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

Clinical characteristics of cerebral infarctions occurring in 15 women (aged 22-51) who had taken oral contraceptives for an average of 24.8 months are described. Aside from 5 atypical cases, the 10 remaining women suffered marked increases in headache pain for only 3 months before their strokes. The subjective severity increased progressively, and in at least 6, the duration of each headache increased. Frequency of headaches in 9 women increased noticeably during the prodrome, and in some was almost constant for a week before the infarct. However only 5 patients had or had just had headaches at the exact time of the stroke. The spatial aspects of headache locations imply etiological relationship to the infarct which follows. Upon recognition of the clinical characteristics of such headache in women taking oral contraceptives, the medication should be stopped immediately. Absolute withdrawal should be recommended for patients with increasing vascular headache and headache associated with focal neurological symptoms. Hypertension in patients with the slightest sign of increasing headache should be cause for discontinuation of the pill. Following withdrawal of the oral contraceptive, synthetic narcotics are the only therapy advised. Vasoconstrictor drugs may aggravate the vasoconstrictor phase leading to infarction.
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PMID:The clinical characteristics of headache during impending cerebral infarction in women taking oral contraceptives. 573 Jan 19

Twenty-five patients requiring infrarenal abdominal aortic clamping were studied during halothane, nitrous oxide anaesthesia. Aortic clamping caused reductions in cardiac index (CI), stroke volume index (SVI) and left ventricular stroke work index (LVSWI). Systemic vascular resistance (SVR) increased. In seven patients CI was less than 1.81 X min-1 X m-2. Intravenous administration of nitroglycerin, 1 microgram X kg-1 X min-1, for 20 minutes, accompanied by volume loading to maintain pulmonary capillary wedge pressure, resulted in a significant improvement in haemodynamic parameters. CI increased 24 per cent as a result of a 14 per cent increase in SVI and an eight per cent increase in heart rate. LVSWI increased 13 per cent and SVR decreased 21 per cent. The plasma nitroglycerin concentration at the time of these measurements was 2.9 +/- 1.0 ng X ml-1. Aortic unclamping resulted in a mean maximum decrease of 14 +/- 2 torr mean arterial pressure. Epinephrine, norepinephrine and plasma renin activity gradually increased during the period of the anaesthetic.
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PMID:Intravenous nitroglycerin administration during infrarenal aortic clamping. 642 26

Isoflurane was used in 10 ASA I or II female patients, undergoing hysterectomy. It was given at a constant inspired concentration of 1.3% in a 50% N2O/50% O2 mixture, after induction of anaesthesia using etomidate (0.3 mg kg-1) and intubation following pancuronium (0.1 mg kg-1). No analgesic supplement was given. The patients were hyperventilated minimally (PaCO2 4.7-5.3 kPa). At standardized times (before induction, after induction, 5', 25', 50' and 75' min after surgical incision, awake and awake +60'), cardiovascular (blood pressure, cardiac output, stroke volume, heart rate), respiratory (blood gases), metabolic (oxygen consumption, blood glucose) and hormonal (noradrenaline, adrenaline, cortisol, prolactin) changes were measured. Blood pressure changes were very moderate (mean values were lower than before induction), but heart rate was increased significantly. Decreases in stroke volume and changes in cardiac output were not significant. Oxygen consumption was decreased below basal values during surgery. Blood glucose levels increased significantly in the course of surgery and remained raised postoperatively. Adrenaline and noradrenaline levels increased significantly. At each examination time, cortisol levels were decreased significantly. Prolactin levels had decreased significantly 75 mins after incision and remained low 60 mins after awakening.
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PMID:Cardiovascular, metabolic and hormonal changes during isoflurane N2O anaesthesia. 644 92

Adrenal catecholamines were determined in Wistar Kyoto rats (WKY), and stroke-prone and stroke-resistant spontaneously hypertensive rats (SHRSP, SHR) treated with hyperbaric oxygen for 90 minutes daily from 6 to 13 weeks of age. The animals were divided into 5 groups. Group I (control group), was handled under the same conditions as pressure-treated groups II and III, but with ambient oxygen pressure and concentration. Group II (pressure-control group), was treated with 2 atmospheric absolute pressures (ATA) of air without any oxygen provided. Group III (high-oxygen group), was exposed to 2 ATA under the environment of air saturating oxygen. Group IV (antihypertensive group), was treated with hydralazine. Group V (adrenalectomized group), was given 1% NaCl solution and bilateral adrenalectomy. The average contents of adrenal norepinephrine of SHR and of SHRSP in Group I were greater (p less than 0.05-p less than 0.001) than those of the WKY in Group I. A similar tendency was also observed for the content of adrenal epinephrine. The average concentrations of adrenal epinephrine and norepinephrine of SHR and SHRSP in Group II and III were significantly (p less than 0.05-p less than 0.001) greater than those of the respective rats in Group I, but no significant differences were noted in the blood pressure between pressure-treated groups (II, III) and the control group (I). Adrenalectomized SHR, SHRSP and WKY rats (Group V) had similar blood pressure levels as the control rats (Group I). The development of hypertension in SHR and SHRSP was effectively suppressed by the treatment with hydralazine, which, however failed to reduce concentrations of adrenal epinephrine and norepinephrine in these rats. These results indicate that increased adrenomedullary function in SHR and SHRSP is further enhanced by hyperbaric oxygenation treatment, but that high concentrations of adrenal catecholamines are not required for the pathogenesis of spontaneous hypertension of these animals at this age.
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PMID:Increased adrenal epinephrine and norepinephrine in spontaneously hypertensive rats treated with hyperbaric oxygen. 652 49

