Biomedical subjects

Amedeo Chiribiri

Publications and source records attributed to Amedeo Chiribiri.

3 recordsLinked to original sources

PubMed2006

Atrio-ventricular synchronization by single VDD lead inserted through persistent left superior vena cava in patient with Turner's syndrome.

A 71-year-old woman with Turner's syndrome underwent pacemaker implantation for complete atrio-ventricular block. During the procedure, the persistence of left sided superior vena cava (LSVC) was observed such that the lead, through the coronary sinus, reached the right atrium. By use of stylets, we could drive the lead against the lateral atrial wall and curve it through the tricuspid valve into the right ventricle. The tip reached an apical stable position, obtaining proper stimulation values. Moreover, the VDD dipole was positioned against high lateral atrial wall, adequately sensing the atrial potential. So, we could obtain an atrial synchronous ventricular pacing with only one VDD lead.

Aged↗

PubMed2003

Coronary endothelial dysfunction after ischemia and reperfusion and its prevention by ischemic preconditioning.

In the coronary circulation, when reperfusion follows ischemia, endothelial dysfunction occurs. This is characterized by a reduced endothelial release of nitric oxide and by an increased release of reactive oxygen species and endothelin. The reduced availability of nitric oxide leads to the adhesion of neutrophils to the vascular endothelium, platelet aggregation and, with the contribution of endothelin, vasoconstriction, which are responsible for the "no-reflow" phenomenon. Neutrophil adhesion is followed by the release of the superoxide anion from neutrophils and endothelial cells. Preconditioning limits the endothelial damage by ischemia-reperfusion. A relevant role is attributed to the increased endothelial release of nitric oxide, while that of adenosine is controversial. Another effect of preconditioning on the coronary vasculature is the acceleration of vasodilation in reactive hyperemia after a brief coronary occlusion. The acceleration is prevented if myocardial protection is achieved by means of the activation of the mitochondrial adenosine triphosphate sensitive potassium channels by diazoxide and persists when ischemic preconditioning is induced after blockade of the same channels by 5-hydroxydecanoate.

Adenosine↗

PubMed2002

Ischemic preconditioning changes the pattern of coronary reactive hyperemia regardless of mitochondrial ATP-sensitive K(+) channel blockade.

Ischemic preconditioning increases the velocity of vasodilatation and reduces the total hyperemic flow (THF) of a subsequent coronary reactive hyperemia (CRH). The increase in the velocity of vasodilatation has been shown to depend on an up-regulation of the endothelial release of nitric oxide, while the reduction of THF is attributed to an adenosine A(1) receptor-mediated mechanism. We investigated whether the changes in CRH induced by preconditioning ischemia (PI) can still be obtained after blockade of mitochondrial ATP-sensitive K(+) channels by sodium 5-hydroxydecanoate (5-HD), and whether the blockade per se affects the pattern of CRH. In anesthetized goats, flow was recorded from the left circumflex coronary artery (LCCA). CRH was obtained with the occlusion of LCCA for 15 s. PI was obtained by 2 cycles of 2.5 min of LCCA occlusion with a 5 min interval of reperfusion between the two occlusions. CRH was studied before and after i.v. administration of 5-HD (20 mg/kg), as well as in the presence of 5-HD after PI. Following 5-HD, the pattern of CRH remained unchanged. After 5-HD and PI, velocity of vasodilatation and total hyperemic flow of CRH showed the same changes as in previous studies after PI alone. It was concluded that the blockade of mitochondrial ATP-sensitive K(+) channels, which is reported to prevent myocardial protection, does not affect CRH and does not prevent PI from increasing the velocity of vasodilatation and reducing THF. These results demonstrate that the changes induced in CRH by preconditioning are independent of the opening of the mitochondrial ATP-sensitive K(+) channels.

Adenosine Triphosphate↗