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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since October 1967 we have performed 76 microsurgical STA--cortical MCA bypass operations. Recently we have had two cases, who died from intracerebellar hematoma following bypass operation. Intracerebellar hematoma is reported primarily due to hypertension (50-80%), and to comprise 10% of all spontaneous intracranial hematomas. Diagnosis of this lesion is frequently missed but can be made by the typical clinical picture (respiratory irregularity, pinpoint pupils, absence of oculovestibular responses, loss of consciousness), and the CT-Scan. If the correct diagnosis is made and operation promptly performed, many patients with subacute or acute intracerebellar hematoma can be saved. The 2 cases presented here had a history of hypertension and anticoagulation (including Colfarit), but had sustained the bypass operation well and showed no neurological deficit immediately after the operation. They had received Rheomacrodex intra- and postoperatively. Quite soon postoperatively, however, the systolic blood pressure rose to 210 mmHg and the patients complained of severe headache. They were treated symptomatically with analgesics and antihypertensive drugs. A short time later they became comatose and died. In order to prevent this complication after bypass surgery, postoperative management of hypertension is mandatory. The combination of antithrombic agents, Colfarit and Rheomacrodox, might have played a role in inducing the hemorrhages. Furthermore strong analgesics should be withheld to prevent their masking neurological deterioration. Intracerebellar hematoma must always be considered in hypertensive or anticoagulated patients, especially because it can be cured with prompt diagnosis and operative treatment.
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PMID:[Intracerebellar Hematoma following microsurgical STA-cortical MCA bypass surgery (author's transl)]. 90 21

A polystyrene-covered platinum electrode (100-150 mum diameter) has been used to measure cortical tissue oxygen tension in baboon brains. The method of preparation, calibration, and the importance of small residual current (less than 40 nA) as an attribute of a reliable electrode, are described. With electrodes of this size, there was a large (16 +/- 12nA/torr) and linear current output with pO2 changes. The effect of avrious gases in addition to oxygen is described; halothane inhalation increases the apparent pO2 and hydrogen, used for blood flow estimations, reduces the recorded pO2. In 48 separate electrode placements in 13 baboons, the mean cortical qo2 was 23.8 +/- 12 mm Hg, with a range from 1-79 mm Hg; following occlusion of one middle cerebral artery, 37 electrodes recorded a pO2 of less then 5 mm Hg pO2 Oscillations were invariably noted in control conditions, independent of blood pressure; these waves disappeared during MCA occlusion and appeared to be augmented following release of the clip. Blood pressure "spikes" produce immediate and synchronous changes in all electrodes entirely different from the spontaneous waves. Such blood pressure changes may mask the true effect of hypercapnia on tissue pO2 and, if ignored, may lead to erroneous assumptions regarding local neural control of the circulation, the increased pO2 secondary to hypertension being regarded as evidence of regional vasodilation. A SUdden change in inspired pO2-the "air test"-was performed in control conditions and following the ischaemic insult, and the rate of change of cortical pO2 compared. The gradient was significantly greater (P less than 0.05) following ischaemia, suggesting a changed ratio in the tissue's flow to oxygen requirements and/or a persisting vasodilatation.
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PMID:Measurements of oxygen tension in the cerebral cortex of baboons. 124 79

