Biomedical subjects

O Scapín

Publications and source records attributed to O Scapín.

5 recordsLinked to original sources

PubMed2001

[The activation of A1 adenosine receptors attenuates myocardial stunning in the rabbit].

Hearts exposed to a prolonged period of ischemia (> or = 30 minutes) present smaller infarct size when reperfused in the presence of adenosine. However, when the period of ischemia is shorter, the infarct areas are not very significant, but a postischemic ventricular dysfunction persists. The objective of this study was to determine the effect of adenosine, (administered only during reperfusion) on systolic and diastolic alterations present in postischemic ventricular dysfunction, as well as to determine whether A1 receptors participate in this effect. Isolated isovolumic rabbit hearts were subjected to 15 minutes of global ischemia followed by 30 minutes of reperfusion. Before ischemia and during reperfusion ventricular function was evaluated. In the control group, the left ventricular developed pressure (LVDP) reached 56 +/- 2% of recovery at 30 minutes of reperfusion. The administration of adenosine improved LVDP 75 +/- 3% (P < 0.05 vs. control). However, when adenosine was given in presence of an A1 receptor selective antagonist (DPCPX), LVDP reached 50 +/- 2% (P < 0.05 vs. control). In the control group, left ventricular end diastolic pressure (LVEDP) (diastolic stiffness), increased 293 +/- 4%, at 30 minutes of reperfusion. Only a 15 +/- 8% (P < 0.05 vs. control) increase in LVEDP was observed with adenosine. Reperfusion with adenosine plus DPCPX did not attenuate an increase of 493 +/- 9% (P < 0.05 vs. control) in diastolic stiffness. Adenosine administered from the beginning of reperfusion attenuated both systolic alterations and diastolic stiffness in postischemic dysfunction. This effect was abolished by DPCPX, suggesting an important role for the A1 receptors in adenosine protection.

Adenosine↗

PubMed2000

Morbidity and mortality following early administration of amiodarone in acute myocardial infarction. GEMICA study investigators, GEMA Group, Buenos Aires, Argentina. Grupo de Estudios Multicéntricos en Argentina.

AIMS: The objective of this study was to ascertain the effect of intravenous and oral amiodarone on morbidity and mortality in patients during the first hours after the onset of an acute myocardial infarction. METHODS AND RESULTS: A cohort of 1073 patients admitted to the CCU within 24 h of the onset of symptoms of an acute myocardial infarction and heart failure (Killip and Kimball A-B) were randomized to receive amiodarone (n=542) or placebo (n=531) for 6 months. Because of the higher mortality, on an interim analysis, from a 'high dose' of amiodarone or placebo (516 patients) the protocol was changed to a 'low dose' or placebo (557 patients). Mortality with high doses of amiodarone was 16.30% vs 10.16% in the placebo group (P=0.04), whereas mortality with low doses was 6.61% vs 9.47% in the control group (P=0.20). Several non-fatal adverse effects were observed in 108 and 73 patients treated with amiodarone and placebo, respectively. CONCLUSION: This study demonstrated that early administration of amiodarone in low doses to patients with an acute myocardial infarction may be used only if life-threatening arrhythmia justify its prescription. Conversely, when given in high doses, it might increase mortality.

Amiodarone↗

PubMed1999

[Exogenous adenosine and postischemic dysfunction in the isolated rabbit heart].

It is recognized that adenosine lessens the systolic alterations of the postischemic ventricular dysfunction ("stunned myocardium"), but little is known about the drug's effects on the diastolic phase of the cardiac cycle. The aim of this work was to determine the effect of adenosine when it was administered: a) before ischemia and during reperfusion, and b) from the early reperfusion period to the end of the experiment on the systolic and diastolic function of the "stunned myocardium". An additional objective was to determine whether adenosine modifies the release of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), in the "stunned myocardium". Rabbit isolated isovolumic hearts were perfused according to Langendorff's technique, and subjected to 15 minutes global ischemia and 30 minutes reperfusion. A small latex balloon was inserted into the left ventricle via the left atrium which allowed to measure the ventricular end-diastolic pressure (diastolic stiffness) and calculate the developed pressure, the maximal rate of pressure generation and maximal rate of pressure decay (+dP/dtmax and -dP/dtmax), the ratio between these two variables (+P/-P), and the time constant of isovolumic relaxation (tau, Tau). The adenosine administered both before the ischemia period, and at the beginning of reperfusion, attenuated the systolic and diastolic stiffness alterations without modifying the isovolumic relaxation. The administration of adenosine did not diminish the CPK and LDH release significantly when it was given before the ischemia period or the beginning of reperfusion.

Adenosine↗

PubMed1998

[Effect of enalaprilat on postischemic systolic and diastolic dysfunction (stunned myocardium) on the isolated rabbit heart].

The aim was to determine: 1) whether Enalaprilat (0.08 mg/kg/min) administration: a) before ischemia or b) at the beginning of reperfusion improved the postischemic systolic and diastolic dysfunction ("stunned myocardium") and attenuated the "hyperfunction" phase at the beginning of reperfusion; and 2) whether creatine kinase (CPK), and lactate dehydrogenase (LDH) activities, and lactate release are involved in the protective effects of Enalaprilat. An isolated isovolumic rabbit heart preparation was used as experimental model and subjected to 15 minutes of ischemia followed by 30 minutes of reperfusion, without (group 1), and with Enalaprilat before the ischemia (group 2) and at the beginning of reperfusion (group 3). Left ventricular developed pressure, and end diastolic pressure (diastolic stiffness) were measured and the time constant of isovolumic relaxation (t, Tau) and the ratio between +dP/dtmax and -dP/dtmax were calculated. For the determinations of lactate release and CPK and LDH activities in the perfusate, samples were taken from the coronary effluent for spectrophotometrical measurements. In comparison to the stunned group (group 1) both Enalaprilat preischemia (group 2) and postischemia (group 3) exerted a significant protective effect on the postischemic recovery of contractile state and diastolic stiffness, and attenuated the "hypercontractile" phase in both groups. However Enalaprilat failed to improve myocardial relaxation. Lactate release was also attenuated, but the enzyme activities were not modified.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1998

Comparison of the effects of ACE inhibition with those of angiotensin II receptor antagonism on systolic and diastolic myocardial stunning in isolated rabbit heart.

The aim was to determine whether enalaprilat (0.08 mg/kg/min) or losartan (0.01 mg/kg/min) administration before ischemia can improve postischemic systolic and diastolic dysfunction ('stunned myocardium') and attenuate the 'hyperfunction' phase at the beginning of reperfusion. An isolated isovolumic rabbit heart preparation was subjected to 15 min of ischemia followed by 30 min of reperfusion without (group 1) or with pretreatment with enalaprilat (group 2) or losartan (group 3). Left ventricular developed pressure and end-diastolic pressure (diastolic stiffness) were measured and the time constant of isovolumic relaxation (T, Tau) and the ratio between +dP/dt and -dP/dt were calculated. In comparison to the stunned group (group 1) both enalaprilat (group 2) and losartan (group 3) exerted a significant protective effect on postischemic recovery of contractile state and diastolic stiffness. Only enalaprilat attenuated the 'hypercontractile' phase. However, both enalaprilat and losartan failed to improve myocardial relaxation. In summary, these data strongly suggest a direct deleterious action of the local renin-angiotensin system on ischemic myocardium and diminution of myocardial stunning with its successful blockade. Although, we can not exclude the possibility that bradykinin has some cardioprotective effect, these data suggest that angiotensin exacerbates myocardial injury.

Angiotensin II↗