It also has usefulness in the treatment ofcocaine-induced cardiovascular complications, where one would generally avoidβ-blockers (e.g.,metoprolol), as they can cause unopposed α-adrenergic mediatedcoronary vasoconstriction, worsening myocardial ischemia and hypertension.[4][5] Phentolamine is not a first-line agent for this indication. Phentolamine should only be given to patients who do not fully respond tobenzodiazepines,nitroglycerin, andcalcium channel blockers.[6][7]
When given by injection, it causes blood vessels todilate, thereby increasing blood flow. When injected into the penis (intracavernosal), it increases blood flow to the penis, which results in an erection.[8]
It may be stored incrash carts to counteract severe peripheral vasoconstriction secondary toextravasation of peripherally placedvasopressor infusions, typically ofnorepinephrine.Epinephrine infusions are less vasoconstrictive than norepinephrine as they primarily stimulate β receptor more than α receptors, but the effect remains dose-dependent.
Phentolamine is marketed in the dental field as a local anesthetic reversal agent. Branded asOraVerse, it is a phentolamine mesylate injection designed to reverse the local vasoconstrictor properties used in many local anesthetics to prolong anesthesia.[10]
Phentolamine is also usedophthalmically under the brand nameRyzumvi to reverse the effects of pharmacologically-inducedmydriasis.[11]
Non-selective α-blockers can cause a much more pronounced reflextachycardia than the selectiveα1 blockers. Like the selective α1 blockers, phentolamine causes a relaxation of systemic vasculature, leading tohypotension. This hypotension is sensed by thebaroreceptor reflex, which results in increased sympathetic nerve firing on the heart, releasingnorepinephrine. In response, theβ1 adrenergic receptors on the heart increase theirrate,contractility, anddromotropy, which help to offset the decrease in systemic blood pressure. Unlike the α1 selective blockers, phentolamine also inhibits the α2 receptors, which function predominantly aspresynapticnegative feedback for norepinephrine release. By abolishing this negative feedback phentolamine leads to even less regulated norepinephrine release, which results in a more drastic increase in heart rate.[16]
^abJewell JR, Longworth DL, Stoller JK, Casey D (2003).The Cleveland Clinic internal medicine case reviews. Hagerstown, MD: Lippincott Williams & Wilkins. p. 32.ISBN0-7817-4266-8.
^Schurr JW, Gitman B, Belchikov Y (December 2014). "Controversial therapeutics: the β-adrenergic antagonist and cocaine-associated cardiovascular complications dilemma".Pharmacotherapy.34 (12):1269–1281.doi:10.1002/phar.1486.PMID25224512.S2CID5282953.
^Freeman K, Feldman JA (February 2008). "Cocaine, myocardial infarction, and beta-blockers: time to rethink the equation?".Annals of Emergency Medicine.51 (2):130–134.doi:10.1016/j.annemergmed.2007.08.020.PMID17933425.
^Hollander JE, Henry TD (February 2006). "Evaluation and management of the patient who has cocaine-associated chest pain".Cardiology Clinics.24 (1):103–114.doi:10.1016/j.ccl.2005.09.003.PMID16326260.
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