Adaptations to iron deficiency: cardiac functional responsiveness to norepinephrine, arterial remodeling, and the effect of beta-blockade on cardiac hypertrophy

Iron deficiency (ID) results in ventricular hypertrophy, believed to involve sympathetic stimulation. We hypothesized that with ID 1) intravenous norepinephrine would alter heart rate (HR) and contractility, 2) abdominal aorta would be larger and more distensible, and 3) the beta-blocker propanolol...

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Bibliographic Details
Published in:BMC physiology 2002-01, Vol.2 (1), p.1-1, Article 1
Main Authors: Turner, Lexa Rae, Premo, Daniel Aaron, Gibbs, Brett Jason, Hearthway, Megan Lesley, Motsko, Madelyne, Sappington, Andrea, Walker, LeeAnn, Mullendore, Michael Eugene, Chew, Jr, Herbert George
Format: Article
Language:English
Subjects:
Adaptation, Physiological
Adrenergic beta-Antagonists - therapeutic use
Animals
Arteries - pathology
Arteries - physiopathology
Body Weight
Cardiomegaly - etiology
Cardiomegaly - physiopathology
Cardiomegaly - prevention & control
Elasticity
Heart - drug effects
Heart - physiopathology
Heart Rate - drug effects
Hematocrit
Hemodynamics
Iron - deficiency
Male
Myocardial Contraction - drug effects
Myocardium - pathology
Norepinephrine - pharmacology
Organ Size
Propranolol - therapeutic use
Rats
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Summary:Iron deficiency (ID) results in ventricular hypertrophy, believed to involve sympathetic stimulation. We hypothesized that with ID 1) intravenous norepinephrine would alter heart rate (HR) and contractility, 2) abdominal aorta would be larger and more distensible, and 3) the beta-blocker propanolol would reduce hypertrophy. 1) 30 CD rats were fed an ID or replete diet for 1 week or 1 month. Norepinephrine was infused via jugular vein; pressure was monitored at carotid artery. Saline infusions were used as a control. The pressure trace was analyzed for HR, contractility, systolic and diastolic pressures. 2) Abdominal aorta catheters inflated the aorta, while digital microscopic images were recorded at stepwise pressures to measure arterial diameter and distensibility. 3) An additional 10 rats (5 ID, 5 control) were given a daily injection of propanolol or saline. After 1 month, the hearts were excised and weighed. Enhanced contractility, but not HR, was associated with ID hypertrophic hearts. Systolic and diastolic blood pressures were consistent with an increase in arterial diameter associated with ID. Aortic diameter at 100 mmHg and distensibility were increased with ID. Propanolol was associated with an increase in heart to body mass ratio. ID cardiac hypertrophy results in an increased inotropic, but not chronotropic response to the sympathetic neurotransmitter, norepinephrine. Increased aortic diameter is consistent with a flow-dependent vascular remodeling; increased distensibility may reflect decreased vascular collagen content. The failure of propanolol to prevent hypertrophy suggests that ID hypertrophy is not mediated via beta-adrenergic neurotransmission.
ISSN:1472-6793
1472-6793
DOI:10.1186/1472-6793-2-1