Medical Students' Attitude Toward Organ Donation: Understanding Reasons for Refusal in Order to Increase Transplantation Rates.

OBJECTIVES: To assess, among medical students, the willingness to donate their own organs or those of a family member, and to establish reasons for refusal. MATERIALS AND METHODS: During the 2016 academic year, an anonymous survey was conducted among University of Buenos Aires School of Medicine second-year students. RESULTS: Of the total 1012 respondents, 81.92% would agree to donate and 18.08% would not. Thirty two percent would not authorize donation of a family member's organ. Almost all (94.1%) students reported they had little information about organ donation. Reasons for refusal included: fears about the possibility of not being really dead when considered for organ ablation (36.4%); lack of confidence in (25.8%) or lack of information about the organ procurement and transplantation system (14.6%); no interest in organ donation (9.3%); and religious reasons (6%). Brain death was considered irreversible by 59.7% of donors and by only 51% of non-donors (P = .036). Contact with a transplanted person was more frequent in the donor group (30.9% vs 21.3%, P = .01). More donors were found among the group who discussed the subject with their families than among the group who did not (69.1% vs 62.9%, P = .053). CONCLUSIONS: A considerable percentage of medical school students would not be willing to donate their own or a family member's organs. Main reasons are mistrust of the system, lack of information about donation programs, and poor understanding of the brain death concept. Contact with an organ recipient and discussing the subject in the family both favored donation.

Cardiometabolic Changes in Different Gonadal Female States Caused by Mild Hyperuricemia and Exposure to a High-Fructose Diet.

BACKGROUND: The objective of this study is to observe if mild hyperuricemia and a high-fructose diet influence the cardiovascular and metabolic systems in hypogonadic female Wistar rats compared to normogonadic female rats. METHODS: Fifty-six (56) adult female Wistar rats were used in the present work. Animals were divided into two groups: normogonadic (NGN) and hypogonadic (HGN). These groups were also divided into four subgroups in accordance with the treatment: control with only water (C), fructose (F), oxonic acid (OA), and fructose + oxonic acid (FOA). Lipid profile, glycemia, uric acid, and creatinine determinations were assessed. Cardiovascular changes were evaluated by measuring blood pressure, myocyte volume, fibrosis, and intima-media aortic thickness. RESULTS: HGN rats had higher levels of total cholesterol (TC) (p < 0.01) and noHDLc (p < 0.01), in addition to higher levels of uric acid (p < 0.05). The OA group significantly increased myocyte volume (p < 0.0001) and the percentage of fibrosis as well as the group receiving FOA (p < 0.001) in both gonadal conditions, being greater in the HGN group. Hypogonadic animals presented a worse lipid profile. CONCLUSION: Mild hyperuricemia produces hypertension together with changes in the cardiac hypertrophy, fibrosis, and increased thickness of the intima media in hypogonadic rats fed high-fructose diet.

Effect of melatonin treatment on oxygen consumption by rat liver mitochondria.

The objective of this study was to examine the in vivo effect of melatonin on rat mitochondrial liver respiration. Two experiments were performed: For experiment 1, adult male rats received melatonin in the drinking water (16 or 50 microg/ml) or vehicle during 45 days. For experiment 2, rats received melatonin in the drinking water (50 microg/ml) for 45 days, or the same amount for 30 days followed by a 15 day-withdrawal period. At sacrifice, a liver mitochondrial fraction was prepared and oxygen consumption was measured polarographically in the presence of excess concentration of DL-3-beta-hydroxybutyrate or L-succinate. Melatonin treatment decreased Krebs' cycle substrate-induced respiration significantly at both examined doses. The stimulation of mitochondrial respiration caused by excess concentration of substrate recovered after melatonin withdrawal. Basal state 4 respiration was not modified by melatonin. Melatonin, by curtailing overstimulation of cellular respiration caused by excess Krebs' cycle substrates, can protect the mitochondria from oxidative damage.

Comparative effects of melatonin and vitamin E in restoring aortic relaxation in pancreatectomized rats.

