Acute pulmonary hemodynamic effects of intravenous copper sulfate

Role of α-adrenergic system

T. Ahmed, A. Januszkiewicz, P. Eyre, M. J. Robinson, M. A. Sackner

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

We investigated the acute pulmonary hemodynamic effects of intravenous copper sulfate (CuSO4) infusion and its mechanism of action in six groups of conscious sheep (total 40). After 300 mg CuSO4 alone, mean pulmonary artery pressure (Ppa) increased from 10.3 to 22.5 Torr and pulmonary artery wedge pressure (Ppaw) from 3.% to 7.6 Torr, whereas systemic arterial pressure (Psa) increased from 95 to 102 Torr. Cardiac output (Qp) decreased from 4.7 to 3.3 l/min. Pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) increased to 320 and 160% of base line, respectively. The hemodynamic changes correlated well with serum copper, which increased from a base-line value of 0.12 to 3.5 mg/dl after the CuSO4. Serum dopamine β-hydroxylase increased from 3.2 U/l before CuSO4 injection to 5.7 after its administration signifying activation of adrenergic nervous system. H1-histamine receptor blockade with chlorpheniramine failed to prevent the effects of CuSO4. Pretreatment with methysergide, a serotonin antagonist, partially attenuated the effects of CuSO4. Phenoxybenzamine, and α-adenergic receptor blocker, and 6-hydroxydopamine, a catecholamine depleting agent, completely blocked the effects of CuSO4. β-Adrenergic receptor blockade with propranolol enhanced the effects of CuSO4. We conclude, that, in conscious sheep, acute infusion of CuSO4 caused a marked reversible increase in PVR with a slight transient increase in SVR, and this pulmonary hypertension was produced by stimulation of the α-adrenergic nervous system.

Original languageEnglish
Pages (from-to)1204-1213
Number of pages10
JournalJournal of Applied Physiology Respiratory Environmental and Exercise Physiology
Volume51
Issue number5
StatePublished - Dec 1 1981
Externally publishedYes

Fingerprint

Copper Sulfate
Vascular Resistance
Adrenergic Agents
Hemodynamics
Lung
Nervous System
Sheep
Chlorpheniramine
Methysergide
Histamine H1 Receptors
Phenoxybenzamine
Serotonin Antagonists
Pulmonary Wedge Pressure
Oxidopamine
Mixed Function Oxygenases
Serum
Pulmonary Hypertension
Propranolol
Cardiac Output
Adrenergic Receptors

ASJC Scopus subject areas

  • Physiology
  • Endocrinology

Cite this

Acute pulmonary hemodynamic effects of intravenous copper sulfate : Role of α-adrenergic system. / Ahmed, T.; Januszkiewicz, A.; Eyre, P.; Robinson, M. J.; Sackner, M. A.

In: Journal of Applied Physiology Respiratory Environmental and Exercise Physiology, Vol. 51, No. 5, 01.12.1981, p. 1204-1213.

Research output: Contribution to journalArticle

Ahmed, T. ; Januszkiewicz, A. ; Eyre, P. ; Robinson, M. J. ; Sackner, M. A. / Acute pulmonary hemodynamic effects of intravenous copper sulfate : Role of α-adrenergic system. In: Journal of Applied Physiology Respiratory Environmental and Exercise Physiology. 1981 ; Vol. 51, No. 5. pp. 1204-1213.
@article{a288deb0e4a34558a489af7a8504a683,
title = "Acute pulmonary hemodynamic effects of intravenous copper sulfate: Role of α-adrenergic system",
abstract = "We investigated the acute pulmonary hemodynamic effects of intravenous copper sulfate (CuSO4) infusion and its mechanism of action in six groups of conscious sheep (total 40). After 300 mg CuSO4 alone, mean pulmonary artery pressure (Ppa) increased from 10.3 to 22.5 Torr and pulmonary artery wedge pressure (Ppaw) from 3.{\%} to 7.6 Torr, whereas systemic arterial pressure (Psa) increased from 95 to 102 Torr. Cardiac output (Qp) decreased from 4.7 to 3.3 l/min. Pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) increased to 320 and 160{\%} of base line, respectively. The hemodynamic changes correlated well with serum copper, which increased from a base-line value of 0.12 to 3.5 mg/dl after the CuSO4. Serum dopamine β-hydroxylase increased from 3.2 U/l before CuSO4 injection to 5.7 after its administration signifying activation of adrenergic nervous system. H1-histamine receptor blockade with chlorpheniramine failed to prevent the effects of CuSO4. Pretreatment with methysergide, a serotonin antagonist, partially attenuated the effects of CuSO4. Phenoxybenzamine, and α-adenergic receptor blocker, and 6-hydroxydopamine, a catecholamine depleting agent, completely blocked the effects of CuSO4. β-Adrenergic receptor blockade with propranolol enhanced the effects of CuSO4. We conclude, that, in conscious sheep, acute infusion of CuSO4 caused a marked reversible increase in PVR with a slight transient increase in SVR, and this pulmonary hypertension was produced by stimulation of the α-adrenergic nervous system.",
author = "T. Ahmed and A. Januszkiewicz and P. Eyre and Robinson, {M. J.} and Sackner, {M. A.}",
year = "1981",
month = "12",
day = "1",
language = "English",
volume = "51",
pages = "1204--1213",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Acute pulmonary hemodynamic effects of intravenous copper sulfate

