Abstract
Doxorubicin (ADM) skin toxicity is a serious complication of inadvertent perivenous drug infiltrations. In an attempt to identify possible antidotes, nine diverse pharmacologic agents were injected intradermally into the hair-free dorsum of BALB/c mice following an intradermal ADM dose of either 0.05 or 0.5 mg. Seven of the compounds were ineffective in reducing ADM-induced ulceration; the compounds included lidocaine, cimetidine, diphenhydramine, sodium heparin, hyaluronidase, N-acetylcysteine, and α-tocopherol. The latter five compounds actually increased ulceration induced by ADM (0.5 mg), especially N-acetylcysteine, which tripled the total toxic effect. Two opposing beta-adrenergic compounds, the antagonist propranolol and the agonist isoproterenol, reduced skin ulceration resulting from experimental treatment with intradermal ADM. A role for the beta-adrenergic receptor in mediating ADM-induced skin ulceration is suggested.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1001-1006 |
| Number of pages | 6 |
| Journal | Cancer Treatment Reports |
| Volume | 65 |
| Issue number | 11-12 |
| State | Published - 1981 |
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ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Pharmacologic antidotes to experimental doxorubicin skin toxicity : A suggested role for beta-adrenergic compounds. / Dorr, Robert T; Alberts, David S.
In: Cancer Treatment Reports, Vol. 65, No. 11-12, 1981, p. 1001-1006.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Pharmacologic antidotes to experimental doxorubicin skin toxicity
T2 - A suggested role for beta-adrenergic compounds
AU - Dorr, Robert T
AU - Alberts, David S
PY - 1981
Y1 - 1981
N2 - Doxorubicin (ADM) skin toxicity is a serious complication of inadvertent perivenous drug infiltrations. In an attempt to identify possible antidotes, nine diverse pharmacologic agents were injected intradermally into the hair-free dorsum of BALB/c mice following an intradermal ADM dose of either 0.05 or 0.5 mg. Seven of the compounds were ineffective in reducing ADM-induced ulceration; the compounds included lidocaine, cimetidine, diphenhydramine, sodium heparin, hyaluronidase, N-acetylcysteine, and α-tocopherol. The latter five compounds actually increased ulceration induced by ADM (0.5 mg), especially N-acetylcysteine, which tripled the total toxic effect. Two opposing beta-adrenergic compounds, the antagonist propranolol and the agonist isoproterenol, reduced skin ulceration resulting from experimental treatment with intradermal ADM. A role for the beta-adrenergic receptor in mediating ADM-induced skin ulceration is suggested.
AB - Doxorubicin (ADM) skin toxicity is a serious complication of inadvertent perivenous drug infiltrations. In an attempt to identify possible antidotes, nine diverse pharmacologic agents were injected intradermally into the hair-free dorsum of BALB/c mice following an intradermal ADM dose of either 0.05 or 0.5 mg. Seven of the compounds were ineffective in reducing ADM-induced ulceration; the compounds included lidocaine, cimetidine, diphenhydramine, sodium heparin, hyaluronidase, N-acetylcysteine, and α-tocopherol. The latter five compounds actually increased ulceration induced by ADM (0.5 mg), especially N-acetylcysteine, which tripled the total toxic effect. Two opposing beta-adrenergic compounds, the antagonist propranolol and the agonist isoproterenol, reduced skin ulceration resulting from experimental treatment with intradermal ADM. A role for the beta-adrenergic receptor in mediating ADM-induced skin ulceration is suggested.
UR - http://www.scopus.com/inward/record.url?scp=0019781919&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0019781919&partnerID=8YFLogxK
M3 - Article
C2 - 7296547
AN - SCOPUS:0019781919
VL - 65
SP - 1001
EP - 1006
JO - Journal of the National Cancer Institute
JF - Journal of the National Cancer Institute
SN - 0027-8874
IS - 11-12
ER -