PMID- 1724530
OWN - NLM
STAT- MEDLINE
DCOM- 19920407
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 18
IP  - 4
DP  - 1991 Oct
TI  - Skeletal muscle blood flow and O2 uptake during intravenous nicotine with and 
      without hypertension.
PG  - 535-41
AB  - The mechanism by which nicotine causes peripheral vasoconstriction and its 
      relationship to the increased risk of peripheral vascular disease in smokers are 
      unknown. To study the peripheral vascular effects of nicotine, we measured 
      hemodynamic responses and oxygen consumption of the in situ gracilis muscle 
      during intravenous (i.v.) nicotine infusions in anesthetized dogs. Nicotine 36.0 
      micrograms/kg/min increased gracilis artery pressure (Pga) 91 +/- 17% and muscle 
      vascular resistance (MVR) 96 +/- 18% whereas muscle blood flow (MBF) and oxygen 
      consumption (MVO2) were unchanged from baseline. In dogs with 
      extracorporeal-controlled normotension during nicotine infusion, however, Pga was 
      held at baseline levels but similar increases in MVR were observed (95 +/- 11%) 
      as flows decreased 52 +/- 9%. Oxygen consumption decreased in direct proportion 
      (53 +/- 5%) to MBF, indicating complete impairment of oxygen extraction (A-VO2). 
      Thus impaired oxygen extraction was masked in dogs in which Pga was allowed to 
      increase because of sustained pressure-dependent flows. Phenoxybenzamine block of 
      muscle alpha-adrenoceptors increased MBF and MVO2 in both normotensive and 
      hypertensive dogs. Combined alpha- and beta-blockade effectively neutralized all 
      sympathoadrenal responses in the muscle. All the above results occurred 
      regardless of innervation. Plasma levels of norepinephrine (NE) and epinephrine 
      (EPI) increased greater than 1,000% during nicotine infusion. Apparently, these 
      levels were high enough to (a) override dilator effects of plasma EPI and (b) 
      cause vasoconstriction in muscle independent of nerve supply. Infusion of 
      nicotine in the gracilis artery had no effect on muscle hemodynamics. 
      Nicotine-induced increase in plasma catecholamines resulted in a powerful 
      constriction of both resistance and oxygen-exchange vessels of skeletal 
      muscle.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Rooney, M W
AU  - Rooney MW
AD  - Department of Anesthesiology, University of Illinois College of Medicine, 
      Chicago.
FAU - Hirsch, L J
AU  - Hirsch LJ
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0TTZ664R7Z (Phenoxybenzamine)
RN  - 6M3C89ZY6R (Nicotine)
RN  - X4W3ENH1CV (Norepinephrine)
RN  - YKH834O4BH (Epinephrine)
SB  - IM
MH  - Animals
MH  - Dogs
MH  - Epinephrine/blood
MH  - Hypertension/*physiopathology
MH  - Infusions, Intra-Arterial
MH  - Infusions, Intravenous
MH  - Muscles/*blood supply/drug effects
MH  - Nicotine/administration & dosage/*pharmacology
MH  - Norepinephrine/blood
MH  - Oxygen Consumption/*drug effects
MH  - Phenoxybenzamine/pharmacology
MH  - Regional Blood Flow/drug effects
MH  - Vascular Resistance/drug effects
EDAT- 1991/10/01 00:00
MHDA- 1991/10/01 00:01
CRDT- 1991/10/01 00:00
PHST- 1991/10/01 00:00 [pubmed]
PHST- 1991/10/01 00:01 [medline]
PHST- 1991/10/01 00:00 [entrez]
AID - 10.1097/00005344-199110000-00009 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1991 Oct;18(4):535-41. doi: 
      10.1097/00005344-199110000-00009.