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)

In cats air embolism of the brain was produced by injecting 0.6 ml blood foam into the innominate artery proximal to the origin of both common carotid arteries. Air embolism caused transient ischemia of the brain, reaching a maximum within 1 min after injection. Resolution of the air embolism began a few minutes later and was completed within 15 min in the center and within 30 min in the border zone of the main supplying arteries. During this phase tissue perfusion was inhomogenous with reduced flow rates in some areas and reactive hyperemia up to 300% in others. This resulted in venous hyperoxia and a decrease of arteriovenous oxygen difference to as low as 2 ml/100 ml blood. Reactive hyperemia was accompanied by brain swelling and an increase in intracranial pressure from 3.6 +/- 1.2 to 12.3 +/- 2.0 mm Hg. The reason for hyperemia was a decrease of cortical pH which fell from 7.33 +/- 0.03 to 7.03 +/- 0.05, and which caused a dilation of pial arteries up to 260%. Immediately after embolism, the EEG flattened and oxygen consumption decreased. After normalization of flow, oxygen consumption returned to normal, but EEG only partially recovered. Air embolism had little effect on the water and electrolyte content of the brain, and produced very little damage to the blood-brain barrier.
Stroke
PMID:Arterial air embolism in the cat brain. 4 47

The influence of sympathetic nervous activity on cerebral circulation and cerebrovascular CO2 reactivity was investigated through inhibition of dopamine beta-hydroxylase (DBH). A PO2 electrode, a PCO2 electrode and a plate-type thermocouple-flowmeter were placed on the pial surface of the cat brain. Cerebrocortical PO2, PCO2, cerebrocortical blood flow and arterial blood pressure were continuously recorded before, during and after intracarotid infusion of 10 mg/kg of fusaric acid, a potent DBH inhibitor. The effects of 5% CO2 inhalation and hyperventilation were measured before and after the inhibition of DBH. Following the intracarotid infusion of fusaric acid, cerebrocortical PO2 and cerebrocortical blood flow increased significantly. After the inhibition of DBH, the degree of the increase in cerebrocortical PO2 during 5% CO2 inhalation was enhanced while the degree of the decrease in cerebrocortical PO2 during hyperventilation did not show any significant change. The cerebral vasodilatation caused by fusaric acid suggests that the sympathetic nervous system takes part in the resting tone of cerebral blood vessels. The increase in the cerebrovascular CO2 reactivity produced by the inhibition of DBH suggests that the sympathetic nervous system modifies cerebrovascular CO2 reactivity.
Stroke
PMID:Modification of cerebrovascular CO2 reactivity by inhibition of dopamine beta-hydroxylase. 4 44

The concensus conclusions reached at a concensus development conference on Estrogen Use and Postmenopausal Women in September 1979 are based on 3 position papers prepared for the conference, the response of the panel, and the general discussion by the audience, followed by the panel and other conference participants. The evidence for the efficacy of estrogens in treating specific conditions associated with menopause was reviewed 1st. It was accepted that estrogens are more effective than placebo in decreasing the frequency and severity of vasomotor symptoms. Estrogens are effective in overcoming the atrophy of the vaginal epithelium and the associated symptoms. Present evidence does not justify the use of estrogens to treat primary psychological problems. The validity of 3 randomized trials indicating that exogenous estrogens can retard bone loss if given around the time of menopause was acknowledged. There is no convincing evidence that estrogens in customary doses increase the risk of thromboembolic phenomena, stroke, or heart disease in women who have undergone natural menopause. Evidence was also reviewed concerning adverse effects associated with post-menopausal estrogen use. In the absence of exogenous estrogens, the incidence of endometrial cancer is about 1/1000 postmenopausal women per year. This rate increases severalfold beginning after about 2-4 years of use of 0.625 or 1.25 mg of conjugated estrogens daily. Cystic hyperplasia of the endometrium, regarded as a premalignant condition, has been associated with unopposed estrogen, whether endogenous or exogenous.
 ...
PMID:Estrogen use and postmenopausal women: a National Institutes of Health Consensus Development Conference. 4 37

