PubMed Health⌕ Search

Biomedical subjects

S P Barnard

Publications and source records attributed to S P Barnard.

15 recordsLinked to original sources

Mechanical ventricular assistance for the failing right ventricle after cardiac transplantation.

Right ventricular failure secondary to elevated pulmonary vascular resistance (PVR) following orthotopic cardiac transplant is a complication with a high mortality; and patients with high resistance are often not accepted on transplant waiting lists. We describe six cases of right ventricular failure after cardiac transplant managed by right ventricular assist device (RVAD), four of whom died and two patients who survived following life-threatening complications.

Adult↗

Right ventricular rupture after coronary surgery.

A 70-year-old woman suffered a fatal right ventricular rupture 12 h after uneventful coronary surgery. Post-mortem examination revealed that the rupture had occurred through an area of fatty infiltration. Myocardium had been replaced by fat cells. The literature is reviewed and pathology of this condition discussed.

Aged↗

Early bioprosthesis calcification in an octogenarian.

Pericardial valves have been advocated for use in the older age group of patients as they avoid the need for anticoagulation and are less liable to calcification than they are in the young. We report here a case of early valve calcification in a Sorin pericardial valve in the aortic position.

Aged↗

Retrieval of broken left-atrial catheter using a rigid bronchoscope.

Left-atrial pressure monitoring continues to be of value in cardiac surgery of the high-risk patient. Complications are fortunately low and include haemorrhage following catheter removal and retained catheter fragments. A simple and safe technique is presented to retrieve retained catheters using a rigid bronchoscope and avoiding the need for resternotomy.

Aortic Valve↗

Straddle embolus--imminent paradoxical embolus diagnosed by echocardiography and treated surgically.

Paradoxical embolus, the passage of an embolus from the right to the left side of the circulation, was formerly recognised as a postmortem diagnosis. More recently, survivors with paradoxical embolus have been described. A case of paradoxical embolus is described in which the diagnosis was made clinically, and an imminent further embolus visualised by transoesophageal echocardiography, which was successfully treated surgically. Treatment strategies are discussed.

Aged↗

The effect of desferal on rat heart mitochondrial function, iron content, and xanthine dehydrogenase/oxidase conversion during ischemia-reperfusion.

Cardiac mitochondrial function as measured by oxidative phosphorylation is impaired by ischemia; and, this deteriorates even further on reperfusion of the heart. Free oxygen radicals, especially the formation of hydroxyl radicals via the iron-catalyzed Haber-Weiss and Fenton reactions have been implicated in the reperfusion injury. In this study, the effect of desferrioxamine (desferal) in the perfusate on mitochondrial function of isolated rat hearts during different periods of normothermic ischemic cardiac arrest (NICA), and subsequent reperfusion was investigated. Mitochondrial functions measured were the QO2 (state 3); ADP/O ratio and oxidative phosphorylation; the mitochondrial, loosely bound (chelateable) iron (LB-iron); the xanthine dehydrogenase and xanthine oxidase activities. Inclusion of desferal in the perfusion solution significantly improved mitochondrial function during the different NICA periods, and prevented the deterioration of mitochondrial function resulting from reperfusion. Desferal did not significantly affect the LB-iron content of the mitochondria or the ratio of xanthine dehydrogenase/xanthine oxidase activities in the mitochondria during NICA or reperfusion. Our experiments suggest that iron, which is free to be chelated by desferal, plays a role in this injury to the rat myocardium.

Animals↗

Purine and oxypurine production in mitochondria of ischemic and reperfused myocardium.

The present study was undertaken to determine whether significant breakdown of adenine nucleotides to purine bases and oxypurines occurred in mitochondria following myocardial ischemia and ischemia followed by reperfusion, and whether allopurinol prevented this effect. The adenine nucleotides adenosine, hypoxanthine, xanthine and uric acid were measured in the mitochondria and the results suggest that breakdown did occur. Malondialdehyde concentration was determined to gauge lipid peroxidation. This substance did not increase during ischemia or reperfusion, but did so in the presence of allopurinol. Xanthine dehydrogenase was converted to xanthine oxidase during reperfusion and the activity of both enzymes were inhibited by allopurinol. The results also suggested the presence of a mitochondrial 5'-nucleotidase. We conclude that significant breakdown of adenine nucleotide took place in myocardial mitochondria during ischemia and ischemia followed by reperfusion and that allopurinol may have a protective effect.

Adenine Nucleotides↗

Effect of normothermic ischemic cardiac arrest and of reperfusion on the free oxygen radical scavenger enzymes and xanthine oxidase (a generator of superoxide anions).

Recent evidence suggests that free oxygen radicals are produced by ischaemic tissues, accounting for at least part of the damage that results. These free oxygen radicals are produced by xanthine oxidase, amongst others, and removed by scavenger enzymes (catalase, superoxide dismutase and glutathione peroxidase) and anti-oxidants. As mitochondria are oxygen-utilising organelles, they are capable of producing free oxygen radicals. Our results indicate that the removal of free oxygen radicals are not diminished during ischaemia, but the activity of the free oxygen radical generator, xanthine oxidase, is increased. This could lead to an increased superoxide anion concentration.

Animals↗

The effect of allopurinol and deferrioxamine on rat heart mitochondrial oxidative phosphorylation after normothermic ischemic cardiac arrest and of reperfusion.

The electron transport chain of the mitochondria is highly sensitive to myocardial ischemia. As free oxygen radicals take part in the damage that occurred during ischemia, this study was undertaken to determine if allopurinol and deferrioxamine had any beneficial effect on mitochondrial function. Our results showed that perfusion with allopurinol did not improve the mitochondrial function, but that reperfusion with allopurinol and deferrioxamine had a beneficial effect. We came to the conclusion that xanthine oxidase, as a generator of superoxide anions, is of minor importance in comparison with the hydroxyl radicals, which are probably formed in the presence of iron in the cell.

Adenosine Diphosphate↗