4 research outputs found
Angiotensin production by the heart: a quantitative study in pigs with the use of radiolabeled angiotensin infusions
BACKGROUND: Beneficial effects of ACE inhibitors on the heart may be
mediated by decreased cardiac angiotensin II (Ang II) production. METHODS
AND RESULTS: To determine whether cardiac Ang I and Ang II are produced in
situ or derived from the circulation, we infused 125I-labeled Ang I or II
into pigs (25 to 30 kg) and measured 125I-Ang I and II as well
Angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade prevent cardiac remodeling in pigs after myocardial infarction: role of tissue angiotensin II
BACKGROUND: The mechanisms behind the beneficial effects of
renin-angiotensin system blockade after myocardial infarction (MI) are not
fully elucidated but may include interference with tissue angiotensin II
(Ang II). METHODS AND RESULTS: Forty-nine pigs underwent coronary artery
ligation or sham operation and were studied up to 6 weeks. To determine
coronary angiotensin I (Ang I) to Ang II conversion and to distinguish
plasma-derived Ang II from locally synthesized Ang II, (125)I-labeled and
endogenous Ang I and II were measured in plasma and in infarcted and
noninfarcted left ventricle (LV) during (125)I-Ang I infusion. Ang II type
1 (AT(1)) receptor-mediated uptake of circulating (125)I-Ang II was
increased at 1 and 3 weeks in noninfarcted LV, and this uptake was the
main cause of the transient elevation in Ang II levels in the noninfarcted
LV at 1 week. Ang II levels and AT(1) receptor-mediated uptake of
circulating Ang II were reduced in the infarct area at all time points.
Coronary Ang I to Ang II conversion was unaffected by MI. Captopril and
the AT(1) receptor antagonist eprosartan attenuated postinfarct
remodeling, although both drugs increased cardiac Ang II production.
Captopril blocked coronary conversion by >80% and normalized Ang II uptake
in the noninfarcted LV. Eprosartan did not affect coronary conversion and
blocked cardiac Ang II uptake by >90%. CONCLUSIONS: Both circulating and
locally generated Ang II contribute to remodeling after MI. The rise in
tissue Ang II production during angiotensin-converting enzyme inhibition
and AT(1) receptor blockade suggests that the antihypertrophic effects of
these drugs result not only from diminished AT(1) receptor stimulation but
also from increased stimulation of growth-inhibitory Ang II type 2
receptors
Massive haemorrhage at resternotomy after stent implantation in ventriculo-pulmonary shunt after Norwood procedure
The ventriculo-pulmonary shunt in hypoplastic left heart syndrome has become an alternative to the arterio-pulmonary shunt. We present
a patient with a severe stenosis in the ventriculo-pulmonary shunt at the proximal anastomosis, for which emergency balloon dilatation
and stent implantation was performed. The location of the stent in the shunt, leaving only a thin compressed infundibular myocardium
directly beneath the sternum, predisposed to massive haemorrhage at resternotomy for bidirectional Glenn procedure.
2006 Published by European Association for Cardio-Thoracic Surgery. All rights reserved