In a previous study we reported the efficacy of melatonin to restore the decreased relaxation response to acetylcholine (ACh) or to sodium nitroprusside (SNP) in aortic rings of rats turned hyperglycemic by subtotal pancreatectomy. The effect was amplified by pre-incubation in a high (44 mmol/l) glucose solution, a situation that resulted in oxidative stress. We hereby compare the effect of another antioxidant, vitamin E, with that of melatonin on ACh response in intact aortic rings or on SNP response in endothelium-denuded aortic rings obtained from pancreatectomized or sham-operated rats. Dose-response curves to ACh or SNP were performed in the presence or absence of melatonin or vitamin E (10-5 mol/1) in 10 or 44 mmol/1 glucose medium. Melatonin was more effective than vitamin E in restoring ACh- or SNP-induced relaxation of aortic rings in a high glucose medium. The differences between the two antioxidants may rely on the ability of melatonin to diffuse readily into intracellular compartments.

Changes of prolactin regulatory mechanisms in aging: 24-h rhythms of serum prolactin and median eminence and adenohypophysial concentration of dopamine, serotonin, (gamma-aminobutyric acid, taurine and somatostatin in young and aged rats.

Twenty-four hour rhythmicity of serum prolactin and median eminence and anterior pituitary content of dopamine (DA), serotonin (5HT), gamma-aminobutyric acid (GABA), taurine and somatostatin were examined in 2 months-old and 18-20 months-old Wistar male rats. The concentration of prolactin was higher in aged rats, with peaks in both groups of rats at the early phase of the activity span. Median eminence DA content of young rats attained its maximum at the middle of rest span and decreased as prolactin levels augmented while the lowest values of adenohypophysial DA were observed at the time of prolactin peak. DA rhythmicity disappeared in aged rats. GABA content of median eminence and adenohypophysis was lower in aged rats, with maximal values of median eminence GABA at light-dark transition in young rats and at the second half of activity span in aged rats. Serum prolactin correlated positively with median eminence GABA in young rats and negatively with pituitary GABA in young and aged rats. Median eminence somatostatin peaked at the beginning of the activity phase (young rats) or at the end of the rest phase (aged rats). Prolactin levels and somatostatin content correlated significantly in young rats only. Median eminence and pituitary 5HT and taurine content did not change with age. The results indicate disruption of prolactin regulatory mechanisms with aging in rats.

Age-dependent changes in 24-hour rhythms of catecholamine content and turnover in hypothalamus, corpus striatum and pituitary gland of rats injected with Freund's adjuvant.

BACKGROUND: Little information is available on the circadian sequela of an immune challenge in the brain of aged rats. To assess them, we studied 24-hour rhythms in hypothalamic and striatal norepinephrine (NE) content, hypothalamic and striatal dopamine (DA) turnover and hypophysial NE and DA content, in young (2 months) and aged (18-20 months) rats killed at 6 different time intervals, on day 18th after Freund's adjuvant or adjuvant's vehicle administration. RESULTS: Aging decreased anterior and medial hypothalamic NE content, medial and posterior hypothalamic DA turnover, and striatal NE concentration and DA turnover. Aging also decreased NE and DA content in pituitary neurointermediate lobe and augmented DA content in the anterior pituitary lobe. Immunization by Freund's adjuvant injection caused: (i) reduction of DA turnover in anterior hypothalamus and corpus striatum; (ii) acrophase delay of medial hypothalamic DA turnover in old rats, and of striatal NE content in young rats; (iii) abolition of 24-h rhythm in NE and DA content of neurointermediate pituitary lobe, and in DA content of anterior lobe, of old rats. CONCLUSIONS: The decline in catecholamine neurotransmission with aging could contribute to the decrease of gonadotropin and increase of prolactin release reported in similar groups of rats. Some circadian responses to immunization, e.g. suppression of 24-h rhythms of neurointermediate lobe NE and DA and of anterior lobe DA were seen only in aged rats.

Effect of melatonin on 24h changes in plasma protein levels during the preclinical phase of Freund's adjuvant arthritis in rats.

The 24h rhythms in plasma protein concentration were examined in rats on the third day after injection of Freund's complete adjuvant or adjuvant's vehicle, performed 3h after light on. In rats treated with adjuvant's vehicle, peak values of albumin and gamma globulin occurred during the nocturnal activity span (P < .02 and P < .0001, respectively), while those of alpha-1, alpha-2, and beta globulins were found late during the rest span (P < .002, P < .0001, and P < .0004, respectively). Freund's adjuvant administration abolished temporal changes in plasma albumin and beta globulin levels. It also decreased the amplitude of daily changes in alpha-1 and alpha-2 globulin (P < .05) and diminished mean values of alpha-2 globulin (P < .01). Pretreatment of rats with melatonin (30 microg daily) for 11 days, 11h after light on, counteracted mycobacterial adjuvant-induced suppression of the 24h rhythms in albumin and alpha-1, alpha-2, and beta globulins. The results further support the existence of preventive properties of a pharmacological dose of melatonin in situations in which a lost of circadian rhythmicity is expected.

