PMID- 3100339
OWN - NLM
STAT- MEDLINE
DCOM- 19870226
LR  - 20220330
IS  - 0014-9446 (Print)
IS  - 0014-9446 (Linking)
VI  - 46
IP  - 1
DP  - 1987 Jan
TI  - Pathway to carrageenan-induced inflammation in the hind limb of the rat.
PG  - 118-26
AB  - A sequential 43-step pathway scheme for the inflammatory response of the rat to 
      interdermal injection of carrageenan (C) was devised. It consisted of a 
      nonphagocytic inflammatory response (NPIR) followed by a phagocytic inflammatory 
      response (PIR) in the dermis and an epidermal NPIR. The dermal NPIR comprised 
      edema, hyperemia, and hyperalgesia followed by hypoalgesia. Antiserotonin agents 
      inhibited the hypoalgesia and part of the edema. These findings and histological 
      observations suggested that dermal mast cells were injured by C. The hyperalgesia 
      and part of the edema were sensitive to arachidonate cyclooxygenase inhibitors 
      (AACOIs). It is speculated that injured mast cells metabolize arachidonic acid 
      and reactive intermediates, not prostaglandins, mediate the NPIR hyperalgesia and 
      part of the edema. The dermal PIR consisted of mobilization of neutrophils, 
      edema, hyperalgesia, mobilization of monocytes, and proliferation of fibroblasts 
      and vascular tissue. Selective drug actions revealed that the edema, 
      hyperalgesia, and monocyte mobilization of the PIR depended on the mobilization 
      of neutrophils. After the mobilization of neutrophils, AACOIs reduced edema 
      formation and hyperalgesia. Arachidonic acid metabolism by neutrophils is 
      speculated to produce the mediators of phagocytic inflammatory (PI) edema and 
      hyperalgesia. Monocyte function was associated with cessation of PI edema 
      formation and phagocytosis of neutrophils and cellular debris. Interleukin 1 is 
      speculated to mediate the adherence of neutrophils to injured dermal endothelium. 
      The epidermal NPIR consisted of edema, hyperplasia, and hyperkeratosis. These 
      parameters were not studied mechanistically. There was no evidence for histamine, 
      bradykinin, platelets, clotting factors, or complement mediating any events in 
      the pathway.
FAU - Vinegar, R
AU  - Vinegar R
FAU - Truax, J F
AU  - Truax JF
FAU - Selph, J L
AU  - Selph JL
FAU - Johnston, P R
AU  - Johnston PR
FAU - Venable, A L
AU  - Venable AL
FAU - McKenzie, K K
AU  - McKenzie KK
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Fed Proc
JT  - Federation proceedings
JID - 0372771
RN  - 0 (Arachidonic Acids)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - 333DO1RDJY (Serotonin)
RN  - 9000-07-1 (Carrageenan)
SB  - IM
MH  - Animals
MH  - Arachidonic Acid
MH  - Arachidonic Acids/metabolism
MH  - Carrageenan/*toxicity
MH  - Cell Adhesion
MH  - Disease Models, Animal/*pathology
MH  - Edema/chemically induced/physiopathology
MH  - Endothelium/pathology
MH  - Hyperalgesia/chemically induced/physiopathology
MH  - Inflammation/chemically induced/pathology/*physiopathology
MH  - Models, Biological
MH  - Neutrophils/physiology
MH  - Phagocytosis
MH  - Rats
MH  - Serotonin/physiology
MH  - Skin/pathology
MH  - Skin Diseases/chemically induced/pathology/*physiopathology
EDAT- 1987/01/01 00:00
MHDA- 1987/01/01 00:01
CRDT- 1987/01/01 00:00
PHST- 1987/01/01 00:00 [pubmed]
PHST- 1987/01/01 00:01 [medline]
PHST- 1987/01/01 00:00 [entrez]
PST - ppublish
SO  - Fed Proc. 1987 Jan;46(1):118-26.