Sodium nitroprusside effects

Figure 4 Experimental results from an individual perfused cat carotid body experiment demonstrating NO donor (sodium nitroprusside) effect, (a) Average ND and tissue PO2 disappearance curve for five measurements with control perfusate and the relationship between tissue PO2 and ND (inset) are shown (left panel). The derivative of the tissue PO2 disappearance curve (open circles) and two-oxidase-model fit (solid curve), with estimated low-affinity pathway (dashed curve) and maximum rate and K, are shown (right panel), (b) Average ND and tissue PO2 disappearance curve for three measurements with 1 pM SNP in the perfusate and relationship between tissue PO2 and ND (inset) are shown (left panel). The derivative of the tissue PO2 disappearance curve (open circles) and two-oxidase-model fit (solid curve), with estimated low-affinity pathway (dashed curve) and maximum rate and K i are shown (right panel).

Maletic, S. D., Dragicevic-Djokovic, L. M., Ognjanovic, B. L. et al. (2004). Effects of exogenous donor of nitric oxide-sodium nitroprusside on energy production of rat reticulocytes. Physiol. Res. 53 (4), 439-47. 

Haywood and Huyser s [43] study of the indophenol blue reaction for ammonia determination showed the effect of pH variation on the final colour and emphasised the necessity for the efficient buffering to obtain reproducible results. The optimum conditions found by the authors (pH 10.8 and using sodium nitroprusside) were similar to those used by Solorzano [37]. Haywood and Huyser also replaced acetone with sodium nitroprusside. 

The answer is d. (Hardman, pp 794-795.) Hydralazine, minoxidil, diazoxide, and sodium nitroprusside are all directly acting vasodilators used to treat hypertension. Because hydralazine, minoxidil, nifedipine, and diazoxide relax arteriolar smooth muscle more than smooth muscle in venules, the effect on venous capacitance is negligible. Sodium nitroprusside, which affects both arterioles and venules, does not increase cardiac output, a feature that enhances the utility of sodium nitroprusside in the management of hypertensive crisis associated with MI. 

Elzubeir, E.A. and R.H. Davis. 1988a. Effect of dietary sodium nitroprusside as a source of cyanide on the selenium status of chicks given diets of varying selenium concentration. Brit. Poult. Sci. 29 769-777. 

Sodium nitroprusside is a mixed arterial-venous vasodilator that acts directly on vascular smooth muscle to increase cardiac index and decrease venous pressure. Despite its lack of direct inotropic activity, nitroprusside exerts hemodynamic effects that are qualitatively similar to those of dobutamine and milrinone. However, nitroprusside generally decreases PAOP, SVR, and blood pressure more than those agents do. 

As well as NONOates, other NO donors also showed anticancer activity independently. Sodium nitroprusside (SNP), a metal-NO complex, showed cytotoxic effects on the cells of some patients with malignant lymphoma (ML), acute myelocytic leukemia (AML) or chronic myelomonocytic leukemia (CMMoL), but not with multiple myeloma [109]. SNP and cytosine arabinoside (Ara-C) did not share the drug resistance. Interestingly, SNP had no effect on lymphocytes of healthy volunteers. These results suggest that SNP has an anti-tumor effect on human hematological malignant cells. 

Sodium nitroprusside (SNP), which is also known as Nipruss or Nipride to medical practitioners, was the first iron nitrosyl complex, prepared as far back as 1850 by Playfair [40]. The hypotensive property of SNP was first demonstrated by Johnson [41] in 1929. It was shown that application of a moderate dose of SNP reduces the blood pressure of a severely hypertensive patient without any side effect [42]. Since that time considerable research has been carried out to understand the mode of action of nitroprusside and its metabolic fate. SNP is now regarded as a potent vasodilator that causes muscle relaxation by releasing NO which activates the cytosolic isozyme of guanylyl cyclase [43-46]. 

Tolerance to nitrates is defined as the reduction in hemodynamic effect or the requirement for higher doses to achieve a persistent effect with continuous use in the face of constant plasma concentrations [15]. Nitrate tolerance was first described for nitroglycerin in 1888 [36] it occurs with all organic nitrates, albeit to different extents. For reasons that are not understood, PETN appears to be the least susceptible to the development of tolerance. No, or much less, tolerance is observed with nitrite esters, such as amyl nitrite [37], molsidomine, and sodium nitroprusside. Earlier investigations suggested that a depletion of intracellular thiols is involved in tolerance development [17], but this has not been substantiated in later studies [38, 39]. As with organic nitrate bioactivation, the precise mechanism(s) involved in nitrate tolerance remain(s) unknown, but it is likely to be complex and multifactorial. Two principal... 

