ABSTRACT
OBJECTIVE: To evaluate the hemodynamic and metabolic effects of terlipressin and naloxone in cardiac arrest. METHODS: Cardiac arrest in rats was induced by asphyxia and maintained for 3.5 minutes. Animals were then resuscitated and randomized into one of six groups: placebo (n = 7), epinephrine (0.02 mg/kg; n = 7), naloxone (1 mg/kg; n = 7) or terlipressin, of which three different doses were tested: 50 µg/kg (TP50; n = 7), 100 µg/kg (TP100; n = 7) and 150 µg/kg (TP150; n = 7). Hemodynamic variables were measured at baseline and at 10 (T10), 20 (T20), 30 (T30), 45 (T45) and 60 (T60) minutes after cardiac arrest. Arterial blood samples were collected at T10, T30 and T60. RESULTS: The mean arterial pressure values in the TP50 group were higher than those in the epinephrine group at T10 (165 vs. 112 mmHg), T20 (160 vs. 82 mmHg), T30 (143 vs. 66 mmHg), T45 (119 vs. 67 mmHg) and T60 (96 vs. 66.8 mmHg). The blood lactate level was lower in the naloxone group than in the epinephrine group at T10 (5.15 vs. 10.5 mmol/L), T30 (2.57 vs. 5.24 mmol/L) and T60 (2.1 vs. 4.1 mmol/L). CONCLUSIONS: In this rat model of asphyxia-induced cardiac arrest, terlipressin and naloxone were effective vasopressors in cardiopulmonary resuscitation and presented better metabolic profiles than epinephrine. Terlipressin provided better hemodynamic stability than epinephrine. .
Subject(s)
Animals , Male , Rats , Epinephrine/pharmacology , Heart Arrest/drug therapy , Lypressin/analogs & derivatives , Models, Animal , Naloxone/pharmacology , Vasoconstrictor Agents/pharmacology , Arterial Pressure/drug effects , Asphyxia/complications , Cardiopulmonary Resuscitation , Epinephrine/metabolism , Heart Arrest/etiology , Heart Arrest/physiopathology , Hemodynamics/drug effects , Lypressin/metabolism , Lypressin/pharmacology , Naloxone/metabolism , Random Allocation , Rats, Wistar , Reference Values , Reproducibility of Results , Time Factors , Vasoconstrictor Agents/metabolismABSTRACT
Se demuesta que, en ratas anestesiadas y perfundidas con solución isotónica de glucosa, la administracíon i.v. previa de lisil-vasopresina, en dosis de 0.1 a 10 m, no inhibe la respuesta diurética y salurética del FNA (2.5 ug); en cambio, la dosis de 50 mU, que produce una elevación transitoria, pero acentuada de la presión arterial, intensifica el efecto del FNA. La pepsanurina obtenida de la hidrólisis de globulinas de 20 ml de plasma humano, administrada i.p., 40 a 60 m antes de la administración i.v. de FNA, produce una significativa inhibición de la respuesta diurética natriurética
Subject(s)
Rats , Animals , Female , Atrial Natriuretic Factor/pharmacology , Diuresis/drug effects , Lypressin/pharmacology , Natriuresis/drug effects , Peptides/pharmacology , Atrial Natriuretic Factor/antagonists & inhibitors , Injections, Intravenous , Lypressin/administration & dosage , Rats, Inbred StrainsABSTRACT
The effect of antidiuretic hormone (ADH) on the release of immunoreactive alpha-melanocyte stimulating hormone (alpha-MSH) from the superfused neurointermediate lobe of the pituitary of the normal Wistar and Brattleboro (diabetes insipidus) rat was studied in vitro. In control experiments, there was usually an initial peak, after which alpha-MSH release fell exponentially over the course of the perfusion. Following the addition of ADH, the levels of alpha-MSH in the superfusate showed a significant rise. It is suggested that ADH is normally involved in the secretion of alpha-MSH by the pars intermedia of the rat, especially in response to osmotic stimuli.