Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experience with a continuous-pressure controlled, external ventricular drainage system (EVD) in 100 patients (n = 49 female, n = 51 male; mean age, 56.3 yr) with acute hydrocephalus is reported. Cerebrospinal fluid circulation disturbances resulted from hemorrhages caused by subarachnoid hemorrhage (n = 45), parenchymal hemorrhages from angioma (n = 4), anticoagulants (n = 7), or hypertension or other reasons (n = 30); in addition, hydrocephalus developed from infections (n = 3), tumors (n = 2), infratentorial infarction (n = 5), or unknown reasons (n = 4); 52 patients had ventricular hemorrhages. No patient died of system-associated morbidity. Mean time of EVD treatment was 9.5 days, with 40 patients being treated for 10 to 29 days; routine refobacin (5 mg) flushing of the system was performed three times a day. Patients without cerebrospinal fluid leakage had a 2% rate of secondary infection compared with 13% in patients with cerebrospinal fluid leakage due to ventricular catheter placement (P < 0.05; overall infection rate, 5%). A clinical mortality rate of 29% during EVD treatment was observed in subarachnoid hemorrhage patients (Hunt and Hess Grades II, III, IV, and V; n = 9, 9, 18, and 9, respectively); recurrent hemorrhages during EVD treatment occurred in 19 patients (26 hemorrhages), and of these, 10 patients died. System occlusion was seen in 19 cases (12 of 45 patients with subarachnoid hemorrhage), requiring catheter and system renewal in 1 case; system extraction was seen in 3 cases, misplacement was seen in 11 cases, and disconnection was seen in 5 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Continuous-pressure controlled, external ventricular drainage for treatment of acute hydrocephalus--evaluation of risk factors. 143 14

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Increasing recognition of the importance of calcium in the pathogenesis of cardiovascular disease has stimulated research into the use of calcium channel blocking agents for treatment of a variety of cardiovascular diseases. The favorable efficacy and tolerability profiles of these agents make them attractive therapeutic modalities. Clinical applications of calcium channel blockers parallel their tissue selectivity. In contrast to verapamil and diltiazem, which are roughly equipotent in their actions on the heart and vascular smooth muscle, the dihydropyridine calcium channel blockers are a group of potent peripheral vasodilator agents that exert minimal electrophysiologic effects on cardiac nodal or conduction tissue. As the first dihydropyridine available for use in the United States, nifedipine controls angina and hypertension with minimal depression of cardiac function. Additional members of this group of calcium channel blockers have been studied for a variety of indications for which they may offer advantages over current therapy. Once or twice daily dosage possible with nitrendipine and nisoldipine offers a convenient administration schedule, which encourages patient compliance in long-term therapy of hypertension. The coronary vasodilating properties of nisoldipine have led to the investigation of this agent for use in angina. Selectivity for the cerebrovascular bed makes nimodipine potentially useful in the treatment of subarachnoid hemorrhage, migraine headache, dementia, and stroke. In general, the dihydropyridine calcium channel blockers are usually well tolerated, with headache, facial flushing, palpitations, edema, nausea, anorexia, and dizziness being the more common adverse effects.
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PMID:Differential effects of 1,4-dihydropyridine calcium channel blockers: therapeutic implications. 332 59

To decrease the risk of iatrogenic thromboembolic complications during interventional procedures with coaxial catheter systems, aspirin and systemic heparinization were used in 57 consecutive cases. No thromboembolic complications occurred. This group was compared with a second group of 25 patients who also had interventional procedures with coaxial systems but who had only a continuous heparinized drip infusion flushing the inside of the coaxial system. Two patients had an embolic complication and two others had thrombus formation inside or outside the catheters without neurologic symptoms. The use of systemic heparinization has been extended to all prolonged angiographic procedures except in cases of acute or recent subarachnoid hemorrhage.
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PMID:Aspirin and systemic heparinization in diagnostic and interventional neuroradiology. 697 49

