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

Ganglioplegic drugs, including trimetaphan, have been imperfect agents of arterial hypotension, liable to produce tachyphylaxis, and not blocking intercurrent attacks of adrenergic hypertension the dose is inconstant and reversibility sometimes doubtful. The association of neuroleptics, in particulier promazines, permits an appreciable economy in dosage, stabilises the curves of hypotension, with the disadvantage of blocking normalisation of blood pressure. Sodium nitroprusside does not have the disadvantage of ganglioplegic drugs. Although usable alone, the blood pressure graphs sometimes have a certain instability mainly due to the difficulty of regulating the ideal perfusion flow rate. The authors show that the association of neuroleptic drugs has here also an effect of economy of dosage and facilitates the rise in blood pressure. Verification of reinforcement of the effect of sodium nitroprusside by chlorpromazine, acepromazine and levomepromazine was carried out in the dog. The authors show significant graphs.
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PMID:[Controlled arterial hypotension produced by nitroprusside combined with neuroleptics]. 1 64

Sodium nitroprusside (SNP) shows a strong hypotensive activity not only in normotensive animals but also in the presence of experimentally induced arterial hypertension. Its use in intravenous perfusion produces the rapid induction of arterial hypotension lasting or only slightly exceeding the time of its administration. Most investigators consider this hypotensive activity related to the fall in peripheral resistance, as is supported by the considerable fall in diastolic blood pressure. However, an effect of SNP on heart function cannot be ruled out. After four weeks' treatment at dosages corresponding to one tenth of the LD 50, no local or general toxicity could be demonstrated.
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PMID:[Toxico-pharmacological study of lyophilized sodium nitroprusside (SNP)]. 1 61

Sodium nitroprusside (SNP) is rarely used in cardiology. It is reserved traditionally for severe episodes of arterial hypertension. Certain states of refractory heart failure represent new indications for use, which implies a double haemodynamic monitoring system: continuous control of systemic blood pressure by intra-arterial catheterization; control of pulmonary pressure and repeated measurements of cardiac output. Prolonged treatment requires continuous biological monitoring of toxicity and careful control of kidney function. As a moderator of blood pressure, SNP is remarkably effective. The hypotensive effect is immediate, readily reversible and generally tachyphylaxis is not observed. The effect of SNP on cardiac work is one of double load reduction: mainly a reduction in afterload or pressure and systemic resistance and a reduction in preload or pressure of ventricular filling. In this respect, SNP can be used effectively for severe cases of heart failure intractable to traditional cardio-stimulatory and diuretic treatments and stemming from diverse causes: acute stage of myocardial infarction, ventricular dilatation, mitral papillary syndrome, heart failure, either subacute or chronic, of various causes. As a rule, the immediate results are positive. Taking the patient off the drug can be difficult and may cause a return to the previous haemodynamic situation.
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PMID:[Use of sodium nitroprusside in cardiology]. 1 64

Sodium nitroprusside has proved to be the most effective and best-tolerated vasodilator drug available for the management of acute hypertension, heart failure, and other vasoconstricted states as well as for the induction of controlled hypotension during surgery. It dilates both arteries and veins, has a rapid onset and offset of action, and is almost uniformly effective in achieving the desired degree of dilation by careful dosage titration. The need for close monitoring of its intravenous administration and the potential toxicity of prolonged infusions limit its general use from periods of hours to a few days, but its unique and usually well-maintained vascular actions make it an ideal agent for short-term therapy and a potentially useful model for development of new, orally effective vasodilator drugs.
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PMID:Nitroprusside. 49 16

We tested the hypothesis that endothelium-dependent afferent arteriolar vasodilation is impaired in the nonclipped kidney of two-kidney, one clip Goldblatt hypertensive rats relative to sham-operated controls. Five to six weeks after positioning of a 0.25-mm clip on the left renal artery, systolic pressure averaged 173 +/- 10 mm Hg in Goldblatt rats and 118 +/- 4 mm Hg in controls (p less than 0.01). The right kidney was harvested for videometric study of the microvasculature using the in vitro blood-perfused juxtamedullary nephron technique. Kidneys from Goldblatt and control rats were perfused at renal arterial pressures of 150 and 110 mm Hg, respectively. Afferent arteriolar inside diameter did not differ between control (20.3 +/- 0.7 microns) and Goldblatt (21.1 +/- 1.7 microns) kidneys. Determination of afferent responses to increasing concentrations of the endothelium-dependent vasodilator acetylcholine (1 nM to 10 microM) in the bathing solution unveiled a shift to the right in the dose-response relation in Goldblatt rats. Afferent arterioles from control kidneys dilated significantly when exposed to 1 nM acetylcholine, whereas a 1,000-fold higher concentration was required to dilate arterioles from Goldblatt rats. Sodium nitroprusside, an endothelium-independent vasodilator, increased afferent diameter to a similar extent in both groups. In a separate group of normal kidneys, vasodilator responses to 10 microM acetylcholine were completely blocked by 1,000 microM nitro-L-arginine, an inhibitor of nitric oxide synthesis. Thus, endothelium-dependent afferent vasodilation appears to be impaired in the nonclipped kidney of Goldblatt hypertensive rats. This phenomenon could contribute to the altered renal hemodynamic status characteristic of Goldblatt hypertension.
Hypertension 1992 Jun
PMID:Attenuated afferent arteriolar response to acetylcholine in Goldblatt hypertension. 159 81