Extracellular acidification related to the stimulation of catecholamines release by strontium in the bovine adrenal medulla.

The possible modifications of extracellular pH associated with the secretion of catecholamines evoked by the introduction of 2.2 mM Sr2+ to a Ca(2+)-free, buffer-free, Locke solution were investigated in decorticated perfused bovine adrenal glands. A progressive and reversible decrease of external pH accompanied the catecholamine release promoted by Sr(2+)-introduction into the perfusion fluid. This extracellular acid shift was practically undetected when the chromaffin tissue was stimulated by the addition of Sr2+ to a buffered medium. Both the secretory response as well as the extracellular pH drop mediated by Sr(2+)-introduction to a Ca(2+)-free, buffer-free, Locke solution were markedly inhibited by methoxyverapamil (0.3 mM), Mg2+ (20 mM) and hyperosmolarity (750 mOsm). The exposure of the adrenal medulla to a Ca(2+)-free, buffer-free, high-K+ solution containing 2.2 mM Sr2+ for 6 min promoted a significant enhancement of both the secretory response and the acidification of the perfusates compared with the responses evoked by Sr2+ in a 5.6 mM K+ medium. These results are consistent with the existence of a close relationship between extracellular acidification and the release of catecholamines triggered by the introduction of Sr2+ to the perfusion fluid.

Blood sugar concentrations during ketamine or pentobarbitone anesthesia in rats with or without alpha and beta adrenergic blockade.

Plasma glucose concentrations were measured in: 1) conscious and anesthetized rats during an iv glucose tolerance test (IVGTT) and 2) conscious and anaesthetized phentolamine/propranolol blocked rats during an IVGTT. Anesthesia was induced with ketamine (120 mg.kg-1) or pentobarbitone (60 mg.kg-1) ip at -30 min of the beginning of the IVGTT, which was followed by 2 injections of the anesthetic agents at intervals of 30 min. Propranolol (2 mg.kg-1) was given ip at -25 and -5 min. An iv infusion of phentolamine (0.015 mg.min-1) was started at -20 min and continued up to the end of the experiment. During the IVGTT, the anesthetized rats showed a moderate hyperglycemic response to glucose load compared to conscious animals (ketamine: p < 0.01 at 5 min; and p < 0.05 at 10-20 min; pentobarbitone: p < 0.05 at 5-20 min). The hyperglycemic response to glucose administration in the conscious rats was not affected by adrenergic blockade (p > 0.05). While in ketamine anesthetized rats the increased glucose response was abolished by adrenergic blockade (p < 0.05 at 5-10 min), this effect was not seen in pentobarbitone anesthetized animals. These results suggest the existence of an inhibitory tone on insulin secretion and a glycogenolytic response in ketamine anesthetized rats, probably mediated by adrenergic inervation of the pancreas and liver and by circulating catecholamines secreted from the adrenal medulla.

Blood sugar concentrations during ketamine or pentobarbitone anesthesia in rats with or without alpha and beta adrenergic blockade.

Plasma glucose concentrations were measured in: 1) conscious and anesthetized rats during an iv glucose tolerance test (IVGTT) and 2) conscious and anaesthetized phentolamine/propranolol blocked rats during an IVGTT. Anesthesia was induced with ketamine (120 mg.kg-1) or pentobarbitone (60 mg.kg-1) ip at -30 min of the beginning of the IVGTT, which was followed by 2 injections of the anesthetic agents at intervals of 30 min. Propranolol (2 mg.kg-1) was given ip at -25 and -5 min. An iv infusion of phentolamine (0.015 mg.min-1) was started at -20 min and continued up to the end of the experiment. During the IVGTT, the anesthetized rats showed a moderate hyperglycemic response to glucose load compared to conscious animals (ketamine: p < 0.01 at 5 min; and p < 0.05 at 10-20 min; pentobarbitone: p < 0.05 at 5-20 min). The hyperglycemic response to glucose administration in the conscious rats was not affected by adrenergic blockade (p > 0.05). While in ketamine anesthetized rats the increased glucose response was abolished by adrenergic blockade (p < 0.05 at 5-10 min), this effect was not seen in pentobarbitone anesthetized animals. These results suggest the existence of an inhibitory tone on insulin secretion and a glycogenolytic response in ketamine anesthetized rats, probably mediated by adrenergic inervation of the pancreas and liver and by circulating catecholamines secreted from the adrenal medulla.