The effect of induced hypertension instituted after a 2-h delay following middle cerebral artery occlusion (MCAO) on brain edema formation and histochemical injury was studied. Under isoflurane anesthesia, the MCA of 14 spontaneously hypertensive rats was occluded. In the control group (n = 7), the mean arterial pressure (MAP) was not manipulated. In the hypertensive group (n = 7), the MAP was elevated by 25-30 mm Hg beginning 2 h after MCAO. Four hours after MCAO, the rats were killed and the brains harvested. The brains were sectioned along coronal planes spanning the distribution of ischemia produced by MCAO. Specific gravity (SG) was determined in the subcortex and in two sites in the cortex (core and periphery of the ischemic territory). The extent of neuronal injury was determined by 2,3,5-triphenyltetrazolium staining. In the ischemic core, there was no difference in SG in the subcortex and cortex in the two groups. In the periphery of the ischemic territory, SG in the cortex was greater (less edema accumulation) in the hypertensive group (1.041 +/- 0.001 vs 1.039 +/- 0.001, P less than 0.05). The area of histochemical injury (as a percent of the cross-sectional area of the hemisphere) was less in the hypertensive group (33 +/- 3% vs 21 +/- 2%, P less than 0.05). The data indicate that phenylephrine-induced hypertension instituted 2 h after MCAO does not aggravate edema in the ischemic core, that it improves edema in the periphery of the ischemic territory, and that it reduces the area of histochemical neuronal dysfunction.
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PMID:Delayed institution of hypertension during focal cerebral ischemia: effect on brain edema. 171 60

Anesthetic management during 85 STA-MCA anastomoses with or without encephalo-myosynangiosis for 64 patients with Moyamoya disease was evaluated retrospectively. Anesthetic agents included nitrous oxide-NLA (GONLA), nitrous oxide-halothane (GOF), nitrous oxide-enflurane (GOE), and their combinations. Slight hypercarbia (40 mmHg less than PaCO2 less than 50 mmHg) was essential to avoid cerebral ischemia. Several procedures to control heart rate by beta blockade or to control hypertension by nitroglycerin were required, because tachycardia and hypertension interfered with fine surgical procedure. During microsurgery HR of GONLA anesthetized patients was significantly lower. Postoperatively the patients anesthetized by GOE showed significantly lower PaCO2 compared with the GONLA anesthetized patients. So we recommend GONLA for anastomosis in patients with Moyamoya disease.
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PMID:[Anesthetic management of revascularization for moyamoya disease]. 192 Jul 89

A model of rat arteriovenous fistula (AVF) was created using a proximal common carotid artery to distal external jugular vein anastomosis. Anatomical dissections revealed that the external jugular vein is the primary vessel draining intracranial venous blood. Physiological measurements were made with the AVF open and closed, and during venous outflow occlusion of the contralateral external jugular vein. Opening the AVF increased torcular pressure from 6.5 +/- 0.6 to 13.5 +/- 1.1 mm Hg and decreased mean arterial pressure from 82.7 +/- 1.8 to 62.8 +/- 1.8 mm Hg (both P less than .05), decreasing cerebral perfusion pressure from 76.2 +/- 1.7 to 49.3 +/- 2.2 mm Hg (P less than .05). Middle cerebral artery blood flow velocity (MCA BFV) decreased from 6.8 +/- 1.1 to 4.2 +/- 0.7 cm/s (P less than 0.05). In rats with an AVF, occlusion of venous outflow increased torcular pressure to 34.8 +/- 3.1 mm Hg (P less than 0.05), MCA BFV decreased to 1.8 +/- 0.5 cm/s (P less than 0.05), and severe ischemic changes were seen on the electroencephalogram. Under this condition, torcular pressure and systemic arterial pressure had a positive linear relationship (P less than 0.05), whereas in control rats torcular pressure and arterial pressure had no relationship. Restoration of cerebral perfusion pressure by release of venous outflow occlusion and AVF closure transiently increased MCA BFV to 69% above baseline (P less than 0.05). Histological examination 1 week after permanent venous outflow occlusion revealed venous infarction, subarachnoid hemorrhage, and severe brain edema in rats with an AVF but not in control rats without an AVF. This model of cerebrovascular steal with venous hypertension reproduces both hemodynamic and hemorrhagic complications of human AVF and emphasizes the importance of venous outflow obstruction and venous hypertension in the pathophysiology of these lesions.
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PMID:Intracranial venous hypertension and the effects of venous outflow obstruction in a rat model of arteriovenous fistula. 192

