Philip H. Heller
University of California, San Francisco
32 Papers
681 Citations
Philip H. Heller is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Analgesic & Pentazocine. The author has an hindex of 24, co-authored 32 publications. Previous affiliations of Philip H. Heller include Kaiser Permanente.
Chat about Author
Papers
Enhancement of morphine analgesia by the GABAB agonist baclofen
Newton C. Gordon,Robert W. Gear,Philip H. Heller,Steven M. Paul,Christine Miaskowski,Jon D. Levine +5 more
TL;DR: While baclofen alone did not affect the level of post-operative pain, morphine analgesia was significantly enhanced by bacl ofen compared to placebo: however, females receiving pentazocine showed significantly greater analgesia than males.
120
Altered autonomic function in patients with arthritis or with chronic myofascial pain.
TL;DR: Physiological responses in patients with inflammatory arthritis or with chronic myofascial pain suggest concurrent increases in tonic pupillary autonomic activity (sympathetic and parasympathetic), with a relative sympathetic dominance, and a decrease intonic parasyMPathetic cardiovascular activity.
107
Mediation of serotonin hyperalgesia by the cAMP second messenger system.
TL;DR: The coupling of the 5-HT1A receptor to the cAMP second messenger system appears to be through guanine regulatory proteins since guanosine 5'-O-(3-thiotriphosphate) and cholera toxin both markedly enhanced 8-OH DPAT hyperalgesia.
87
Further substantiation of a significant role for the sympathetic nervous system in inflammation
TL;DR: It is shown that bradykinin is able to release norepinephrine in the knee-joint, indicating action on the sympathetic postganglionic neuron, and substantial additional evidence supporting a significant contribution of the sympatheticPostganglionics neuron terminal to inflammatory plasma extravasation is provided.
86
Characterization of distinct phospholipases mediating bradykinin and noradrenaline hyperalgesia.
TL;DR: This study evaluated the hypothesis that bradykinin and norepinephrine stimulate prostaglandin production in the rat, via distinct phospholipases, and found that, in normal skin, brady Kinin hyperalgesia is inhibited by the phospholIPase A2 inhibitor, mepacrine, but not by theospholipase C inhibitor, neomycin and is mimicked by phospholips A2.
69