[Cardiovascular effects of ketamine anesthesia in rats treated with enalapril and propranolol]. / Efectos cardiocirculatorios de la anestesia con ketamina en ratas tratadas con enalapril y propranolol.

It is well-known that ketamine (Kt) anaesthesia produces a rise in blood pressure and heart rate in man. These cardiostimulatory effects were adscribed to several factors such as: a) increased sympathetic nervous system activity by direct stimulation of central nervous structures, b) increased catecholamine release from the peripheral sympathetic system, c) high plasmatic renin levels. However, the quantitative participation of these mechanisms in the cardiovascular effects of this anaesthetic agent is unknown. While some authors have shown a major rise in serum renin activity in experimental anaesthesia, others have been unable to confirm these results. The present study was undertaken to assess if the cardiostimulatory effects of Kt anaesthesia were due to an activation of renin-angiotensin system or to increased sympathetic activity. In consequence we used rats treated with enalapril (an angiotensin-converting enzyme inhibitor) or propranolol prior to anaesthetic procedures. Thirty male Wistar and six spontaneously hypertensive rats (SHR) weighing 240-300 g were used in all the experiments. The rats were randomly grouped into six groups. I- Non-anaesthetized rats, II- Anaesthetized rats (trained in the experimental procedures), III- Anaesthetized rats (without training), IV- Anaesthetized rats previously treated with enalapril, V- Anaesthetized rats pretreated with propranolol, VI- SHR treated with enalapril. The rats of groups IV and VI received enalapril p.o. for three weeks (25 mg/Kg body wt). The animals of group V were submitted to acute beta-adrenergic blockade. Propranolol dose: 10 mg/Kg body wt, was given i.p. 15 min before Kt anaesthesia. Blood pressure and heart rate were measured with a sphygmomanometer and photoelectric sensors and recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Efectos cardiocirculatorios de la anestesia con ketamina en ratas tratadas con enalapril y propranolol. / [Cardiovascular effects of ketamine anesthesia in rats treated with enalapril and propranolol]

It is well-known that ketamine (Kt) anaesthesia produces a rise in blood pressure and heart rate in man. These cardiostimulatory effects were adscribed to several factors such as: a) increased sympathetic nervous system activity by direct stimulation of central nervous structures, b) increased catecholamine release from the peripheral sympathetic system, c) high plasmatic renin levels. However, the quantitative participation of these mechanisms in the cardiovascular effects of this anaesthetic agent is unknown. While some authors have shown a major rise in serum renin activity in experimental anaesthesia, others have been unable to confirm these results. The present study was undertaken to assess if the cardiostimulatory effects of Kt anaesthesia were due to an activation of renin-angiotensin system or to increased sympathetic activity. In consequence we used rats treated with enalapril (an angiotensin-converting enzyme inhibitor) or propranolol prior to anaesthetic procedures. Thirty male Wistar and six spontaneously hypertensive rats (SHR) weighing 240-300 g were used in all the experiments. The rats were randomly grouped into six groups. I- Non-anaesthetized rats, II- Anaesthetized rats (trained in the experimental procedures), III- Anaesthetized rats (without training), IV- Anaesthetized rats previously treated with enalapril, V- Anaesthetized rats pretreated with propranolol, VI- SHR treated with enalapril. The rats of groups IV and VI received enalapril p.o. for three weeks (25 mg/Kg body wt). The animals of group V were submitted to acute beta-adrenergic blockade. Propranolol dose: 10 mg/Kg body wt, was given i.p. 15 min before Kt anaesthesia. Blood pressure and heart rate were measured with a sphygmomanometer and photoelectric sensors and recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Efectos cardiocirculatorios de la anestesia con ketamina en ratas tratadas con enalapril y propranolol. / [Cardiovascular effects of ketamine anesthesia in rats treated with enalapril and propranolol]

