Biomedical subjects

Martín Donato

Publications and source records attributed to Martín Donato.

6 recordsLinked to original sources

PubMed2006

Effects of low-calcium reperfusion and adenosine on diastolic behavior during the transitory systolic overshoot of the stunned myocardium in the rabbit.

The aims of the present study were to determine whether the transitory systolic overshoot (TSO) that occurs in the early reperfusion (R) of the stunned myocardium is accompanied by diastolic alterations, and to determine whether the R with low Ca2+ Krebs-Henseleit's solution or with adenosine modifies these alterations. Isolated-isovolumic rabbit hearts were divided in 3 groups (G). G1 (n = 11) was perfused with Krebs-Henseleit's solution, subjected to 15 min of global ischemia and 30 min R; G2 (n = 10) was reperfused during the first 10 min with Krebs-Henseleit's solution [Ca2+] = 1 mmol/L, which was increased in the perfusate to 1.5 mmol/L up to 20 min R and at 2.5 mmol/L from 20 to 30 min R. G3 (n = 12) was perfused with Krebs-Henseleit's solution with adenosine (0.03 microg x kg(-1) x min(-1)) from 10 min before ischemia and during all R. Left ventricular (LV) +dP/dtmax (mmHg/s), LV end diastolic pressure (LVEDP, mmHg), and 1 relaxation index (t(1/2)) were measured in preischemic state, at 30, 50, 60, 70, 90, and 120 s R, and then at 5 and 30 min R. The +dP/dtmax recovered to 621 +/- 77 mmHg/s (p > 0.05), 346 +/- 31 mmHg/s (p < 0.05 vs. G1), and 533 +/- 76 mmHg/s (p > 0.05) from preischemic value of 730 +/- 39, 690 +/- 32, and 758 +/- 57 in G1, G2, and G3, respectively. The LVEDP in G1 and G3 increased early in the R, and it was negatively correlated with the +dP/dtmax (r = -0.63, p = 0.0369; and r = -0.71, p = 0.0090, respectively). The R with low Ca2+ abolished this correlation and attenuated the TSO phase. The correlation between LVEDP and +dP/dtmax in G1 and G3 and the lack of correlation in G2 suggests there are common mechanisms for the systolic and diastolic alterations during the TSO phase that are possibly related to Ca2+ overload but not with the vascular tone.

Adenosine↗

PubMed2006

[Evaluation of diastolic function during and post-exercise in patients with arterial hypertension].

UNLABELLED: It is known that patients with arterial hypertension and ventricular hypertrophy have diastolic alterations, in particular during exercise. However, it is controversial if diastolic dysfunction continues once exercise had concluded. The objective was to assess the effects of isometric exercise on the diastolic function in patients with arterial hypertension. Five control patients (group 1, G1) and 7 patients with arterial hypertension (group 2, G2) were studied. All patients underwent cardiac catheterization and performed isometric exercise until heart rate increased 43 +/- 7%. Left ventricular systolic pressure (LVSP) and end diastolic pressure (LVEDP) were measured. We calculated, +dP/dt(max), the time constant of isovolumic pressure decay (tau) and t1/2 were all measured. RESULTS: The LVSP increased in G1 and G2 during exercise from 140 +/- 3 to 195 +/- 14 mm Hg (p < 0.05) and 161 +/- 9 to 238 +/- 15 mm Hg, respectively; returning to their basal values once exercise had concluded. The tau (tau) and t1/2 increased, while exercising in G2, from 23 +/- 2 and 15 +/- 2 msec to 35 +/- 7 and 23 +/- 4 msec, respectively. After exercise both variables continued elevated reaching 41 +/- 6 msec (p < 0.05) and 23 +/- 3 msec (p < 0.05), respectively. In conclusion, isometric exercise decreases relaxation rate and increases LVEDP in patients with arterial hypertension and ventricular hypertrophy. After exercise, isovolumic relaxation remained altered suggesting the presence of stunned myocardium.

Aged↗

PubMed2005

Effects of isometric exercise on the diastolic function in patients with severe aortic stenosis with or without coronary lesion.

BACKGROUND: There is no literature evaluating the effect of exercise on patients with aortic stenosis, in which patients with and without coronary artery disease were assessed separately. OBJECTIVE: To assess the effects of isometric exercise on the diastolic function in patients with aortic stenosis (AS). METHODS: 18 patients with AS, and 5 control patients were studied (group 1, G1). Patients with AS were divided in: group 2 (G2, n=10), without coronary lesion, and group 3 (G3, n=8), with coronary lesion. All patients underwent cardiac catheterization and performed isometric exercise until heart rate increased 32+/-9%. Left ventricular systolic pressure and end diastolic pressure (LVEDP), t1/2 (relaxation index), and the +dP/dt(max) were all measured. RESULTS: The +dP/dt(max) increased in G1, G2, and G3 during exercise returning to their basal values once exercise had concluded. While exercising, the LVEDP increased in G1, G2 and G3, returning to its original baseline value only in G1 and G2. The t1/2 increased, while exercising, in G2 and G3, and continued to be elevated after the exercise in both groups although it was only statistically significant in G3. The control group did not show significant changes. CONCLUSIONS: Isometric exercise decreases relaxation rate and increases LVEDP in patients with AS. After exercise, relaxation and LVEDP remained altered only in the patients with coronary lesion. The alteration in lusitropism and increased LVEDP after exercising suggest the presence of stunned myocardium.

Aged↗

PubMed2005

Hypercholesterolemia attenuates postischemic ventricular dysfunction in the isolated rabbit heart.

