Originally Posted by fmichael

Yes, is you use any product with a vaso-constrictive decongestant, e.g., Sudafed (Pseudoephedrine HCL), in which case you're basically stimmulating the flighlt or flight response of sudden stress, and we all know how well that can trigger an instant flair. I learbed that one the hard way.) See, e.g.:

Mechanism of action
Pseudoephedrine is a sympathomimetic amine. Its principal mechanism of action relies on its indirect action on the adrenergic receptor system. The vasoconstriction that pseudoephedrine produces is believed to be principally an α-adrenergic receptor response.[6]

While it may have weak or no direct agonist activity at α- and β-adrenergic receptors, the principal mechanism is to cause the release of endogenous norepinephrine (noradrenaline) from storage vesicles in presynaptic neurons. The displaced noradrenaline is released into the neuronal synapse where it is free to activate the postsynaptic adrenergic receptors. These adrenergic receptors are located on the muscles lining the walls of blood vessels. When activated by pseudoephedrine, the muscles contract, causing the blood vessels to constrict (vasoconstriction). The constricted blood vessels now allow less fluid to leave the blood vessels and enter the nose, throat and sinus linings, which results in decreased inflammation of nasal membranes as well as decreased mucus production. Thus, by constriction of blood vessels, mainly those located in the nasal passages, pseudoephedrine causes a decrease in the symptoms of nasal congestion.

Note
6. Drew, et al. Comparison of the effects of D-(-)-ephedrine and L-(+)-pseudoephedrine on the cardiovascular and respiratory systems in man. Br J Clin Pharmacol. 1978; 6, p 225; PDF [at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1429447/].

Pseudoephedrine, From Wikipedia, the free encyclopedia (updated April 2, 2010; last accessed April 17, 2010).

http://en.wikipedia.org/wiki/Pseudoephedrine

Nor may Phenylephrine HCL, the active ingrediant in the new OTC formulation "Su-Phedrine PE" among many others, be much better. See, e.g., Smooth muscle α1D-adrenoceptors mediate phenylephrine-induced vasoconstriction and increases in endothelial cell Ca2+ in hamster cremaster arterioles, W F Jackson, E M Boerman, E J Lange et al., Br J Pharmacol. 2008 October; 155(4): 514–524, full text at http://www.ncbi.nlm.nih.gov/pmc/arti...jp2008276a.pdf

In fact, there is some doubt as to whether Phenylephrine HCL is even effective as a nasal decongestant in the first place. See, Substitution of phenylephrine for pseudoephedrine as a nasal decongeststant. An illogical way to control methamphetamine abuse, Eccles R, Br J Clin Pharmacol. 2007 Jan;63(1):10-4. Epub 2006 Nov 20, full text at http://www.ncbi.nlm.nih.gov/pmc/arti...p0063-0010.pdf:

Abstract
The aim of this review was to investigate the rationale for replacing the nasal decongestant pseudoephedrine (PDE) with phenylephrine (PE) as a means of controlling the illicit production of methamphetamine. A literature search was conducted in electronic databases and use of textbooks. Restrictions have been placed on the sale of PDE in the USA in an attempt to control the illicit production of methamphetamine. This has caused a switch from PDE to PE in many common cold and cough medicines. PE is a poor substitute for PDE as an orally administered decongestant as it is extensively metabolized in the gut and its efficacy as a decongestant is unproven. Both PDE and PE have a good safety record, but the efficacy of PDE as a nasal decongestant is supported by clinical trials. Studies in the USA indicate that restricting the sale of PDE to the public as a medicine has had little impact on the morbidity and number of arrests associated with methamphetamine abuse. Restricting the sale of PDE in order to control the illicit production of methamphetamine will deprive the public of a safe and effective nasal decongestant and force the pharmaceutical industry to replace PDE with PE, which may be an ineffective decongestant. Restrictions on sales of PDE to the public may not reduce the problems associated with methamphetamine abuse.

PMID: 17116124 [PubMed - indexed for MEDLINE]PMCID: PMC2000711

http://www.ncbi.nlm.nih.gov/pubmed/17116124

Personally, I think the 5 mg. zinc gluconate lozenges (forget the now banned nose spray- see below) are still the best way to go. See, Zinc gluconate lozenges for treating the common cold. A randomized, double-blind, placebo-controlled study, Mossad SB, Macknin ML, Medendorp SV, Mason P, Ann Intern Med. 1996 Jul 15;125(2):81-8, full text at http://www.annals.org/content/125/2/81.full.pdf:

