PMID- 10559840
OWN - NLM
STAT- MEDLINE
DCOM- 20000201
LR  - 20190516
IS  - 0100-879X (Print)
IS  - 0100-879X (Linking)
VI  - 32
IP  - 11
DP  - 1999 Nov
TI  - Role of nitric oxide in hypoxia-induced hyperventilation and hypothermia: 
      participation of the locus coeruleus.
PG  - 1389-98
AB  - Hypoxia elicits hyperventilation and hypothermia, but the mechanisms involved are 
      not well understood. The nitric oxide (NO) pathway is involved in hypoxia-induced 
      hypothermia and hyperventilation, and works as a neuromodulator in the central 
      nervous system, including the locus coeruleus (LC), which is a noradrenergic 
      nucleus in the pons. The LC plays a role in a number of stress-induced responses, 
      but its participation in the control of breathing and thermoregulation is 
      unclear. Thus, in the present study, we tested the hypothesis that LC plays a 
      role in the hypoxia-induced hypothermia and hyperventilation, and that NO is 
      involved in these responses. Electrolytic lesions were performed bilaterally 
      within the LC in awake unrestrained adult male Wistar rats weighing 250-350 g. 
      Body temperature and pulmonary ventilation (V E) were measured. The rats were 
      divided into 3 groups: control (N = 16), sham operated (N = 7) and LC lesioned (N 
      = 19), and each group received a saline or an N G-nitro-L-arginine methyl ester 
      (L-NAME, 250 microg/microl) intracerebroventricular (icv) injection. No 
      significant difference was observed between control and sham-operated rats. 
      Hypoxia (7% inspired O2) caused hyperventilation and hypothermia in both control 
      (from 541.62 +/- 35.02 to 1816.18 +/- 170.7 and 36.3 +/- 0.12 to 34. 4 +/- 0.09, 
      respectively) and LC-lesioned rats (LCLR) (from 694.65 +/- 63.17 to 2670.29 +/- 
      471.33 and 36 +/- 0.12 to 35.3 +/- 0.12, respectively), but the increase in V E 
      was higher (P<0.05) and hypothermia was reduced (P<0.05) in LCLR. L-NAME caused 
      no significant change in V E or in body temperature under normoxia, but abolished 
      both the hypoxia-induced hyperventilation and hypothermia. Hypoxia-induced 
      hyperventilation was reduced in LCLR treated with L-NAME. L-NAME also abolished 
      the hypoxia-induced hypothermia in LCLR. The present data indicate that 
      hypoxia-induced hyperventilation and hypothermia may be related to the LC, and 
      that NO is involved in these responses.
FAU - Fabris, G
AU  - Fabris G
AD  - Departamento de Fisiologia, Faculdade de Medicina de Ribeirao Preto, Universidade 
      de Sao Paulo, Ribeirao Preto, SP, Brasil.
FAU - Anselmo-Franci, J A
AU  - Anselmo-Franci JA
FAU - Branco, L G
AU  - Branco LG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Brazil
TA  - Braz J Med Biol Res
JT  - Brazilian journal of medical and biological research = Revista brasileira de 
      pesquisas medicas e biologicas
JID - 8112917
RN  - 0 (Enzyme Inhibitors)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
SB  - IM
MH  - Animals
MH  - Enzyme Inhibitors/pharmacology
MH  - Hyperventilation/etiology/*physiopathology
MH  - Hypothermia/etiology/*physiopathology
MH  - Hypoxia, Brain/complications/*physiopathology
MH  - Locus Coeruleus/*physiology
MH  - Male
MH  - NG-Nitroarginine Methyl Ester/pharmacology
MH  - Nitric Oxide/*physiology
MH  - Rats
MH  - Rats, Wistar
EDAT- 1999/11/24 00:00
MHDA- 1999/11/24 00:01
CRDT- 1999/11/24 00:00
PHST- 1999/11/24 00:00 [pubmed]
PHST- 1999/11/24 00:01 [medline]
PHST- 1999/11/24 00:00 [entrez]
AID - S0100-879X(99)03201109 [pii]
AID - 10.1590/s0100-879x1999001100009 [doi]
PST - ppublish
SO  - Braz J Med Biol Res. 1999 Nov;32(11):1389-98. doi: 
      10.1590/s0100-879x1999001100009.