It is well-known that ketamine (Kt) anaesthesia produces a rise in blood pressure and heart rate in man. These cardiostimulatory effects were adscribed to several factors such as: a) increased sympathetic nervous system activity by direct stimulation of central nervous structures, b) increased catecholamine release from the peripheral sympathetic system, c) high plasmatic renin levels. However, the quantitative participation of these mechanisms in the cardiovascular effects of this anaesthetic agent is unknown. While some authors have shown a major rise in serum renin activity in experimental anaesthesia, others have been unable to confirm these results. The present study was undertaken to assess if the cardiostimulatory effects of Kt anaesthesia were due to an activation of renin-angiotensin system or to increased sympathetic activity. In consequence we used rats treated with enalapril (an angiotensin-converting enzyme inhibitor) or propranolol prior to anaesthetic procedures. Thirty male Wistar and six spontaneously hypertensive rats (SHR) weighing 240-300 g were used in all the experiments. The rats were randomly grouped into six groups. I- Non-anaesthetized rats, II- Anaesthetized rats (trained in the experimental procedures), III- Anaesthetized rats (without training), IV- Anaesthetized rats previously treated with enalapril, V- Anaesthetized rats pretreated with propranolol, VI- SHR treated with enalapril. The rats of groups IV and VI received enalapril p.o. for three weeks (25 mg/Kg body wt). The animals of group V were submitted to acute beta-adrenergic blockade. Propranolol dose: 10 mg/Kg body wt, was given i.p. 15 min before Kt anaesthesia. Blood pressure and heart rate were measured with a sphygmomanometer and photoelectric sensors and recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of beta-adrenergic blocking with propranolol on the mechanisms of glucose regulation in the dog]. / Efectos del bloqueo beta-adrenérgico con propranolol sobre los mecanismos de regulación de la glucemia en el perro.

Propranolol (P) administration is known to cause hypoglycemia in insulin-dependent diabetic patients. The mechanisms whereby this response is produced remain controversial. Some authors postulate an inhibition in the beta-adrenergic action of catecholamines, responsible for hepatic glycogenolysis, while others indicate that these hormones are not so important in the regulation of blood sugar (BS) level. The present studies were undertaken to assess the mechanism whereby hypoglycemia is developed in the dog, with or without beta-adrenergic blockade. Unanesthetized male mongrel dogs were used, weighing 10-20 kg body wt., fed on dog chow pellets and water ad libitum up to 18-22 hours before the test performances. The dogs were randomly grouped into two groups, A and B in which the effect of P on several hormonal and metabolic responses basally and during insulin (I) test, were respectively studied. Group A was constituted by two subgroups of 6 animals each; the animals of one subgroup were beta-blocked, receiving P p.o. for 10 days (80 mg every 8 hours); the dogs of the remaining subgroup received only P excipient in the same way as the treated ones, for the same period. As P treatment was completed, blood samples were taken by venipuncture, in a peripheral vein, at 0 and 60 min. Some biological controls of beta-blockade, assessed at 0, 30 and 60 min, indicated that mean pulse rate (+/- SE) in the control dogs was 123 +/- 2, 128 +/- 2 and 128 +/- 3 beats/min while in the P treated ones was 106 +/- 2, 103 +/- 1 and 103 +/- 3 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Efectos del bloqueo ß-adrenergico con propranolol sobre los mecanismos de regulación de la glucemia en el perro / Effects of ßeta-adrenergic blocking with propranolol about mechanisms of glucose regulation in the dog

Conociendo que el bloqueo ß-adrenérgico con propranolol (P) puede provocar cuadros hipoglucémicos en pacientes diabéticos insulino-dependientes, hemos analizado la respuesta de algunas variables hormonales (insulina (I) y cortisol (C) séricos, adrenalina (A) y noradrenalina (NA) plasmáticas) y metabólicas (glucemia y ácidos grasos libres (AGL) séricos) a la administración de esta droga a perros machos por la vía oral (dosis: 80 mg, 3 veces por día, durante 10 días) (grupo A) o endovenosa (dosis: 1 mg/Kg a -30 min) (grupo B), estudiándose en estos últimos, el comportamiento de dichas variables durante la hipoglucemia insulinica (HI). Se controló la frecuencia cardíaca como índice del bloqueo. Se obtuvieron muestras de sangre en condiciones basales en los perros del grupo A, a 0 y 30 min., y en los del grupo B a -30 y o min., continuandose durante la HI cada 30 min. por 2 horas. En los animales con bloqueo crónico, el P no afectó los niveles de glucemia, I sérica y catecolaminas plasmáticas, pero redujo los de AGL y C séricos cuando se los comparó con los respectivos controles. Durante la HI (grupo B), el tratamiento con P no afectó el comportamiento de la glucemia o de la insulinemia, observándose descensos en los niveles de AGL (p < 0,001) y C (p < 0,05) séricos junto con un aumento de la repsuesta adrenalínica a la hipoglucemia, al compararlos con los de los perros no bloqueados. Los resultados expuestos indican que el mecanismo ß-adrenérgico no desempeña un papel importante en la recuperación de la HI (AU)

