Nitroprusside clinical studies: Difference between revisions

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==clinical studies==
 
Baseline-controlled clinical trials have uniformly shown that sodium nitroprusside has a prompt hypotensive effect, at least initially, in all populations. With increasing rates of infusion, sodium nitroprusside has been able to lower blood pressure without an observed limit of effect.
 
Clinical trials have also shown that the hypotensive effect of sodium nitroprusside is associated with reduced blood loss in a variety of major surgical procedures.
 
In patients with acute congestive heart failure and increased peripheral vascular resistance, administration of sodium nitroprusside causes reductions in peripheral resistance, increases in cardiac output, and reductions in left ventricular filling pressure.
 
Many trials have verified the clinical significance of the metabolic pathways described above. In patients receiving unopposed infusions of sodium nitroprusside, cyanide and thiocyanate levels have increased with increasing rates of sodium nitroprusside infusion. Mild to moderate metabolic acidosis has usually accompanied higher cyanide levels, but peak base deficits have lagged behind the peak cyanide levels by an hour or more.
 
Progressive [[tachyphylaxis]] to the hypotensive effects of sodium nitroprusside has been reported in several trials and numerous case reports. This [tachyphylaxis]]has frequently been attributed to concomitant cyanide toxicity, but the only evidence adduced for this assertion has been the observation that in patients treated with sodium nitroprusside and found to be resistant to its hypotensive effects, cyanide levels are often found to be elevated. In the only reported comparisons of cyanide levels in resistant and nonresistant patients, cyanide levels did not correlate with tachyphylaxis. The mechanism of [tachyphylaxis]]to sodium nitroprusside remains unknown.<ref name="dailymed.nlm.nih.gov">{{Cite web  | last =  | first =  | title = NITROPRESS (SODIUM NITROPRUSSIDE) INJECTION, SOLUTION, CONCENTRATE [HOSPIRA, INC.] | url = http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=6a44bcac-a0e1-4069-5691-db7b83dbb4b7 | publisher =  | date =  | accessdate = 27 February 2014 }}</ref>
 
==References ==
{{Reflist|2}}
 
{{Nonsympatholytic vasodilatory antihypertensives}}
 
[[Category:Cyanides]]
[[Category:Vasodilators]]
[[Category:Coordination compounds]]
[[Category:World Health Organization essential medicines]]
[[Category:Iron compounds]]
[[Category:Nitrosyl compounds]]
[[Category:Cardiovascular Drugs]]
[[Category:Drugs]]

Latest revision as of 22:13, 21 July 2014