The effects of the chronic administration of cholesterol on the stunned myocardium have not been studied. The objective was to determine the effect of a cholesterol enriched diet on postischemic ventricular dysfunction. In group 1 (G1, n = 7) isolated rabbit hearts underwent a follow up of ventricular function during 30 min in aerobic conditions. In group 2 (G2, n = 6) G1 was repeated but the animals were subjected to a 1% cholesterol enriched diet during 4 weeks (hypercholesterolemic animals). In group 3 (G3, n = 8) hearts underwent 15 min of global ischemia followed by 30 min of reperfusion. In Group 4 (G4, n = 11) G3 was repeated, but in hypercholesterolemic animals. Since cholesterol decreased the inotropism in basal situation, and this makes the comparison between groups difficult, we performed a Group 5 (G5, n = 7), in which G4 protocol was repeated but isoproterenol (8 microg/kg/min) was administered 10 min before ischemia, in order to match the preischemic inotropic state with respect to the normocholesterolemic ones. G1 and G2 maintained a stable inotropism during the 30 min of perfusion. The preischemic left ventricular developed pressure (LVDP) in G3 and G4 was 91.4 +/- 4.3 and 70.8 +/- 3.4 mmHg (p < 0.05), respectively, and after 30 min of reperfusion differences were not observed between G3 and G4. Nevertheless, when LVDP is expressed as a percentage, we detected an attenuation of postischemic systolic alterations in hypercholesterolemic animals (67.3 +/- 3.6 in G4 vs. 90.8 +/- 3.1% in G3, p < 0.05). When LVDP in G5 was increased until matching the one of G3, there were no differences after 30 min of reperfusion. Left ventricular end diastolic pressure increased 285 +/- 46%, 61 +/- 25% (p < 0.05 vs. G3 and G5) and 216 +/- 25% in G3, G4 and G5 at 30 min of reperfusion. There were no differences either in the values of tau or infarct size between groups. Thus, in hypercholesterolemic animals, a decrease of the preischemic inotropism exists and there is an attenuation of the stunned myocardium. When contractility of the normo and hypercholesterolemic animals is matched, the beneficial effect disappears.

Animals↗

PubMed2003

Adenosine and cardioprotection during reperfusion--an overview.

Ischemic heart disease includes a number of entities that have been grouped in accordance with physiopathology and evolutive criteria. In recent years 'new' ischemic syndromes have been described. Within the 'new' ischemic syndromes, ventricular post-ischemic dysfunction--also known as 'stunned myocardium'--is worth mentioning. In this route, several studies have suggested that reperfusion per se could cause cellular injury (reperfusion injury). In previous years, a protective effect on the injury caused by ischemia and reperfusion in the heart has been attributed to adenosine. These effects have been documented in different experimental in vivo and in vitro models. Thus, the administration of exogenous adenosine, or agonists of adenosine receptors prior to ischemia reduces the size of the infarction, improves the recovery of the ventricular function during reperfusion (attenuating stunning) and prolongs the time period to the ischemic contracture. However, focusing on a potential therapeutic application, it is of the utmost importance to find this protection and learn the mechanisms involved when procedures are applied during early reperfusion. We showed that adenosine, administered from the beginning of reperfusion, attenuated systolic and diastolic (myocardial stiffness) alterations of the stunned myocardium. This protective effect was mediated by the activation of A1 adenosine receptors, and without modification on infarct size. According to some authors, adenosine can decrease the release of endothelin, during early reperfusion, and reduce an overload of Ca2+ that could cause a cellular lesion. Finally, ischemic preconditioning involves a series of intracellular events that are initiated with the activation of the A1 receptor, and end at the sensitive K+ ATP channels of the mitochondria. The phosphorylation and opening of these channels would cause the protective effect. Activation of this specific mechanism during reperfusion has not been studied extensively.

Adenosine↗

PubMed2003

[Diastolic behavior during postischemic hypercontraction phase in rabbit stunned myocardium].

UNLABELLED: The objective was to determine whether "hypercontraction" (HC) that occurs at the beginning of reperfusion (R) in stunned myocardium is accompanied by diastolic alterations and determine if the R with low Ca2+. Ringer's solution modifies these alterations. Isolated isovolumic rabbit hearts were divided into 2 groups. Group 1 (G1, n = 11) was perfused with Ringer's solution ([Ca2+] = 2 mM) and subjected to 15 min of global ischemia and 30 min of R. Group 2 (G2, n = 10) was R during the first 10 min with ([Ca2+] = 1 mM), which was increased to 1.5 mM and 2 mM in the perfusate at 30 min of R. The left ventricular +dP/dtmax, left ventricular end diastolic pressure (LVEDP) (stiffness index), and relaxation rate (t 1/2 and +P/-P ratio) were measured, from the beginning of R every 10 sec for 2 min, and then at 5 and 30min. At 60 sec of R the +dP/dtmax in G1 was increased (76.88 +/- 5.37% vs preischemic value) and was attenuated in G2 (48.22 +/- 3.40%; P < 0.05 vs G1). The LVEDP in G1 was increased early in the R, although it was negatively correlated with HC degree (r = .0.7477; p = 0.008). This increase was attenuated in G2 (P < 0.05 vs G1) at 60 sec R. There was a dealy in the relaxation at 60 secR in both group (G1 vs G2, NS). IN CONCLUSION: HC is accompanied by diastolic alterations. The improvement of HC is inversely related with LVEDP. During R the stiffness during the relaxation rate was normal. The R with low Ca2+ attenuated the HC and the diastolic stiffness.

Animals↗