Nicardipine is a second generation dihydropyridine calcium antagonist which selectively inhibits vascular smooth muscle contraction. In elderly patients, the drug has demonstrated clinical efficacy in the management of hypertension, angina pectoris and ischaemia-related cerebrovascular disease. In particular, nicardipine effectively controls blood pressure in elderly hypertensive patients with or without coexistent disease. In noncomparative trials, a regimen containing nicardipine has been associated with an improvement of symptoms in hypertensive patients with concurrent coronary artery, cerebrovascular or peripheral vascular disease, while in essentially 'healthy' elderly hypertensive patients, nicardipine monotherapy has resulted in improved indices of mobility and cognitive function. As yet, however, there is no evidence that nicardipine (and/or other calcium channel antagonists) decreases cardiovascular morbidity and mortality in elderly patients, as has been demonstrated for more established antihypertensive therapies, namely diuretics and/or beta-blockers. The pharmacokinetic properties of nicardipine in elderly hypertensive patients appear to be similar to those in younger patients. The main adverse events associated with nicardipine in the elderly are related to the vasodilator properties of the drug and include pedal oedema, headache and flushing. However, the drug does not exacerbate spontaneous postural hypotension in the elderly, nor does it adversely affect the coronary artery disease risk profile, even in patients with type II diabetes mellitus. In summary, widespread clinical experience in the elderly indicates that nicardipine monotherapy or a regimen containing nicardipine is useful for the treatment of hypertension, particularly in patients with coexistent coronary artery, cerebrovascular or peripheral vascular disease. Nicardipine monotherapy has also demonstrated efficacy in angina pectoris and shown promise in the management of ischaemia-related cerebrovascular diseases, notably subarachnoid haemorrhage.
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PMID:Nicardipine. A review of its pharmacology and therapeutic efficacy in older patients. 847 49

A double blind, placebo controlled, escalating dose study was undertaken in five healthy, conscious volunteers to investigate the effects of human synthetic alpha calcitonin gene-related peptide (CGRP) on middle cerebral artery (MCA) blood flow velocity using transcranial Doppler sonography. During placebo infusion, there was no significant change in any of the parameters studied. During CGRP infusion, all subjects showed flushing of the face and neck. Infusion of CGRP caused a significant increase in arterial pulse pressure and heart rate and a fall in diastolic and mean arterial blood pressure when compared to baseline. Peak and mean MCA velocity did not change significantly. There was a significant increase in pulsatility index though interpretation of this was confounded by the central systemic effects of CGRP. The observed haemodynamic changes may be explained by a prompt sympathetic nervous system response in order to maintain mean arterial blood pressure. Our data suggest that if cerebral vasodilatation had occurred, it was not associated with increased blood flow as an increase in MCA velocity might have been expected. An alternative explanation is that, at the doses employed, CGRP did not cause dilatation of normal cerebral vessels in healthy subjects. This does not however exclude the fact that CGRP may cause dilatation of a spastic artery as seen in cerebral vasospasm following subarachnoid haemorrhage.
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PMID:In vivo effect of calcitonin gene related peptide on middle cerebral artery blood flow velocity in humans. 1581 48

The risk of pial or brain injury while dissecting the cerebral cistern to treat acute subarachnoid hemorrhage might be higher than that of unruptured aneurysms, because visualizing the arachnoid trabeculae between the pia mater and the vessels can be complicated by thick subarachnoid clots filling the cerebral cistern. The author describes technical points of dissecting the cerebral cistern and the removal of subarachnoid hematomas during acute surgical treatment for subarachnoid hemorrhage. Tough arachnoid trabeculae form a "perivascular cistern" around the relatively major vessels in both the sylvian and interhemispheric fissures. The cistern can be separated without pial injury by identifying the microstructure surrounding the major vessels in the cistern and then cutting the arachnoid trabeculae. After bloodless dissection of the cistern, the subarachnoid hematoma can easily be irrigated and removed. The subarachnoid clot must be repeatedly irrigated by flushing the micro-space between arachnoid trabeculae with jets of water to ensure efficient removal. When the arachnoid trabeculae become transparent, small vessels and the arachnoid trabeculae can be differentiated as well as whether or not they can be cut. To treat sylvian hematoma, subpial hematomas extending from the insular cistern and intra-cisternal clots must be removed. Furthermore, inducing complete hemostasis by coagulating the subpial vessels is indispensable to prevent postoperative rebleeding.
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PMID:[Less invasive cistemal approach and removal of subarachnoid hematoma for the treatment of ruptured cerebral aneurysms]. 1722 64