The therapeutic effects of sodium nitroprusside depend on release of nitric oxide which relaxes vascular muscle. Sodium nitroprusside is best formulated as a nitrosonium (NO+) complex. Its in vivo activation is probably achieved by reduction to [Fe(CN)5NO]3, which then releases cyanide to give [Fe(CN)4NO]2, which in turn releases nitric oxide and additional CN to yield aquated Fe(II) species and [Fe(CN)6]4 (502). There are problems associated with its use, namely reduced activity due to photolysis (501) and its oxidative breakdown due to the action of an activated immune system (503), both of which release cyanide from the low-spin d6 iron complex. 

Sodium nitroprusside is a powerful, instantaneous-acting intravenous drug used to lower blood pressure in hypertensive crises. The hypotensive effect is caused by peripheral vasodilation resulting from a direct effect on both arterial and venous vessels. 

Side effects also appear very quickly however, they last for a very short time because of their extremely short half-life. Sodium nitroprusside is biotransformed to cyanide and thiocyanate, which upon overdose can result in thiocyanate and cyanide intoxication. The presence of drugs such as diazoxide and sodium nitroprusside has significantly decreased the possibility of a sharp drop in arterial blood pressure and urgent situations which, however, should be used under the constant care of medical personnel. Synonyms of this drug are nipride, nipruton, and others. 

This chapter describes four vasodilators in detail. Two of these agents, hydralazine and minoxidil, are effective orally and are used for the chronic treatment of primary hypertension. The other two drugs, diazoxide and sodium nitroprusside, are effective only when administered intravenously. They are generally used in the treatment of hypertensive emergencies or during surgery. 

Sodium nitroprusside is used in the management of hypertensive crisis. Although it is effective in every form of hypertension because of its relatively favorable effect on cardiac performance, sodium nitroprusside has special importance in the treatment of severe hypertension with acute myocardial infarction or left ventricular failure. Because the drug reduces preload (by venodila-tion) and after load (by arteriolar dilation), it improves ventricular performance and in fact is sometimes used in patients with refractory heart failure, even in the absence of hypertension. 

The most commonly encountered side effects of sodium nitroprusside administration are nausea, vomiting, and headache, which quickly dissipate when the infusion is terminated. When sodium nitroprusside treatment extends for several days, there is some danger of toxicity owing to the accumulation of its thiocyanate metabolite. Thiocyanate intoxication includes signs of delirium and psychosis hypothyroidism also may occur. If nitroprusside is administered for several days, thiocyanate levels should be monitored. 

Attention then turned to the mechanism of glutamate-induced neurotoxicity in the brain. Evidence was provided that NO mediates glutamate neurotoxicity in primary cortical cultures (Dawson et ai, 1991). NO synthase inhibitors and hemoglobin prevented NMDA- and glutamate-induced neurotoxicity on the other hand, L-arginine reversed the effect of NO synthase inhibitors, and sodium nitroprusside (which decomposes to NO) caused neurotoxicity that paralleled cyclic GMP formation. In the cerebral cortex, NO synthase immunoreactivity was found to be confined to a discrete population of aspiny neurons comprising... 

It is usually recommended that ACE inhibitors be continued peri-operatively in common with other antihypertensives. There is some evidence that postoperative haemodynamic stability is improved and renal function protected. Pretreatment with ACE inhibitors may reduce tachyphylaxis to sodium nitroprusside and help to prevent rebound hypertension. On the other hand, there is evidence that ACE inhibitors may predispose to hypotension during anaesthesia and that they reduce cerebral blood flow during any period of systemic hypotension. Furthermore, the response to and recovery from hypotensive episodes due to blood loss or circulatory depletion may be impaired. At present, the advice concerning these drugs would be to continue therapy up to and including the day of operation. Another rare side-effect of ACE inhibitors is angioneurotic oedema, which has occasionally been seen complicating intubation. 

Calcium channel blockers with vasodilator effects, such as nifedipine, nicardipine, and nimodipine, will potentiate the effect of vasodilator effects of, e.g. halothane or isoflurane, potentiating any hypotension. This is especially obvious in hypertensive patients and when combined with similarly acting agents, such as sodium nitroprusside or nitroglycerin. Similarly, they also enhance the tendency of volatile anaesthetics to reduce hypoxic pulmonary vasoconstriction, which might exacerbate ventilation/perfusion mismatching during anaesthesia. 

Structure-activity relationship. The endothelium-independent vasodilator effects showed by flavonoids are related to the structure of the compound tested. Structure- activity relationships have been studied to flavonoids selected from five groups flavonols, flavones, flavanones, isoflavones, and flavanols in rat isolated aorta on the contractions induced by noradrenaline, KC1 and the phorbol ester derivative PMA, as well as the interactions of these flavonoids with isoprenaline and sodium nitroprusside, Table (2). 

B) The pattern of hydroxylation in B-rings is very important for the activity, (i) The absence or the methylation of the hydroxyl group in position 3 accounts for a lower vasodilator potency. In contrast, the lack of the 3 -hidroxyl group is related with a potentiation of the effects in the presence of sodium nitroprusside suggesting a reduced inhibitory effect on cyclic guanosine monophosphate (cGMP) PDE activity, (ii) Morin, with a... 

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