern on the skin. It is probably caused by patchy impairment of cutaneous arteriolar circulation, resulting in reflectory venous dilation and stasis of blood. Livedo may accompany diseases such as atherosclerosis, diseases with intravascular occlusion, and collagen disorders, indicating a need for a careful search for an underlying condition. These 3 patients demonstrated several risk factors for atherosclerosis: hypertension (1 patient), oral contraceptive use (2 patients), and smoking (2 patients). The clinical findings in these 3 cases provide support to the theory that a chronic endarteritis obliterans of the small and medium-sized arteries is the underlying cause for the skin and neurologic manifestations in livedo racemosa associated with stroke.
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PMID:Livedo racemosa generalisata and stroke. 402 92

The aggregation properties of washed SHRSP platelets were investigated in comparison with normotensive WKY platelets at prehypertensive (4 weeks), early hypertensive (11 weeks) and late hypertensive (17 weeks) ages in the absence of plasma factors. The number of platelets in SHRSP was markedly lower with the development of hypertension than that in WKY. The thrombin- and collagen-induced aggregation was markedly reduced in the platelets from 11 and 17 week old SHRSP compared with that of age-matched WKY, whereas the degree of platelet aggregation in 4 week old SHRSP showed a tendency to be even greater than that in WKY. The changes in blood pressure and platelet aggregability were correlated inversely. ADP did not induce aggregation in the same system used for thrombin and collagen stimulation but in another system it aggregated washed rat platelets. Aggregation responses to ADP and ionophore A23187 were also significantly lower in 14 week old SHRSP platelets than age-matched WKY platelets. Together with other evidence, these results suggest that defective Ca2+ function, rather than the presence of exhausted platelets, is responsible for hypoaggregability in SHRSP platelets.
Stroke
PMID:Hypoaggregability of washed platelets from stroke-prone spontaneously hypertensive rats (SHRSP). 642 Sep 47

A variety of mechanisms may cause intravascular coagulation. Fibrinolysis is nearly always secondary to the initial clotting. In the acute form, ICF is characterized by depletion of platelets and several coagulation factors together with active fibrinolysis. There is a decrease in Factors V and VIII because they are sensitive to coagulation. The stable coagulation factors may be decreased as well because after activation they are removed from the circulation by the liver and reticuloendothelial system. Severe bleeding is the usual accompaniment of the acute syndrome, which may also occur in cancer and infection of all types. The acute syndrome may also occur in prolonged, extensive operations, after transfusion of incompatible blood, heat stroke, acute injury, certain snake bites, and with the administration of certain drugs. The chronic syndrome of intravascular coagulation is much more common and is associated with many diseases, including collagen diseases or immune diseases and malignancy. Many patients with chronic intravascular coagulation have normal or even increased levels of coagulation factors, and these patients have no unusual bleeding. The diagnosis depends on the demonstration of circulating complex of "soluble" fibrin revealed by the ethanol gel and protamine sulfate gelation tests. The secondary fibrinolysis results in elevation of FSP. Many laboratories are investigating the use of other procedures in the diagnosis of intravascular coagulation, including fibrinopeptides A and B, the VIII:C VIIIR:AG ratio, antithrombin III, PF 4, beta-thromboglobulin, D dimer, urinary FSP, and fibrinogen chromatography.
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PMID:The clinical pathology of intravascular coagulation. 642 Dec 71

In an effort to accelerate development of a biologic lining on the fibrillar surface of a left ventricular assist pump, the blood-contacting interface was covered with bovine fetal fibroblasts immediately prior to implantation into the animal. Selection of these syngeneic cells was based on their demonstrated prolificacy and abundant collagen production. Comparative studies, carried out in 17 Holstein calves, indicated that an adherent, thin, collagenous lining developed on the fibroblast-seeded polyurethane pump chamber in nine animals. Similar implantations of eight non-cell-seeded (control) devices resulted in formation of a predominantly acellular, fibrinous membrane, varying in thickness from 1 to 8 mm. Pump chamber compliance was significantly reduced when the histologic surface exceeded 3 mm in thickness, resulting in impaired filling and an inadequate stroke volume. The use of 14C-thymidine-labeled fibroblasts permitted later identification of the donor cells in the collagenous linings by radioautography. Serial immunologic studies undertaken to detect evidence of rejection in recipient Holstein calves were negative.
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PMID:Development of collagenous linings on impermeable prosthetic surfaces. 644 87

Investigations to develop an implantable assist pump for prolonged circulatory support have been impeded by accumulation of friable thrombus on the prosthetic interface, with subsequent embolization. To circumvent this problem, the textured, fibril surface of a polyurethane pump chamber (mat thickness 430 microns) was inoculated with cultured bovine fetal fibroblasts (labelled with thymidine-14C) prior to animal implantation. The pneumatically actuated device (stroke volume 75 ml), maintained a pulsatile blood flow throughout each study. In 20 calf experiments, extending up to 335 days, 30 X 10(6) fibroblasts (in 50 ml media) derived from a single Holstein fetus were distributed on the urethane surface (360 +/- 50 cells/mm2) by rotation of a sealed device for three hours (12 revolutions/hour). Following connection to the circulation, cell washout was minimal. Resultant biologic linings, examined after animal sacrifice, were densely adherent to the underlying polymer matrix, and varied in thickness from 250 micron-1.5 mm. Microscopically, fibroblasts were identified from the surface to base, accompanied by numerous collagen bundles and abundant ground substance. Amino acid analysis in 10/20 pumps implanted for 31--335 days, revealed 50 +/- 5 Hydroxyproline residues/1000 residues (50% collagen) and scant elastin. Donor fibroblasts were identified by radioautography and karyotyping. Lack of immunologic response in 12 Hereford pump recipients as confirmed by serial fibroblast cytotoxicity assays. In conclusion, an induced collagenous-blood interface permitted prolonged mechanical circulatory support in animals without thromboembolic complications.
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PMID:Development of a nonthrombogenic collagenous blood-prosthetic interface. 644 27

