Cardiovascular research
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Cardiovascular research · Aug 1994
Brief perfusion with diluted whole blood after global myocardial ischaemia increases reperfusion injury.
In vivo studies indicate that blood components, especially leucocytes, contribute to reperfusion injury after myocardial ischaemia. This study was designed to: (1) develop a small animal heart model of ischaemia-reperfusion that demonstrates the contribution of blood to reperfusion injury; (2) determine when the presence of blood in the heart--that is, during ischaemia or during early reperfusion--caused greater dysfunction; and (3) attempt to limit the blood contribution to reperfusion injury by leucocyte depletion. ⋯ Thirty min of global, normothermic ischaemia caused significant cardiac dysfunction early during reperfusion. Perfusion with unstimulated blood for a limited period further impaired the recovery of function and enhanced myocardial oedema. Dysfunction was particularly evident when diluted whole blood was perfused during the first minutes of reperfusion. The leucocyte depletion studies suggest that leucocytes are necessary, but may not be sufficient, to demonstrate the blood contribution to reperfusion injury.
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Cardiovascular research · Jun 1994
Comparative StudyAssessment of ability of levcromakalim and sodium nitroprusside to reverse the cardiovascular effects of nitric oxide synthase inhibition in the anaesthetised pig.
The aim was to test the ability of levcromakalim, a potassium channel opener, and sodium nitroprusside, a nitric oxide donor, to reverse the systemic and pulmonary vasoconstrictor actions of NG-nitro-L-arginine methyl ester (L-NAME), and thus to restore cardiac output in anaesthetised pigs. ⋯ Increased systemic vascular resistance following a bolus of L-NAME (10 mg.kg-1) is reversed by subsequent administration of levcromakalim (10-40 micrograms.kg-1) or sodium nitroprusside (1-4 micrograms.kg-1.min-1) associated with partial restoration of cardiac output. The degree to which cardiac output is restored by these two agents is limited by a concomitant reduction in preload.
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Cardiovascular research · Jan 1994
Randomized Controlled Trial Comparative Study Clinical TrialEffects of a nitric oxide synthase inhibitor in humans with septic shock.
Studies in animals have indicated that increased production of nitric oxide from an inducible isoform of nitric oxide synthase contributes to the pathophysiology of endotoxic and cytokine induced shock. The aim of this study was to determine the role of nitric oxide in septic shock in humans. ⋯ Low doses of L-NMMA cause a widespread increase in vascular tone and raise blood pressure in patients with septic shock. Overproduction of nitric oxide appears to be an important mechanism in septic shock in patients, and inhibition of nitric oxide synthesis might provide a novel therapeutic approach to this condition. However, L-NMMA produced a fall in cardiac output and it is possible that this would worsen tissue perfusion. Larger studies examining the effects of L-NMMA on mortality and morbidity are now required.
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Cardiovascular research · Jan 1994
Left ventricular remodelling and disparate changes in contractility and relaxation during the development of and recovery from experimental heart failure.
Canine pacing induced heart failure is characterised by impaired left ventricular contractility and relaxation, and clinical recovery after cessation of pacing. It is unclear whether the impairment is responsive to adrenergic stimulation. The aim of this study was to assess left ventricular contractility and relaxation and their response to beta adrenergic stimulation during heart failure and after recovery. ⋯ In pacing induced heart failure, there is a dissociation between the normal ability of beta adrenergic stimulation to augment contractility and shorten relaxation, and a differential capacity for recovery of contractility and relaxation.
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Cardiovascular research · Nov 1993
Comparative StudyMechanisms causing coronary microvascular dysfunction following crystalloid cardioplegia and reperfusion.
The aim was to examine the mechanisms of coronary microvascular dysfunction during cardiopulmonary bypass and ischaemic arrest using a crystalloid cardioplegic solution. ⋯ Ischaemic cardioplegia-reperfusion induced endothelium dependent and direct smooth muscle microvascular dysfunction is at least partially mediated by prolonged exposure of vessels to hyperkalaemia and to the generation of oxygen derived free radicals. Leucocytes probably mediate injury during reperfusion, while hypothermia has minimal effect on recovery of vasomotor function.