Abstract
BACKGROUND: The common cold is one of the most frequent human illnesses and is responsible for substantial morbidity and economic loss. No consistently effective therapy for the common cold has been well documented, but evidence suggests that several possible mechanisms may make zinc an effective treatment. OBJECTIVE: To test the efficacy of zinc gluconate lozenges in reducing the duration of symptoms caused by the common cold. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: Outpatient department of a large tertiary care center. PATIENTS: 100 employees of the Cleveland Clinic who developed symptoms of the common cold within 24 hours before enrollment. INTERVENTION: Patients in the zinc group (n = 50) received lozenges (one lozenge every 2 hours while awake) containing 13.3 mg of zinc from zinc gluconate as long as they had cold symptoms. Patients in the placebo group (n = 50) received similarly administered lozenges that contained 5% calcium lactate pentahydrate instead of zinc gluconate. MAIN OUTCOME MEASURES: Subjective daily symptom scores for cough, headache, hoarseness, muscle ache, nasal drainage, nasal congestion, scratchy throat, sore throat, sneezing, and fever (assessed by oral temperature). RESULTS: The time to complete resolution of symptoms was significantly shorter in the zinc group than in the placebo group (median, 4.4 days compared with 7.6 days; P < 0.001). The zinc group had significantly fewer days with coughing (median, 2.0 days compared with 4.5 days; P = 0.04), headache (2.0 days and 3.0 days; P = 0.02), hoarseness (2.0 days and 3.0 days; P = 0.02), nasal congestion (4.0 days and 6.0 days; P = 0.002), nasal drainage (4.0 days and 7.0 days; P < 0.001), and sore throat (1.0 day and 3.0 days; P < 0.001). The groups did not differ significantly in the resolution of fever, muscle ache, scratchy throat, or sneezing. More patients in the zinc group than in the placebo group had side effects (90% compared with 62%; P < 0.001), nausea (20% compared with 4%; P = 0.02), and bad-taste reactions (80% compared with 30%; P < 0.001), CONCLUSION: Zinc gluconate in the form and dosage studied significantly reduced the duration of symptoms of the common cold. The mechanism of action of this substance in treating the common cold remains unknown. Individual patients must decide whether the possible beneficial effects of zinc gluconate on cold symptoms outweigh the possible adverse effects.

PMID: 8678384 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/8678384

Then too if you are lucky enough to develop a cough, we now have the a pure form of the cough suppressant Dextromethorphan HBr, which is the strongest cough suppressant available without a prescription* - a relatively powerful NDMA-receptor antagonist, now available OTC as an oral spray, irononically marketed in the U.S. as "Cough Max" under the Zicam label: the same folks who brought us the zinc nose spray that permanently took out some folks sense of smell. Zicam-induced damage to mouse and human nasal tissue, Lim JH, Davis GE, Wang Z, Li V, Wu Y, Rue TC, Storm DR, PLoS One. 2009 Oct 30;4(10):e7647 full text at http://www.plosone.org/article/fetch...esentation=PDF

What can I say? We win a few, we lose a few.

Mike

* A qualitative systematic review of the role of N-methyl-D-aspartate receptor antagonists in preventive analgesia. McCartney CJ, Sinha A, Katz J, Anesth Analg. 2004 May;98(5):1385-400, full text at http://www.anesthesia-analgesia.org/.../1385.full.pdf:

Abstract
We evaluated in a qualitative systematic review the effect of N-methyl-D-aspartate (NMDA) receptor antagonists on reducing postoperative pain and analgesic consumption beyond the clinical duration of action of the target drug (preventive analgesia). Randomized trials examining the use of an NMDA antagonist in the perioperative period were sought by using a MEDLINE (1966-2003) and EMBASE (1985-2003) search. Reference sections of relevant articles were reviewed, and additional articles were obtained if they evaluated postoperative analgesia after the administration of NMDA antagonists. The primary outcome was a reduction in pain, analgesic consumption, or both in a time period beyond five half-lives of the drug under examination. Secondary outcomes included time to first analgesic request and adverse effects. Forty articles met the inclusion criteria (24 ketamine, 12 dextromethorphan, and 4 magnesium). The evidence in favor of preventive analgesia was strongest in the case of dextromethorphan and ketamine, with 67% and 58%, respectively, of studies demonstrating a reduction in pain, analgesic consumption, or both beyond the clinical duration of action of the drug concerned. None of the four studies examining magnesium demonstrated preventive analgesia. IMPLICATIONS: We evaluated, in a qualitative systematic review, the effect of N-methyl D-aspartate antagonists on reducing postoperative pain and analgesic consumption beyond the clinical duration of action of the target drug (preventive analgesia). Dextromethorphan and ketamine were found to have significant immediate and preventive analgesic benefit in 67% and 58% of studies, respectively.

PMID: 15105220 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/15105220