This report summarizes the protocol of a randomized trial of superficial temporal artery-middle cerebral artery (STA-MCA) bypass procedure and presents the entry characteristics of its patients. The trial has been designed to determine whether this EC/IC bypass reduces the rate of subsequent stroke among patients with recent hemispheric or retinal strokes and/or transient ischemic attacks who have angiographically proven atherosclerotic narrowing or occlusion of the ipsilateral internal carotid or middle cerebral artery. Of the 1377 eligible patients entered from the 71 participating centers, 714 (52%) have been assigned to medical treatment alone (daily aspirin and aggressive hypertension control) while 663 (48%) have been assigned to receive STA-MCA bypass in addition to medical therapy. The two treatment groups have been well balanced for important prognostic factors. Bypass patency rates of 95% have been documented. At the end of the study in mid-1985, an average follow-up of five years and a minimum follow-up of 33 months will have been achieved. On both clinical and methodologic grounds, this study will have provided a rigorous test of the STA-MCA bypass procedure.
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PMID:The International Cooperative Study of Extracranial/Intracranial Arterial Anastomosis (EC/IC Bypass Study): methodology and entry characteristics. The EC/IC Bypass Study group. 286 Jul 39

We tested the hypothesis that blood flow through cerebral collateral vessels is lower in stroke-prone spontaneously hypertensive rats (SHRSP) than in normotensive Wistar-Kyoto rats (WKY) after occlusion of the middle cerebral artery and during maximal vasodilatation. Cerebral blood flow, measured with microspheres, was similar in adult male SHRSP and WKY under control conditions. In both strains, occlusion of the middle cerebral artery reduced blood flow and vascular conductance to the territory of the occluded artery, as compared with homologous tissue on the side contralateral to the occlusion. The territory distal to the site of occlusion was identified by intravital demarcation with neutral red dye. In both strains, vasodilatation produced by seizures after occlusion of the middle cerebral artery produced minimal increases in blood flow to the territory of the occluded artery. Blood flow and vascular conductance to the territory of the occluded MCA were significantly lower in SHRSP than in WKY (p less than 0.05) after occlusion and during seizure after occlusion. We conclude that after occlusion of the middle cerebral artery, there is less blood flow through cerebral collateral vessels in SHRSP than in WKY. We speculate that the lower blood flow through collateral vessels in SHRSP may be related to structural differences in those vessels. Thus, the tendency toward infarction after occlusion of the middle cerebral artery in SHRSP may be related, at least in part, to a more limited dilator reserve of cerebral collateral vessels in SHRSP.
Hypertension 1986 Jun
PMID:Blood flow through cerebral collateral vessels in hypertensive and normotensive rats. 372 59

Two cases of cerebral aneurysm combined with polycystic kidneys (PCKs) were presented. Case 1, a 24-year-old hypertensive male, was referred to our clinic owing to sudden onset of severe headache at August 20, 1982. Neurological findings on admission were stuporous, right vitreous hemorrhage (so-called Terson's syndrome), and hypertension. CT scans showed subarachnoid hemorrhage, and right MCA bifurcation aneurysm with marked vasospasms by cerebral angiography was revealed. Intentional delayed operation with V-P shunt was performed. He discharged with mild left upper limb paresis, and visual impairment on the right. Bilateral PCKs were confirmed by postoperative DIP and CT scan. Case 2, a 51-year-old female, who suddenly complained of severe headache, was referred to our department 3 days after subarachnoid hemorrhage. One year previously, she had been pointed out PCKs. Neurological findings on admission at February 29, 1980, were drowsy, left third cranial nerve palsy, and hypertension. Cerebral angiography showed multiple aneurysms (bilateral IC-PC & A-com). Neck clipping (1-IC-PC & A-com) and coating (r-IC-PC) were performed at the next day of admission, and V-P shunt operation was followed about 8 weeks after first operation. About 2 weeks after discharge, she suddenly became loss of consciousness and expired. Autopsy revealed intracerebral hemorrhage in left basal ganglia and thalamus. Both kidneys were PCKs of Potter type 3 and cysts of the liver were also noted. In young hypertensive patients with cerebral aneurysms, it should be in mind whether PCKs may be combined or not, and cerebral angiography in PCKs were reasonable to find out harbored cerebral aneurysm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of cerebral aneurysms combined with polycystic kidneys]. 652 33