Sodium nitroprusside is widely used in the treatment of hypertension after coronary artery bypass surgery despite its toxicity and its deleterious effect on the coronary circulation. The aim of this study was to compare the safety and effectiveness of nicardipine with sodium nitroprusside in a randomized study. Nicardipine and sodium nitroprusside are effective for controlling hypertension after coronary artery surgery. Oxygen myocardial balance was more often improved by nicardipine than by sodium nitroprusside. Hemodynamic stability was better with nicardipine which was also devoid of toxicity and might therefore have advantages over sodium nitroprusside in the management of hypertension after coronary artery surgery.
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PMID:Comparison of nicardipine and sodium nitroprusside in the treatment of hypertension after coronary bypass surgery (a pilot study). 163 77

Forty patients who had undergone coronary artery graft surgery and who required vasodilator therapy for postoperative hypertension were given infusions of either propofol (2,6,di-isopropylphenol) or midazolam, together with an infusion of morphine for analgesia while ventilation was controlled artificially. Sodium nitroprusside was administered to patients in both groups using a computer-controlled closed loop system. Both agents produced good quality of sedation. Overall times to spontaneous ventilation and tracheal extubation were shorter in the propofol group, but this was not statistically significant. Ease of control of arterial pressure was satisfactory clinically with both agents, although propofol appeared to be associated with a statistically greater incidence of hypotension.
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PMID:Sedation after cardiac bypass surgery: comparison of propofol and midazolam in the presence of a computerized closed loop arterial pressure controller. 173 76

Rapid lowering of severe hypertension is essential to prevent irreversible damage to vital organs. The patient's clinical status should be evaluated, noting particularly cardiac, neurologic, and renal functions. Choice of treatment should be based on speed and efficacy of action and on hemodynamic, vascular, and renal consequences. It is also important to preserve circulatory homeostasis and vital organ function. Sodium nitroprusside, labetalol, diazoxide, and hydralazine have been used parenterally for rapid control of severe hypertension, but they do not always produce optimal, balanced hemodynamic effects. Calcium antagonists have been advocated because of their beneficial circulatory effects. Nicardipine, a new dihydropyridine calcium antagonist, produces significant antihypertensive effects, and when given intravenously, results in a rapid fall in blood pressure. Studies have confirmed that nicardipine is effective and safe in the management of severe hypertension and hypertensive crises. Because the aim of rapidly controlling severe hypertension is to prevent target organ dysfunction, nicardipine therapy offers a useful additional option in the clinical management of severe hypertension and hypertensive crises.
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PMID:Management of hypertensive emergencies: changing therapeutic options. 176 27

The nitrovasodilators, nitroglycerin and sodium nitroprusside, cause both arterial and venous smooth muscle dilation by the intracellular release of nitric oxide. Nitric oxide activates guanylate cyclase, resulting in an accumulation of cyclic GMP. The endogenous formation of nitric oxide results in vasodilatory activity similar to the nitrovasodilators. Nitroglycerin is commonly used in the treatment of angina pectoris because of its ability to decrease myocardial oxygen consumption. Most likely, this response occurs as a result of a reduction in preload, which can decrease arterial wall tension and improve coronary blood flow. This pharmacologic effect warrants the use of nitroglycerin in the treatment of myocardial ischemia or infarction, congestive heart failure, and hypertension. Sodium nitroprusside is effective in reducing arterial blood pressure in hypertensive crisis as a result of systemic vasodilation leading to a reduction in preload and afterload. Sodium nitroprusside is not as effective in the treatment of angina pectoris or in diminishing of myocardial ischemia because it does not preferentially improve blood flow to ischemic myocardium over nonischemic myocardium. Inhibition of platelet aggregation has been demonstrated with these drugs, but the clinical applications need further investigation. Nursing interventions for the patient on nitrovasodilator therapy include careful hemodynamic monitoring and drug infusion, along with elimination of physical and emotional stimuli that can aggravate the patient's underlying pathology.
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PMID:Pharmacology of the nitrovasodilators. Antianginal, antihypertensive, and antiplatelet actions. 190 76

The recent discovery of endothelium-derived relaxation factor (EDRF) has altered the traditional classification of vasodilators used in angina pectoris and heart failure. If a vasodilator induces release of EDRF from the epithelium it is classified as endothelium-dependent, if not it is independent. Sodium nitroprusside and SIN-1 (active metabolite of molsidomine) are the main independent vasodilators since the endothelium relaxation factor appears to be principally a nitric oxide radical in these synthetic vasodilators. In contrast, calcium-channel blockers and a good number of endogenous chemical mediators (acetylcholine, bradykinin, serotonin, etc.) are endothelium-dependent. Furthermore, simple increase in blood flow through the large vessels can result in endothelium-dependent vasodilation (flow rate-dependence) the extent of which depends on the drug examined. The fact that the pharmacologic response of a vasodilator can be altered under certain pathologic conditions (atherosclerosis, hypertension, diabetes, etc.) further increases the importance of the role of the vascular endothelium in the action of vasodilators since endothelial modulation may then be completely diverted to secretion of endothelium-derived contracting factors (EDCFS).
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PMID:[Vasodilator agents and the vascular endothelium]. 262 13


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