The physiological integrity of the in situ perfused heart of the ocean pout was established by its ability to maintain cardiac output (Q) over a range of work loads, and by the dependence of Q upon the filling pressure of the heart. Similar observations have been reported previously for the in situ perfused heart of the sea raven. Physiological levels of extracellular acidosis (pH 7.6/1% CO2 and pH 7.4/2% CO2) significantly depressed cardiac performance in sea raven and ocean pout hearts in situ. Negative chronotropic and inotropic responses were observed. Adrenaline (AD; 10(-7) M) under control conditions (pH 7.9/0.5% CO2) produced a sustained tachycardia. The tachycardia reduced filling time of the ventricle and stroke volume was compromised because of the constant preload to the heart. Consequently, AD produced only an initial, transient increase in stroke volume and Q. Thereafter, stroke volume was reduced in proportion with the increase in heart rate, and Q remained unchanged. The combined challenge of extracellular acidosis and AD demonstrated interactive effects between AD and acidosis in situ. Q and power output were maintained in both species at both levels of extracellular acidosis during the combined challenge. Thus AD alone can maintain (but not improve upon) basal Q during extracellular acidosis. The effects of extracellular acidosis, circulating catecholamines and venous return pressure to the heart are discussed in relation to the regulation of Q following exhaustive exercise.
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PMID:Cardiac performance in the in situ perfused fish heart during extracellular acidosis: interactive effects of adrenaline. 666 60

Forty-four untreated patients with an enlarged sella were studied (excluding patients with acromegaly, Cushing's disease, and those with radiological evidence of suprasellar extension). In 20 patients CT revealed a completely or partially empty sella. Based on recent studies we take this finding to signify the previous presence of a pituitary adenoma which has undergone complete or partial necrosis. Ten of the 20 patients had in fact experienced symptoms typical of a pituitary apoplexy compared with only one out of the other 24 patients. Adrenal, thyroid, and growth-hormone insufficiency occurred as often in patients with an empty sella as in those with a solid pituitary tumour. In contrast, plasma prolactin levels were much lower in patients with an empty sella than in patients with a solid tumour (11 vs 166 ng/ml). It is assumed that this discrepancy reflects previous necrosis occurring in an adenoma hypersecreting prolactin. These results emphasize the importance of taking the spontaneous course of pituitary adenomas into account when assessing the effect of various treatment protocols.
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PMID:Pituitary function in patients with evidence of spontaneous disappearance of a pituitary adenoma. 688 32

Cardiac output was determined to 70 patients with hypertonic disease I, II and III stage by dye-dilution method and urine excretion of adrenaline and noradrenaline was determined by fluorescence method. The extent of stroke and minute volume was determined depending on the stage of the disease, degree of arterial hypertension and patients' age. Noradrenaline excretion was normal in 75.8 per cent from the whole group of the patients examined and decreased in 24.2 per cent. Adrenaline excretion was increased in 7.1 per cent and with normal values--in 92.9 per cent of the patients. No discrepancies in adrenaline and noradrenaline excretion were found in the patients with hypertonic disease, depending both on the degree of arterial hypertension and patients' age. A moderate positive correlation was found between noradrenaline excretion and cardiac index and stroke index.
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PMID:[Urinary catecholamine excretion and cardiac output in hypertensive patients]. 710 94