A case of an acutely beginning histologically proved panarteritis is described which was initiated by hepatitis B caused by blood transfusions. After one year of steroid therapy the arteritis was no longer seen histologically, Australia-antigen became negative. Terminally the patient developed an apoplexy, renewed gastric bleeding, septicemia with obstructive jaundice, nose bleeding, increasing renal insufficiency, and cardiac failure. The Australia-antigen reappeared in the serum. It could be assumed that the panarteritis had progressed. Immune complexes of Australia-antigen and corresponding antibodies which are deposited in the vascular wall and cause an inflammatory reaction, are being held responsible for the panateritis. They were proved serologically and by immunofluorescence in the vascular wall. In cases of panarteritis of unknown origin Australia-antigen can be found in a high percentage, as was demonstrated by a second case.
 ...
PMID:[Hepatitis-B-surface antigen and panarteritis (author's transl)]. 4 44

The relationship between preload and inotropy on left ventricular function was studied in anaesthetized open-chest dogs, by measuring left ventricular dimensions and stroke volume before and during saline infusion at different levels of inotropy. Left ventricular dimensions were continuously estimated by recording myocardial chord length (MCL) in the anterior wall of the left ventricle by ultrasonic technique. The effects of isoproterenol, a stimulator of adrenergic beta-receptors (high inotropy), and propranolol, an inhibitor of adrenergic beta-receptors (low inotropy), were examined during right atrial pacing at constant heart rate averaging 161 +/- 5 beats/min. Stroke volume was varied within the range 9.0 +/- 1.7 ml to 28.6 +/- 3.2 ml by increasing inotropy and preload. To increase preload, saline was infused intravenously until end-diastolic MCL increased by about 10% and left ventricular end-diastolic pressure was higher than 10 mmHg. At constant heart rate and blood volume, both before and during saline infusion, end-diastolic MCL was not influenced by isoproterenol or propranolol administration. End-systolic MCL was reduced by raising inotropy. The difference between end-diastolic and end-systolic MCL, the systolic myocardial shortening (MS), increased during saline infusion; the relative increase in MS was the same at high and low inotropy. On average, MS was more than 50% longer at high than at low inotropy, both before and after saline infusion. Thus, left ventricular end-diastolic volume is increased by saline infusion and end-systolic volume is reduced by increasing inotropy. Preload and inotropy exert independent effects on stroke volume.
 ...
PMID:Role of preload and inotropy in stroke volume regulation at constant heart rate. 4 64

To determine optimal heart rate for the maximal cardiac output at various levels of inotropy and blood volume, the relationship between heart rate (HR) and stroke volume (SV) was examined in anaesthetized dogs during right atrial pacing. Myocardial inotropy was raised by intravenous infusion of isoproterenol, a stimulator of adrenergic beta-receptors, and reduced by propranolol, an inhibitor of adrenergic beta-receptors. Circulating blood volume was increased by saline infusion. Within the range of optimal heart rate, SV and HR were inversely related: SV = k (HR0-HR), where k indicates the relationship between changes in SV and HR. The intercept with the HR axis is HR0. At constant HR a rise in inotropy increased SV and a fall in inotropy reduced SV. These changes in SV were eual at every HR, and k was therefore constant. In contrast, blood volume expansion increased SV more at low than at high HR (k increased), but HR0 was not significantly changed. Calculated maximal cardiac output: k.HR02/4, and optimal heart/rate: HR0/2, agreed with observations when maximal cardiac output was raised from 1900 to 4500 ml/min by increasing blood volume and inotropy. Optimal HR was not influenced by changes in blood volume, but was increased from 160 to 200 beats/min by increasing inotropy. We conclude that the optimal heart rate and the maximal cardiac output can be predicted from the linear relationship between SV and HR during right atrial pacing.
 ...
PMID:Cardiac performance: optimal heart rate for maximal cardiac output. 4 65