T2 - Role of α-adrenergic system

AU - Ahmed, T.

AU - Januszkiewicz, A.

AU - Eyre, P.

AU - Robinson, M. J.

AU - Sackner, M. A.

PY - 1981/12/1

Y1 - 1981/12/1

N2 - We investigated the acute pulmonary hemodynamic effects of intravenous copper sulfate (CuSO4) infusion and its mechanism of action in six groups of conscious sheep (total 40). After 300 mg CuSO4 alone, mean pulmonary artery pressure (Ppa) increased from 10.3 to 22.5 Torr and pulmonary artery wedge pressure (Ppaw) from 3.% to 7.6 Torr, whereas systemic arterial pressure (Psa) increased from 95 to 102 Torr. Cardiac output (Qp) decreased from 4.7 to 3.3 l/min. Pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) increased to 320 and 160% of base line, respectively. The hemodynamic changes correlated well with serum copper, which increased from a base-line value of 0.12 to 3.5 mg/dl after the CuSO4. Serum dopamine β-hydroxylase increased from 3.2 U/l before CuSO4 injection to 5.7 after its administration signifying activation of adrenergic nervous system. H1-histamine receptor blockade with chlorpheniramine failed to prevent the effects of CuSO4. Pretreatment with methysergide, a serotonin antagonist, partially attenuated the effects of CuSO4. Phenoxybenzamine, and α-adenergic receptor blocker, and 6-hydroxydopamine, a catecholamine depleting agent, completely blocked the effects of CuSO4. β-Adrenergic receptor blockade with propranolol enhanced the effects of CuSO4. We conclude, that, in conscious sheep, acute infusion of CuSO4 caused a marked reversible increase in PVR with a slight transient increase in SVR, and this pulmonary hypertension was produced by stimulation of the α-adrenergic nervous system.

AB - We investigated the acute pulmonary hemodynamic effects of intravenous copper sulfate (CuSO4) infusion and its mechanism of action in six groups of conscious sheep (total 40). After 300 mg CuSO4 alone, mean pulmonary artery pressure (Ppa) increased from 10.3 to 22.5 Torr and pulmonary artery wedge pressure (Ppaw) from 3.% to 7.6 Torr, whereas systemic arterial pressure (Psa) increased from 95 to 102 Torr. Cardiac output (Qp) decreased from 4.7 to 3.3 l/min. Pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) increased to 320 and 160% of base line, respectively. The hemodynamic changes correlated well with serum copper, which increased from a base-line value of 0.12 to 3.5 mg/dl after the CuSO4. Serum dopamine β-hydroxylase increased from 3.2 U/l before CuSO4 injection to 5.7 after its administration signifying activation of adrenergic nervous system. H1-histamine receptor blockade with chlorpheniramine failed to prevent the effects of CuSO4. Pretreatment with methysergide, a serotonin antagonist, partially attenuated the effects of CuSO4. Phenoxybenzamine, and α-adenergic receptor blocker, and 6-hydroxydopamine, a catecholamine depleting agent, completely blocked the effects of CuSO4. β-Adrenergic receptor blockade with propranolol enhanced the effects of CuSO4. We conclude, that, in conscious sheep, acute infusion of CuSO4 caused a marked reversible increase in PVR with a slight transient increase in SVR, and this pulmonary hypertension was produced by stimulation of the α-adrenergic nervous system.

UR - http://www.scopus.com/inward/record.url?scp=0019817952&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019817952&partnerID=8YFLogxK

M3 - Article

VL - 51

SP - 1204

EP - 1213

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 5

ER -