Tags

Type your tag names separated by a space and hit enter

Effects of aminoguanidine and N(omega)-nitro-L-arginine methyl ester on vascular hyporeactivity induced by endotoxaemia.
Eur J Surg. 2001 Nov; 167(11):803-9.EJ

Abstract

OBJECTIVE

To investigate the effects of endotoxaemia on the reactivity of the aortic bed in rats, and to compare the effects of the nitric oxide (NO) synthase inhibitors aminoguanidine and N(omega)-nitro-L-arginine methyl ester (L-NAME), on endotoxaemia-induced changes in vascular reactivity.

DESIGN

Randomised experiment.

SETTING

University laboratory, Turkey.

SUBJECTS

54 Wistar rats.

INTERVENTIONS

Rats were divided into control (n = 24) and endotoxaemia (n = 30) groups and were treated with an intraperitoneal injection of saline (control) and lipopolysaccharide (20 mg/kg), respectively. Subgroups of control and endotoxaemic rats were given either aminoguanidine or L-NAME by the same route.

MAIN OUTCOME MEASURES

Contractile responses to phenylephrine and relaxation responses to acetylcholine 4 hours after treatment.

RESULTS

Incubation with aminoguanidine and L-NAME potentiated the phenylephrine-induced contractile response and inhibited acetylcholine-induced relaxation in aortic rings in the control group. The vascular responses to phenylephrine and acetylcholine were less pronounced in the endotoxaemia group, and in vitro incubation with aminoguanidine and L-NAME partially restored the contraction induced by phenylephrine but did not affect the impaired response to acetylcholine. Aminoguanidine given in vivo prevented the impairment of vascular responses to both phenylephrine and acetylcholine whereas L-NAME gave no such protection.

CONCLUSION

Aminoguanidine acted similarly to L-NAME when incubated with the tissues in vitro, and did not show selectivity to inducible compared with constitutive isoforms of NO synthase. The finding that aminoguanidine but not L-NAME, prevented the endotoxin-induced impairment of vascular reactivity when administrated in vivo, therefore, suggested a role other than inhibition of NO synthase.

Authors+Show Affiliations

Faculty of Pharmacy, Department of General Surgery, Hacettepe University, Ankara, Turkey.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

11848232

Citation

Ismailoglu, U B., et al. "Effects of Aminoguanidine and N(omega)-nitro-L-arginine Methyl Ester On Vascular Hyporeactivity Induced By Endotoxaemia." The European Journal of Surgery = Acta Chirurgica, vol. 167, no. 11, 2001, pp. 803-9.
Ismailoglu UB, Pekiner C, Yorganci K, et al. Effects of aminoguanidine and N(omega)-nitro-L-arginine methyl ester on vascular hyporeactivity induced by endotoxaemia. Eur J Surg. 2001;167(11):803-9.
Ismailoglu, U. B., Pekiner, C., Yorganci, K., & Sahin-Erdemli, I. (2001). Effects of aminoguanidine and N(omega)-nitro-L-arginine methyl ester on vascular hyporeactivity induced by endotoxaemia. The European Journal of Surgery = Acta Chirurgica, 167(11), 803-9.
Ismailoglu UB, et al. Effects of Aminoguanidine and N(omega)-nitro-L-arginine Methyl Ester On Vascular Hyporeactivity Induced By Endotoxaemia. Eur J Surg. 2001;167(11):803-9. PubMed PMID: 11848232.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of aminoguanidine and N(omega)-nitro-L-arginine methyl ester on vascular hyporeactivity induced by endotoxaemia. AU - Ismailoglu,U B, AU - Pekiner,C, AU - Yorganci,K, AU - Sahin-Erdemli,I, PY - 2002/2/19/pubmed PY - 2002/7/31/medline PY - 2002/2/19/entrez SP - 803 EP - 9 JF - The European journal of surgery = Acta chirurgica JO - Eur J Surg VL - 167 IS - 11 N2 - OBJECTIVE: To investigate the effects of endotoxaemia on the reactivity of the aortic bed in rats, and to compare the effects of the nitric oxide (NO) synthase inhibitors aminoguanidine and N(omega)-nitro-L-arginine methyl ester (L-NAME), on endotoxaemia-induced changes in vascular reactivity. DESIGN: Randomised experiment. SETTING: University laboratory, Turkey. SUBJECTS: 54 Wistar rats. INTERVENTIONS: Rats were divided into control (n = 24) and endotoxaemia (n = 30) groups and were treated with an intraperitoneal injection of saline (control) and lipopolysaccharide (20 mg/kg), respectively. Subgroups of control and endotoxaemic rats were given either aminoguanidine or L-NAME by the same route. MAIN OUTCOME MEASURES: Contractile responses to phenylephrine and relaxation responses to acetylcholine 4 hours after treatment. RESULTS: Incubation with aminoguanidine and L-NAME potentiated the phenylephrine-induced contractile response and inhibited acetylcholine-induced relaxation in aortic rings in the control group. The vascular responses to phenylephrine and acetylcholine were less pronounced in the endotoxaemia group, and in vitro incubation with aminoguanidine and L-NAME partially restored the contraction induced by phenylephrine but did not affect the impaired response to acetylcholine. Aminoguanidine given in vivo prevented the impairment of vascular responses to both phenylephrine and acetylcholine whereas L-NAME gave no such protection. CONCLUSION: Aminoguanidine acted similarly to L-NAME when incubated with the tissues in vitro, and did not show selectivity to inducible compared with constitutive isoforms of NO synthase. The finding that aminoguanidine but not L-NAME, prevented the endotoxin-induced impairment of vascular reactivity when administrated in vivo, therefore, suggested a role other than inhibition of NO synthase. SN - 1102-4151 UR - https://www.unboundmedicine.com/medline/citation/11848232/Effects_of_aminoguanidine_and_N_omega__nitro_L_arginine_methyl_ester_on_vascular_hyporeactivity_induced_by_endotoxaemia_ DB - PRIME DP - Unbound Medicine ER -