In 10 patients following open heart surgery, adrenaline, dobutamine and dopamine were administered, and the changes in hemodynamic parameters and renal blood flow (RBF) were examined. RBF was determined by the local thermodilution method. Prior to the application of this method in clinical measurement, reliability of the method was checked using a model circuit. The correlation between the actual flow and flow obtained with this method was high (r = 0.999, p less than 0.005, n = 8). Reproducibility in repeated measurements was excellent, r = 0.997 (p less than 0.005, n = 8) in the model circuit and r = 0.985 (p less than 0.005, n = 89) in the clinical measurement. Adrenaline at rates of 0.02--0.08 microgram/kg/min showed a marked inotropic action without any significant change in RBF. With 0.04 microgram/kg/min of adrenaline, the RBF/CO (cardiac output) ratio declined significantly. We conclude that adrenaline is often effective in patients following open heart surgery, but renal vasoconstriction is the major disadvantage. After a 10-min administration of 2, 4 and 8 micrograms/kg/min of dobutamine, cardiac index (CI) and stroke volume index (SVI) showed a stepwise increase in accordance with an increase of dosage, and RBF also increased with CO. Consequently, no significant change in RBF/CO was found. Mean left atrial pressure (LAP) or mean pulmonary arterial wedge pressure (PAWP) decreased in 4 of 7 patients with 8.0 micrograms/kg/min of dobutamine. Thus, dobutamine is an excellent beta 1-adrenergic agonist with a weak alpha-action on both peripheral and renal vessels. With 2.0--2.5 micrograms/kg/min of dopamine, RBF increased by 15.5% (p less than 0.05). while no significant increase appeared in CI. With 4.0 micrograms/kg/min or more of dopamine, CI and SVI increased. With 16--20 micrograms/kg/min of dopamine, RBF increased by up to 44.8%. Significant increase of mean LAP or mean PAWP was observed with 8.0--10.0 micrograms/kg/min or more of dopamine. These findings indicate that the potential increase o LVEDP (left ventricular end-diastolic pressure) with 8--10 micrograms/kg/min or more of dopamine exerts a disadvantageous effect in patients following open heart surgery. However, the effect on the renal hemodynamics, especially with small doses of dopamine, is unique and not observed with adrenaline or dobutamine.
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PMID:Comparative study of effects of adrenaline, dobutamine and dopamine on systemic hemodynamics and renal blood flow in patients following open heart surgery. 712 Jun 50

The mechanisms by which elevated levels of vasopressin (ADH) in man and animals cause serious myocardial dysfunction, evidenced by arrhythmias, reduction in cardiac output and coronary blood flow, are not settled. Experiments were conducted in 16 isolated working left ventricles to examine their metabolic and hemodynamic responses to the infusion of vasopressin and the combination of vasopressin and epinephrine. Contractile performance was evaluated by analysis of positive dP/dt, contractile element velocities, and ventricular work-curves using stroke work/end-diastolic pressure. Relaxation parameters, including negative dP/dt and the early diastolic relaxation time constant, were also studied. Coronary blood flow was reduced 22% or less by vasopressin while cardiac output was maintained at a constant level. Myocardial oxygen consumption, lactate and potassium balances were determined from arterial and coronary sinus concentrations. Vasopressin produced myocardial dysfunction indicated by decrements in contractile and relaxation indices, without evidence of global ischemia. Epinephrine restored the mechanical performance to normal without significant change in coronary blood flow, myocardial oxygen consumption, or lactate and potassium balance.
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PMID:Mechanisms of impaired cardiac function by vasopressin. 736 15

The relationship between circulating adrenaline and blood pressure was examined by manipulating plasma adrenaline levels in both normotensive and hypertensive rats: bilateral adrenalmedullectomy was performed in spontaneously hypertensive rats and stroke-prone spontaneously hypertensive rats; adrenaline bitartrate was infused chronically (25-32 micrograms/kg/h s.c.) into Wistar Kyoto, Sprague Dawley and stroke-prone rats via osmotic minipumps. Arterial and venous catheters were subsequently implanted for direct measurement of mean arterial pressure, blood sampling and drug administration in conscious rats. Adrenaline infusion for 5-6 weeks in Wistar Kyoto rats did not affect resting blood pressure (118 +/- 3 versus 119 +/- 1 mmHg in controls) even though plasma adrenaline was elevated 12-fold. Plasma noradrenaline was marginally elevated. Blood pressure was also unaffected by adrenaline infusion in Sprague Dawley or stroke-prone hypertensive rats. One week after adrenal medullectomy, plasma adrenaline was reduced 89% in spontaneously hypertensive rats, but blood pressure was unaffected. Ten weeks after adrenal medullectomy in young stroke-prone rats, resting blood pressure was slightly higher (167 +/- 2 mmHg) than in control rats (157 +/- 2 mmHg), although adrenaline was reduced by 34% in plasma and 67% in adrenal glands. Nitroprusside was infused acutely to lower blood pressure and reflexly elevate plasma noradrenaline. Neither of these responses were affected by chronic adrenaline infusion or adrenal medullectomy. In both adrenaline-infused Wistar Kyoto and medullectomised stroke-prone rats, autonomic blockade reduced blood pressure to a similar extent as in controls, indicating that the degree of sympathetic vasoconstriction was not altered by either treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of influence of circulating adrenaline on blood pressure in normotensive and hypertensive rats. 819 11


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