IQUIMEFA   05518
INSTITUTO QUIMICA Y METABOLISMO DEL FARMACO
Unidad Ejecutora - UE
artículos
Título:
Diastolic function during hemorrhagic shock in rabbits
Autor/es:
V. DANNUNZIO ; M. DONATO; A. FELLET; B. BUCHHOLZ; T. ZAOBORNYJ; M. C. CARRERAS,; C.MORALES, ; A. BOVERIS, ; J. J. PODEROSO,; A. M. BALASZCZUK,; R.J. GELPI
Revista:
MOLECULAR AND CELLULAR BIOCHEMISTRY
Editorial:
SPRINGER
Referencias:
Lugar: La Haya; Año: 2012 vol. 359 p. 169 - 176
ISSN:
0300-8177
Resumen:
Hemorrhage (H) is associated with a left ventricular (LV) dysfunction. However, the diastolic function has not been studied in detail. The main goal was to assess the diastolic function both during bleeding and 120 minutes after bleeding, in the absence and in the presence of L-NAME. Also the changes in mRNA and protein expression of nitric oxide synthase (NOS) isoforms were determined. New Zealand rabbits were divided into three groups: Sham group, H group (Hemorrhage 20% blood volume), and H L-NAME group (Hemorrhage treated with L-NAME). We evaluated systolic and diastolic ventricular function in vivo and in vitro (Langendorff technique). Hemodynamics parameters, LV function were measured before, during, and at 120 min after bleeding. We analyzed the isovolumic relaxation using t ½ in vivo (closed chest). After that hearts were excised and perfused in vitro to measure myocardial stiffness. Samples were frozen to measure NOS mRNA and protein expression. The t½, increased during bleeding, and returned to basal values 120 min after bleeding. L-NAME blunted this effect. Data from the H group revealed a shift to the left in the LV end diastolic pressure-volume curve at 120 min after bleeding, which was blocked by L-NAME. iNOS and nNOS protein expression and mRNA levels increased at 120 min after the hemorrhage. Acute hemorrhage induces early and transient isovolumic relaxation impairment and an increase in myocardial stiffness 120 min after bleeding. L-NAME blunted the LV dysfunction, thus suggesting that NO modulates ventricular function through iNOS and nNOS isoforms.