PubMed · 689801
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
R M Fine. 1978. The fine page.. https://doi.org/10.1111/j.1365-4362.1978.tb06001.x
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Histamine-sensitive nerve endings are assumed to terminate in the superficial epidermis. Heat-sensitive nociceptors that are excited by brief carbondioxide-laser pulses must also terminate within the epidermis, because this infrared radiation has an extinction length of about 10 microns. We now compared laser heat stimuli (10 W, 50 ms, 20 mm2) with intradermal injections of histamine (10(-10) to 10(-8) mol) in their capacity to cause cutaneous vasodilatation (flare) in awake human subjects. Cutaneous blood flow was measured with a two-channel laser-Doppler device. The radiant heat pulses caused a transient cutaneous vasodilatation that spread at least 15 mm from the stimulus site. There was no visible flare and vasodilatation could only be detected by laser Doppler measurements. Although the heat pulses elicited enough nociceptor activity to be perceived as moderately painful, the magnitude of the vasodilatation was smaller and its duration shorter than after the smallest dose of histamine. In contrast, nociceptor activation by heat is usually stronger than by histamine. These data indicate that flare and pain are two different aspects of cutaneous small fiber function.
Although histamine is the principal mediator of the immediate allergic reaction, other inflammatory mediators as well as neuropeptides also contribute to rhinorrhea and nasal congestion. Within minutes of exposure to allergen, mast cells produce histamine, leukotriene C4, and prostaglandin D2. A concomitant increase occurs in neuropeptides and bradykinin. In vitro mast cell activation also leads to the release of tumor necrosis factor--alpha, several interleukins, and granulocyte-macrophage colony--stimulating factor. Because all these various mediators and neuropeptides may play a role in producing rhinorrhea and congestion, antihistamines alone cannot control all of the symptoms of allergic rhinitis. However, the combination of antihistamines with topical corticosteroids can inhibit the generation, release, and activity of most if not all of the mediators potentially involved in the allergic response.
Despite advances in dialysis treatment, pruritus remains a common and distressing manifestation of chronic renal failure. Two-thirds of patients on maintenance hemodialysis experience persistent itching, however, the etiology of this condition is unknown. Although pruritic patients have higher serum levels of parathyroid hormone (PTH) than nonpruritic patients, subsequent studies do not support a role for PTH as a peripheral itch mediator. Experimental itching induced by intracutaneous histamine injections is significantly stronger in patients with uremic itching, indicating an enhanced sensitivity to pruritogens in these patients. Immunohistochemistry of skin nerve fibers has shown conflicting results and the innervation pattern of uremic skin clearly needs further elucidation. The possibility of uremic itching being a neuropathic manifestation awaits future investigations.