Treatment of ischemic deficits caused by vasospasm relies on enhancing cardiac output, inducing arterial hypertension, and expanding the intravascular volume in an attempt to improve CBF. Different treatment protocols exist from institution to institution to achieve these goals. The role of calcium-channel blockers now is well established. The newest focus on prevention of vasospasm includes tPA and a variety of anti-inflammatory drugs and potential neuroprotective drugs under research. Endovascular therapy for vasospasm has an increasing role in treating patients who are unable to tolerate induced hypertension or aggressive volume augmentation. We will return to our index case of the 63-year-old woman with SAH caused by an ACoA aneurysm to review some major management issues. After placing a ventriculostomy and slowly lowering ICP, the patient became alert and was fully oriented. She had aneurysm surgery on hospital day 2, with an uncomplicated immediate postoperative course. A Swan-Ganz catheter, placed for intraoperative monitoring, was kept in place and she was hydrated with 125 mL/hour of normal saline, achieving a PAWP of 10 to 16 mm Hg. Her mean arterial blood pressure without pharmacologic intervention was 95 to 110 mm Hg. She had continued clinical improvement with resolution of her left hemiparesis. On hospital day 5, her ventriculostomy was clamped because cerebrospinal fluid drainage was minimal. The following morning, the patient was arousable only to deep pain and her left side was flaccid. An emergent CT scan demonstrated no new hemorrhage, no increase in ventricular size, and no infarct. Vasospasm was considered the most likely cause. Hypertensive therapy was about to be initiated with a phenylephrine drip, but within an hour she was fully alert and moving all extremities equally. A search for other potential causes of neurologic decline was undertaken and revealed a phenytoin level of 5.5. It was thought that the patient most likely had had a seizure and that her clinical deterioration represented a postictal state. She received a bolus infusion of phenytoin. On hospital day 7, the patient became confused, insisting that her nurse was her son and ordering him out of her "apartment." Lower extremity weakness was detected. CT scan was unchanged. Phenylephrine was started but she developed precordial lead ST elevation and elevated cardiac enzymes. Topical nitrate therapy was initiated and phenylephrine was discontinued. The patient underwent emergent cerebral angiography, which demonstrated moderate to severe bilateral ACA spasm and moderate right MCA spasm.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Management of aneurysmal subarachnoid hemorrhage. 747 15

The authors studied intracranial hemodynamics in experimental animals (Macaca Fuscatus) with acute intracranial hypertension by use of transcranial Doppler (TCD) ultrasound. The blood mean flow velocity in the middle cerebral artery (MCA-FV) and pulsatility index (PI) was recorded using TCD ultrasound (TC2-64, EME) as in the clinical study. Acute intracranial hypertension was produced to determine the correlation of MCA-FV with intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in 11 monkeys, and the correlation of PI with ICP and CPP in 7 monkeys. ICP was elevated by infusing 0.1-0.2 ml/min of saline into the balloon using infusion pump. ICP was raised until maximum level. Changes of MCA-FV, PI, ICP and CPP were evaluated until the CPP of 0mmHg. There was a significant correlation between MCA-FV and ICP (p < 0.01) as well as between MCA-FV and CPP (p < 0.01) in all 11 monkeys. There was also a significant correlation between PI and ICP (p < 0.01) and between PI and CPP (p < 0.01) in 7 monkeys. PI increased markedly when ICP was 80mmHg or greater or when CPP was 60mmHg or less. ICP was always above 80mmHg when PI was above 1.2. All PI values were above 1.0 when CPP was 40mmHg or less. Thus, we could not estimate the absolute values of ICP or CPP from MCA-FV and PI. It seems possible, however, to follow changes in intracranial hemodynamics at the time of increased ICP if MCA-FV and PI are measured continuously while paying attention to factors influencing MCA-FV.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transcranial Doppler sonography in acute intracranial hypertension model--usefulness of pulsatility index]. 810 43


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