Efectos del bloqueo ß-adrenergico con propranolol sobre los mecanismos de regulación de la glucemia en el perro / Effects of ßeta-adrenergic blocking with propranolol about mechanisms of glucose regulation in the dog

Conociendo que el bloqueo ß-adrenérgico con propranolol (P) puede provocar cuadros hipoglucémicos en pacientes diabéticos insulino-dependientes, hemos analizado la respuesta de algunas variables hormonales (insulina (I) y cortisol (C) séricos, adrenalina (A) y noradrenalina (NA) plasmáticas) y metabólicas (glucemia y ácidos grasos libres (AGL) séricos) a la administración de esta droga a perros machos por la vía oral (dosis: 80 mg, 3 veces por día, durante 10 días) (grupo A) o endovenosa (dosis: 1 mg/Kg a -30 min) (grupo B), estudiándose en estos últimos, el comportamiento de dichas variables durante la hipoglucemia insulinica (HI). Se controló la frecuencia cardíaca como índice del bloqueo. Se obtuvieron muestras de sangre en condiciones basales en los perros del grupo A, a 0 y 30 min., y en los del grupo B a -30 y o min., continuandose durante la HI cada 30 min. por 2 horas. En los animales con bloqueo crónico, el P no afectó los niveles de glucemia, I sérica y catecolaminas plasmáticas, pero redujo los de AGL y C séricos cuando se los comparó con los respectivos controles. Durante la HI (grupo B), el tratamiento con P no afectó el comportamiento de la glucemia o de la insulinemia, observándose descensos en los niveles de AGL (p < 0,001) y C (p < 0,05) séricos junto con un aumento de la repsuesta adrenalínica a la hipoglucemia, al compararlos con los de los perros no bloqueados. Los resultados expuestos indican que el mecanismo ß-adrenérgico no desempeña un papel importante en la recuperación de la HI

Efectos del bloqueo beta-adrenérgico con propranolol sobre los mecanismos de regulación de la glucemia en el perro. / [Effects of beta-adrenergic blocking with propranolol on the mechanisms of glucose regulation in the dog]

Propranolol (P) administration is known to cause hypoglycemia in insulin-dependent diabetic patients. The mechanisms whereby this response is produced remain controversial. Some authors postulate an inhibition in the beta-adrenergic action of catecholamines, responsible for hepatic glycogenolysis, while others indicate that these hormones are not so important in the regulation of blood sugar (BS) level. The present studies were undertaken to assess the mechanism whereby hypoglycemia is developed in the dog, with or without beta-adrenergic blockade. Unanesthetized male mongrel dogs were used, weighing 10-20 kg body wt., fed on dog chow pellets and water ad libitum up to 18-22 hours before the test performances. The dogs were randomly grouped into two groups, A and B in which the effect of P on several hormonal and metabolic responses basally and during insulin (I) test, were respectively studied. Group A was constituted by two subgroups of 6 animals each; the animals of one subgroup were beta-blocked, receiving P p.o. for 10 days (80 mg every 8 hours); the dogs of the remaining subgroup received only P excipient in the same way as the treated ones, for the same period. As P treatment was completed, blood samples were taken by venipuncture, in a peripheral vein, at 0 and 60 min. Some biological controls of beta-blockade, assessed at 0, 30 and 60 min, indicated that mean pulse rate (+/- SE) in the control dogs was 123 +/- 2, 128 +/- 2 and 128 +/- 3 beats/min while in the P treated ones was 106 +/- 2, 103 +/- 1 and 103 +/- 3 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)