In 18 patients with documented ischaemic heart disease the cardiovascular effects of ketamine (1.5 mg/kg iv) were studied under three different conditions: 1. in awake premedicated patients (n = 6); 2. after the previous administration of flunitrazepam (0.015 mg/kg iv, n = 6) and 3. under conditions of neuroleptanalgesia and muscle relaxation (n = 6). Flunitrazepam prevented or at least attenuated the increases in heart rate (30%), mean arterial pressure (37%), mean pulmonary artery pressure (165%), left ventricular filling pressure (230%), total peripheral resistance (50%), pulmonary vascular resistance (100%) and in the rate-pressure product (66%) which were associated with the use of ketamine as the sole anaesthetic agent. In addition, the flunitrazepam-pretreatment abolished the fall in cardiac index and stroke index which occured in patients given ketamine alone. Flunitrazepam therefore appears to be a promising drug to prevent adverse cardiovascular reactions, when ketamine should be chosen for induction of anaesthesia. Neuroleptanalgesia and muscle relaxation also proved effective in controlling the sympathomimetic actions of ketamine. The response of the mean pulmonary artery pressure and of the ventricular filling pressures to ketamine in this group was even more damped than in the patients pretreated with flunitrazepam alone.
 ...
PMID:[Flunitrazepam-pretreatment for prevention of adverse cardiovascular effects following ketamine]. 4 95

1 After acute intravenous administration labetalol reduced mean values for BP, total peripheral resistance, heart rate and cardiac output. All changes were more pronounced during bicycle exercise. 2 After a mean duration of 20 months' treatment with oral labetalol the haemodynamic findings were broadly similar except for a more marked reduction in the total peripheral resistance and cardiac output had returned to pretreatment level due to an increased stroke volume which had counter balanced the reduction in heart rate. These changes occurred at rest, in the erect position and during exercise but the reductions in BP and peripheral resistance were most marked during exercise. 3 Left ventricular filling pressures and stroke volume/filling pressure ratios were not significantly altered after intravenous labetalol compared with pretreatment values. 4 Systolic BP x heart rate product was lowered particularly during exercise after both intravenous and oral labetalol. 5 After long-term oral labetalol, the most striking haemodynamic change was in the elevated resting stroke volume supine and standing.
 ...
PMID:Cardiovascular dynamics after acute and long-term alpha- and beta-adrenoceptor blockade at rest, supine and standing, and during exercise. 4 62

Sixteen patients scheduled for abdominal aortic resection and grafting were randomly assigned to two groups to study the cardiovascular effects of infrarenal aortic cross-clamping. The patients in the first group had received a thoracic epidural block followed by intravenous administration of the selective beta-1-adrenoreceptor agonist prenalterol prior to induction of general anaesthesia. The patients in the second group served as controls and received no specific treatment prior to general anaesthesia. In both groups, aortic cross-clamping was followed by an equal rise in pulmonary artery diastolic pressure and mean systemic arterial pressure. There was a significant difference in systemic vascular resistance, as the control group had a 46% increase 30 s after cross-clamping, while the pretreated patients had only a 7% increase at the same time. Moreover, the patients given the thoracic epidural block followed by prenalterol increased their stroke volume and cardiac indices, as compared to the patients in the control group who showed a significant decrease in these parameters. Possible mechanisms for the mode of action of the combined thoracic epidural block and beta-1-adrenoreceptor agonist pretreatment are discussed.
 ...
PMID:Effects of thoracic epidural block and the beta-1-adrenoreceptor agonist prenalterol on the cardiovascular response to infrarenal aortic cross-clamping in man. 4 50

Cerebral blood flow was measured by means of a 10-channel cerebrograph in anesthetised patients before and during 2% enflurane. This investigation was carried out after carotid angiography; 2-3 mCi Xe133 was injected into the internal carotid artery. The clearance curves of Xe133 were captured by 10 scintillation counters. In addition to regional cerebral blood flow (rCBF), arterial blood pressure, heart rate, stroke volume, cardiac output and arterial blood gases were measured in seven adult patients. During 2% enflurane, a small, and in two regions a significant decrease in rCBF was observed. Mean arterial pressure and heart rate decreased significantly, but cardiac output did not. The decrease in PaCO2 was not significant.
 ...
PMID:Influence of enflurane on cerebral blood flow in man. 4 55


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