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The purpose of this study was to evaluate the haemodynamic and metabolic effects of captopril during reperfusion of pig hearts following 360 min global hypothermic cardioplegia and storage (HCS). The hearts were perfused with one litre of cold crystalloid cardioplegia (Bretschneider solution no. 3), excised and stored in saline at 4 degrees C for 360 min. The hearts were then reperfused with blood in a modified Langendorff model for 60 min. Left ventricular function, myocardial blood flow, and arteriovenous differences in oxygen, glucose and lactate were monitored intraoperatively and during reperfusion. Two groups of hearts were studied. Group I (captopril treated, n = 9): the pigs were pre-medicated with increasing oral doses of captopril for 3 weeks (12.5 mg-150 mg daily) and an intravenous dose (25 mg) upon arrival at the laboratory. Captopril was added to the cardioplegia (1000 microg/l) and to the reperfusion media (1000 microg/l). Group II (controls, n = 8): the pigs were given no premedication, captopril-free cardioplegia and the hearts were reperfused with captopril-free blood. Captopril increased myocardial oxygen and glucose extraction during reperfusion (p < 0.05 for both) while lactate remained unchanged after 360 min HCS. Treatments with captopril increased developed left ventricular pressure (DLVP) and relaxation (-dP/dtmax) during reperfusion (p < 0.05 for both), while contractility (+dP/dtmax) was unchanged. Heart rate was reduced in captopril-treated hearts (p < 0.05) while myocardial blood flow (MBF) was similar in the two groups. Captopril administration prior to and during HCS and postcardioplegic reperfusion improves oxygen and glucose extraction in large spontaneously beating porcine hearts during reperfusion. The underlying mechanisms seem to involve metabolic modulation, since myocardial uptake of oxygen and glucose was increased in the absence of changes in myocardial blood flow.

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INTRODUCTION: Patients with carotid stenosis are at high risk of vascular events and therefore require an optimal control of risk factors such as hypertension. As the treatment of hypertension differs according to the cause, we examined the prevalence of resistant hypertension, and the cause of hypertension, among patients with carotid stenosis followed closely in two randomized trials of carotid endarterectomy. OBJECTIVE: The purpose of this study was to determine the prevalence of resistant hypertension and of secondary hypertension among patients with carotid stenosis. METHODS: A chart review was performed of all patients from our center who participated in the North American Symptomatic Carotid Endarterectomy Trial or the Asymptomatic Carotid Artery Study to determine the prevalence of renovascular hypertension. RESULTS: Among 170 patients with carotid stenosis followed in these two trials, 145 (83.5%) were hypertensive (systolic >160 or diastolic >90 mm Hg); at least 24 (14.1% overall, 16.6% of hypertensives) had renovascular hypertension based on either nuclear medicine renography, renal angiography or both; among the 79 patients with resistant hypertension (mean arterial pressure >130 mm Hg despite treatment), 20 (25.3%) had renovascular hypertension. Adrenocortical hyperplasia was the underlying cause of hypertension in 12 (7.1% of cases, 8.3% of hypertensives, 8.8% of resistant hypertensives). Blood pressures were significantly higher for patients with renovascular and adrenocortical hypertension (p < 0.0001 for systolic, p = 0.024 for diastolic pressures). CONCLUSION: Among patients with carotid stenosis, renovascular hypertension is unusually common. Resistant hypertension among such patients should lead to investigation and management directed at the cause of hypertension. Appropriate investigations might include plasma renin/aldosterone ratio, captopril renography and MRA of the renal arteries or renal angiography. Copyright 2000 S. Karger AG, Basel

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Br J Pharmacol. 2000 Jul;130(5):1076-82.
Participation of kinins in the captopril-induced inhibition of intimal hyperplasia caused by interruption of carotid blood flow in the mouse.

Emanueli C, Bonaria Salis M, Figueroa C, Chao J, Chao L, Gaspa L, Capogrossi MC, Madeddu P.

Laboratorio di Patologia Vascolare, Istituto Dermopatico dell'Immacolata (IDI, IRCCS), Roma, Italy [corrected].

1. In the rat balloon injury model, angiotensin-converting enzyme (ACE) inhibitors prevent vascular remodelling by inhibiting angiotensin II generation and kinin breakdown. We investigated if ACE inhibition also prevents the structural vascular responses to disruption of carotid artery blood flow and if kinin potentiation plays a role in such a protection. 2. Morphometric analysis of the structural alterations caused by ligation of the left carotid artery was performed 14 days after surgery in J129Sv wild-type mice (B(2)(+/+)) drinking normal tap water or water containing captopril (120 mg kg(-1) per day). In addition, the effect of captopril on vascular remodelling was tested in B(2)(+/+) given the bradykinin (BK) B(1) receptor antagonist des-Arg(9)-[Leu(8)]-BK (DALBK, 50 nmol kg(-1) per day, intraperitoneally) or the BK B(2) receptor antagonist D-Arg, [Hyp(3),Thi(5)D-Tic(7),Oic(8)]-BK (icatibant, 1 micromol kg(-1) per day, intraperitoneally), and in B(2) receptor gene knockout mice (B(2)(-/-)). 3. Interruption of blood flow resulted in carotid artery intimal hyperplasia and media thickening in untreated B(2)(+/+), these responses being partially suppressed by captopril. The inhibition of intimal thickening exerted by captopril was reduced in B(2)(+/+) given DALBK or icatibant (P<0.05 for both comparisons) as well as in B(2)(-/-) (P<0.05). Neither antagonism of kinin receptors nor disruption of the B(2) receptor gene altered the suppressive effect of captopril on media thickening. The protection of vascular wall structure was independent of the reduction in blood pressure by captopril. 4. These results demonstrate that kinins participate in the inhibitory effect of captopril on intimal hyperplasia via B(1) and B(2) receptor signalling. Our findings may have important implications in treating vascular remodelling evoked by altered shear stress conditions.

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