Cardiovascular research
-
Cardiovascular research · Apr 1995
Preischaemic as well as postischaemic application of a calcium antagonist affords cardioprotection in the isolated guinea pig heart.
The aim was to answer the following questions: (1) Does treatment with calcium antagonists have to be begun before ischaemia or is postischaemic application also protective? (2) When applied before ischaemia, do calcium antagonists have to depress preischaemic cardiac function in order to elicit protection? (3) Is cardioprotection a matter of improved reflow or do the agents influence the degree of oxidative injury during reperfusion? ⋯ Short term postischaemic application of the calcium antagonist gallopamil is almost as effective at restoring pump function as preischaemic application which, in turn, does not have to depress preischaemic cardiac function in order to elicit protection. A reduction of oxidative stress during reperfusion seems to contribute to the beneficial effects of postischaemic application of gallopamil, but a direct oxygen radical scavenging activity of gallopamil is not involved.
-
Cardiovascular research · Apr 1995
Adenosine and PAF dependent mechanisms lead to myocardial reperfusion injury by neutrophils after brief ischaemia.
The aim was to establish whether polymorphonuclear neutrophils can, by themselves, elicit depression of postischaemic heart function immediately after short periods of ischaemia, and to examine the involvement of endogenous adenosine and platelet activating factor (PAF) in the observed phenomena. ⋯ Even after brief ischaemia, neutrophils introduced into the coronary system can exacerbate reperfusion injury. Adenosine, through its A1 receptor, and PAF appear to play a significant role as mediators of this action.
-
Cardiovascular research · Feb 1995
Intracellular pH in vascular smooth muscle: regulation by sodium-hydrogen exchange and multiple sodium dependent HCO3- mechanisms.
The aim was to determine the mechanisms, particularly bicarbonate dependent mechanisms, of intracellular pH (pHi) recovery from various acidoses in vascular smooth muscle and to explore the ATP dependency of the respective mechanisms. ⋯ At least three transporters contribute to recovery from acidosis in vascular smooth muscle: Na+/H+ exchange, an Na(+)-HCO3- cotransporter which is sensitive to EIPA, and an Na+ dependent HCO3-/Cl- exchange sensitive to both SITS and EIPA. The Na(+)-HCO3- cotransporter appears to be similar to that described in human vascular smooth muscle. When the Na+/H+ exchanger is attenuated by cellular ATP depletion, the alternative pathways, particularly the Na(+)-HCO3- cotransporter, ensure that substantial pHi regulatory capacity is maintained.
-
Cardiovascular research · Nov 1994
Randomized Controlled Trial Comparative Study Clinical TrialDofetilide reduces the incidence of ventricular fibrillation during acute myocardial ischaemia. A randomised study in pigs.
The aim was to investigate whether dofetilide, a new selective cardiac potassium channel blocker, would reduce the incidence of ischaemia induced ventricular fibrillation in closed chest pigs. ⋯ Dofetilide significantly reduces the incidence of ischaemia induced ventricular fibrillation in closed chest pigs.
-
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.