The role of heart rate in the modulation of the decreased cardiac output induced by acute nitric oxide synthesis inhibition in anaesthetized dogs

Abstract

1. The role of the heart rate modulating the decrease in cardiac output induced by the nitric oxide synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was investigated in anaesthetized dogs. This was achieved in dogs in which a positive pacemaker (PM) cable was located at the right ventricle. 2. The haemodynamic events were evaluated: mean arterial blood pressure (MABP), systemic vascular resistance index (SVRI), stroke volume index (SVI), heart rate (HR) and cardiac index (CI). 3. The infusion of L-NAME (0.01-10 mg kg(-1)) in the animals with the PM off caused a dose-dependent rise in MABP and SVRI, accompanied by significant decreases of HR and SVI. A resulting decrease in CI was observed at all doses of L-NAME used. 4. In the animals with the PM on, HR was maintained stable. Under this condition, the increase in MABP and SVRI as well as the decrease in SVI induced by the L-NAME infusion did not significantly differ from the PM-off animals. However, the resulting decreased CI was markedly attenuated compared to PM-off animals but significant decreases in CI were still observed at higher doses of L-NAME. 5. The results suggest that HR plays an important role in the L-NAME-mediated decreased cardiac output but other factors might also be involved.

Aminoguanidine produces beneficial haemodynamic effects in a canine model of acute pulmonary thromboembolism

“…The animals were randomly assigned to one of six experimental groups as follows: (1) a group of Sham‐operated, non‐embolized animals ( n = 4), which received only saline infusions; (2) NAME group ( n = 3), which received a 5‐min bolus infusion of l ‐NAME (Sigma‐Aldrich, St Louis, MO, USA) 10 mg kg −1 i.v. followed by l ‐NAME 4 mg kg −1 h −1 throughout the study (Faro et al. 1999); (3) AG group ( n = 3), which received a 5‐min bolus infusion of aminoguanidine (Sigma‐Aldrich) 10 mg kg −1 i.v.…”

“…The doses of l ‐NAME and aminoguanidine used in the present study were based on previous studies showing that these doses produced marked inhibition of NOS activity (by more than 60%) (Zappellini et al. 1996, Faro et al. 1999) and significant haemodynamic effects (Evgenov et al.…”

“…(1) a group of Sham-operated, non-embolized animals (n = 4), which received only saline infusions; (2) NAME group (n = 3), which received a 5-min bolus infusion of l-NAME (Sigma-Aldrich, St Louis, MO, USA) 10 mg kg )1 i.v. followed by l-NAME 4 mg kg )1 h )1 throughout the study (Faro et al 1999); (3) AG group (n = 3), which received a 5-min bolus infusion of aminoguanidine (Sigma-Aldrich) 10 mg kg )1 i.v. followed by aminoguanidine 2 mg kg )1 h )1 throughout the study; (4) Emb group (n = 9), which received saline infusion and were embolized 30 min after the saline infusion was started.…”

“…This model of APT is very similar to that previously reported (Lee et al 2001); (5) NAME + Emb group (n = 4), which received the same l-NAME infusions as described above and were embolized 30 min after the l-NAME infusions were started; (6) AG + Emb group (n = 7), which received the same aminoguanidine infusions as described above and were embolized 30 min after the aminoguanidine infusions started. The doses of l-NAME and aminoguanidine used in the present study were based on previous studies showing that these doses produced marked inhibition of NOS activity (by more than 60%) (Zappellini et al 1996, Faro et al 1999) and significant haemodynamic effects (Evgenov et al 2000) respectively. Corresponding to the lung embolization with the clots produced from 5 mL kg )1 blood, the dogs in the Sham, NAME and AG groups received a saline 5 mL injection via the cannula placed in the right atrium.…”

Nitric oxide synthase blockade and body fluid volumes

“…In addition to the increase in vascular reactivity induced by NOS blocking, the extracellular fluid volume increase may provoke an increase of cardiac output which, after a variable period of time, may induce an increase in peripheral resistance by an autoregulation mechanism (12). However, the effects of L-NAME administration on cardiac output remain unclear, and the different results reported in the literature may be due to differences in the experimental designs (10,13,14).…”