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Hemodynamic response to norepinephrine with and without inhibition of nitric oxide synthase in porcine endotoxemia.
Am J Respir Crit Care Med. 1999 Dec; 160(6):1987-93.AJ

Abstract

The objective of this study was to determine the circuit and cardiac effects of norepinephrine (NE) with and without endotoxin, and how these responses are modified by the inhibition of nitric oxide synthase (NOS). We anesthetized eight pigs and instrumented them for measurements of cardiac output (Q), arterial pressure (Part), and mean pulmonary arterial pressure (Ppa). We also placed a 40-ml balloon in the right atrium for transient obstruction of flow and measurement of the mean circulatory filling pressure (MCFP) and resistance to venous return (RVR). After baseline measurements, animals were treated with 10 microg/kg/h of Escherichia coli endotoxin. At 105 min the measurements were repeated. We then infused 12.5 mg/kg of N(G)-nitro-L-arginine methyl ester (L-NAME) for 10 min and repeated the measurements. At baseline, at the end of endotoxin infusion, and after L-NAME infusion we infused 3, 9, and 27 microg/min of NE for 10 min each, and recorded hemodynamic measurements at each dose. NE shifted the venous return curve (i.e., increased MCFP) to the right without changing RVR, and increased cardiac output (CO) both at baseline and after endotoxin. Endotoxemia markedly flattened the dose-response curves for the change in Part, Ppa, CO, and heart rate with NE. The peak response of Part to NE after endotoxemia was restored with L-NAME, but the other dose-response curves were not affected. NE also did not shift the venous return curve after L-NAME. Furthermore, the increase in Part with NE was of shorter duration after L-NAME than in the baseline condition. In conclusion, NE shifts the venous return curve to the right and improves CO in endotoxic and nonendotoxic conditions. Endotoxemia decreases the arterial responsiveness to NE. L-NAME partly restored this loss of responsiveness in arteries but not in the venous circulation.

Authors+Show Affiliations

Departments of Medicine and Physiology, Critical Care Division, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10588618

Citation

Datta, P, and S Magder. "Hemodynamic Response to Norepinephrine With and Without Inhibition of Nitric Oxide Synthase in Porcine Endotoxemia." American Journal of Respiratory and Critical Care Medicine, vol. 160, no. 6, 1999, pp. 1987-93.
Datta P, Magder S. Hemodynamic response to norepinephrine with and without inhibition of nitric oxide synthase in porcine endotoxemia. Am J Respir Crit Care Med. 1999;160(6):1987-93.
Datta, P., & Magder, S. (1999). Hemodynamic response to norepinephrine with and without inhibition of nitric oxide synthase in porcine endotoxemia. American Journal of Respiratory and Critical Care Medicine, 160(6), 1987-93.
Datta P, Magder S. Hemodynamic Response to Norepinephrine With and Without Inhibition of Nitric Oxide Synthase in Porcine Endotoxemia. Am J Respir Crit Care Med. 1999;160(6):1987-93. PubMed PMID: 10588618.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hemodynamic response to norepinephrine with and without inhibition of nitric oxide synthase in porcine endotoxemia. AU - Datta,P, AU - Magder,S, PY - 1999/12/10/pubmed PY - 2001/7/4/medline PY - 1999/12/10/entrez SP - 1987 EP - 93 JF - American journal of respiratory and critical care medicine JO - Am J Respir Crit Care Med VL - 160 IS - 6 N2 - The objective of this study was to determine the circuit and cardiac effects of norepinephrine (NE) with and without endotoxin, and how these responses are modified by the inhibition of nitric oxide synthase (NOS). We anesthetized eight pigs and instrumented them for measurements of cardiac output (Q), arterial pressure (Part), and mean pulmonary arterial pressure (Ppa). We also placed a 40-ml balloon in the right atrium for transient obstruction of flow and measurement of the mean circulatory filling pressure (MCFP) and resistance to venous return (RVR). After baseline measurements, animals were treated with 10 microg/kg/h of Escherichia coli endotoxin. At 105 min the measurements were repeated. We then infused 12.5 mg/kg of N(G)-nitro-L-arginine methyl ester (L-NAME) for 10 min and repeated the measurements. At baseline, at the end of endotoxin infusion, and after L-NAME infusion we infused 3, 9, and 27 microg/min of NE for 10 min each, and recorded hemodynamic measurements at each dose. NE shifted the venous return curve (i.e., increased MCFP) to the right without changing RVR, and increased cardiac output (CO) both at baseline and after endotoxin. Endotoxemia markedly flattened the dose-response curves for the change in Part, Ppa, CO, and heart rate with NE. The peak response of Part to NE after endotoxemia was restored with L-NAME, but the other dose-response curves were not affected. NE also did not shift the venous return curve after L-NAME. Furthermore, the increase in Part with NE was of shorter duration after L-NAME than in the baseline condition. In conclusion, NE shifts the venous return curve to the right and improves CO in endotoxic and nonendotoxic conditions. Endotoxemia decreases the arterial responsiveness to NE. L-NAME partly restored this loss of responsiveness in arteries but not in the venous circulation. SN - 1073-449X UR - https://www.unboundmedicine.com/medline/citation/10588618/Hemodynamic_response_to_norepinephrine_with_and_without_inhibition_of_nitric_oxide_synthase_in_porcine_endotoxemia_ L2 - https://www.atsjournals.org/doi/10.1164/ajrccm.160.6.9808019?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -