Peripheral vasospasm

Unlabeled Uses Control of paroxysmal hypertension before and during surgery for pheochromocytoma, peripheral vasospasm caused by ergot alkaloid overdose, treatment adjunct for MI, valvular regurgitation... 

BETA-BLOCKERS ERGOT DERIVATIVES Three reported cases of arterial vasoconstriction and one of T BP occurred when ergotamine or methysergide was added to propanolol or oxprenolol Ergotamine can cause peripheral vasospasm, and absence of beta-adrenergic activity can t the risk of vasoconstriction Ergot derivatives and beta-blockers are often co-administered without trouble however, monitor BP at least weekly until stable (watch for t BP) and warn patients to stop the ergot derivative and seek medical attention if they develop cold, painful feet... 

Case Conclusion KO is experiencing peripheral vasospasm from an interaction between his ergotamine and the erythromycin. It is also recommended that KO not exceed 6 tablets of ergotamine per migraine attack or 10 tablets per week. Acute ergotism can be manifested when these agents are u d concurrently, manifesting as peripheral ischemia. Nitro-prusside IV may be required In more severe cases. 

The antagonistic action of tolazoline is relatively weak, but its histaminc-like and acclylcholinc-like agonistic actions probably conlribule to its vasodilatory activity. Its his-laminc-like effects include stimulation of ga.stric acid secretion, rendering it inappropriate for administration to patients who have gastric or peptic ulcers. Il has been used to treat Raynaud s syndrome and other conditions involving peripheral vasospasm. Tolazoline is available in an injectable form and is indicated for use in persi.stent pulmonary hypertension of the newborn when supportive measures are not successful. 

This drug is useful in the treatment of peripheral vasospasm secondary to ergot alkaloid overdose, and as an adjunct in the treatment of valvular regurgitation. 

B. Theoretically, this dmg may have additive effects with other ergot alkaloids, and its potential to cause peripheral vasospasm may be exacerbated by propranolol. 

The pathophysiology of peripheral vasospasm is unclear. The author of this chapter would like to propose the hypothesis that it is a result of endothelial dysfunction. In the late 1920s, Sir Thomas Lewis hypothesized that Raynaud s disease is a result of a local vascular fault (99), but after all these years, fault has not been adequately defined. An attrac-... 

Calcium channel blockers (CCBs) are the most widely used pharmacologic agents for the treatment of peripheral vasospasm (110-112). Sympatholytic agents have also been used in the treatment of Raynaud s phenomenon. Topical nitroglycerin ointment can be applied with a nocturnal nitrate-free interval to avoid nitrate tolerance. 

Severe gangrene of all four Umbs due to cocaine-associated peripheral vasospasm has been reported [25 ]. 

The authors suggested that cocaine-induced peripheral vasospasm with associated delayed and persistent vasospasm was a probable mechanism for this outcome. The vasospastic action of cocaine peaks at 1 hour after use and correlates with an increased serum concentration of cocaine (benzoylmethylecgonine). Delayed and persistent vasospasm can occur, as the major metabolites of cocaine, benzyolecgonine and ecgonine methyl ester, can also reportedly cause vasospasm [26 ]. 

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