Experimental cerebral vasospasm was induced in the canine basilar artery by an intracisternal injection of fresh autogenous arterial blood. Delayed vasospasm was defined as a reduction to less than 75% of the caliber of control basilar artery 5 days after the intracisternal blood injection. A selective inhibitor of thromboxane A2 synthetase, sodium(E)-3-[4-(3-pyridylmethyl) phenyl]-2-methyl-2-propenoate, was infused intravenously for 1 or 2 hrs at 50 micrograms/kg/min in normal animals exhibiting vasospasm. Angiographic evidence of cerebral vasospasm was not reversed. Mean regional cerebral blood flow was not significantly increased in normal and vasospastic animals, but a mean difference of regional cerebral blood flow was significantly increased only in vasospastic animals. Mean arterial blood pressure and pulse rate were not seriously changed in normal and spastic animals. Another selective thromboxane A2 synthetase inhibitor, (E)-3-[4-(1-imidazolylmethyl)phenyl]-2-propenoic acid hydrochloride monohydrate, showed a similar effect on the caliber of the basilar artery, regional cerebral blood flow, blood pressure, and pulse rate, in vasospastic animals. Venous blood was taken from the internal jugular vein, and the mean platelet aggregation induced by 10 micrograms/ml of collagen was inhibited by the infusion of either selective inhibitor at 50 micrograms/kg/min for 2 hrs. However, mean platelet aggregation rates in vasospastic animals before and after treatment with either selective inhibitor were not significantly different to those in normal animals.
Stroke
PMID:Effect of selective inhibitor of thromboxane A2 synthetase on experimental cerebral vasospasm. 653 55

A permanent, implantable, circulatory support system for patients with irreversible cardiomyopathy is gradually becoming a reality. Progress has been achieved toward formation of a stable, nonthrombogenic, blood-prosthesis interface, and an electrically actuated ventricular assist device has reached an advanced stage of fabrication. The two most important components of the system, an electromechanical energy converter and a contiguous, pusher-plate, blood pump (stroke volume 85 ml) were employed in these studies. The energy converter consisted of a 50 volt, low-speed, brushless, torque motor and a mechanism to convert rotary motion into a pulsatile output. An electronic controller and variable-volume compliance chamber were not evaluated. Left ventricular bypass experiments were conducted in 13 calves for periods of 30 to 149 days. Preoperatively, four devices were inoculated with bovine, fetal fibroblasts to accelerate formation of a collagenous lining, and nine nonseeded pumps served as controls. The collagen-lined devices functioned for longer periods of time with unrestricted blood flow and no thromboembolic complications when compared to the control devices. Additional studies are contemplated employing a complete VAD system prior to undertaking preclinical trials.
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PMID:Investigations with an implantable, electrically actuated ventricular assist device. 673 93

Systemic hypertension (secondary to aortic coarctation) produces in monkeys, multifocal brain lesions where capillaries show increased diameter, endothelial degeneration and deposition of collagen and other substances in the basement membrane. In one animal, capillary changes were detected as early as 8 weeks after induction of hypertension. Similar capillary alterations were demonstrated in brain samples of hypertensive humans obtained at autopsy. We suggest that the above abnormalities may be the result of successive episodes of regional ischemia and/or hyperperfusion. Validation of these observations requires careful evaluation of additional human and animal brains.
Stroke
PMID:Arterial hypertension injures brain capillaries. Definition of the lesions. Possible pathogenesis. 679 8

Most earlier studies of platelet function in stroke patients have been performed in the acute phase and are hampered by diagnostic insecurity. A sample of totally 67 young adults below the age of 55, with ischemic cerebrovascular disease (TIA and minor stroke) were investigated at a late stage after acute disease and compared to 20 healthy controls. Patients with atherosclerotic signs at cerebral angiography had significantly (p less than 0.05) higher platelet factor 3 availability than angionegative patients. Unexpectedly, female patients compared to male patients had significantly (p less than 0.05) larger ADP-release after stimulation with collagen in vitro. Furthermore, when female patients were compared to female controls a significantly (p less than 0.05) increased platelet factor 3 availability was found. The results indicate that platelets in female patients may have an increased tendency to aggregate in vivo. Patients had significantly (p less than 0.01) shortened platelet cyclooxygenase regeneration half times (PRT). This was correlated to high levels of factor VIII related antigen (r=0.59) and high levels of factor VIII biological activity (r=0.67), indicating that platelets may be consumed by platelet adhesion and mural thrombi formation in abnormal vessel walls. PRT appears to be a reliable method to assess platelet function in vivo and to optimize aspirin dose and dose intervals in the individual.
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PMID:A study of hemostasis in ischemic cerebrovascular disease. II. Abnormalities in platelet ADP release, platelet cyclooxygenase regeneration time and platelet factor 3 availability. 681 Apr 97


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