Social impact of behavioral disorders in psychiatric patients.

Background: Violent behavior is often met in patients with mental health disorders. An important area of research studied different factors that can influence aggressive behavior in psychiatric patients. Objectives: The paper's aim was to compare different characteristics between two groups of patients, who presented with psychiatric disorders and aggressive behavior. Demographic characteristics, diagnosis, use of alcohol, history of brain injury, physical and verbal aggression were analyzed in both groups. Methods: The first group was formed of 23 mentally ill patients framed into the Article 114 Criminal Code who presented aggressive behavior and committed various offences. In the second group, 45 patients admitted at psychiatry without their consent were included, after having committed different acts of aggression. Results: The patients from the first group had significantly more psychiatric admissions in their history than the patients from the second group. A higher percentage of alcohol users was registered in the first group, compared to the second one. More patients with personality disorders and concomitant use of alcohol were present in the first group, compared to the second group. In both groups, aggressive behavior was more frequent in patients having psychotic disorders, compared to other diagnosis. Even if overall aggression was more frequent in the second group, when alcohol use (with or without brain injury) was present, aggressive behavior became more frequent in the first group. Conclusions: Results of the study suggest that when certain conditions are met, they can significantly influence the behavior of psychiatric patients, with notable differences in each group.

The renin-angiotensin system and the effect of propranolol upon the cerebral cortical and hypothalamic circulation in hypoxia.

The regulatory mechanisms of the cerebral blood flow have preoccupied the physiology department of Cluj since the end of the 4th decade. These studies continued over the last years. The researches progressed from the studies of regulation by blood pressure changes to the nervous regulation and to the metabolic one. This paper's subject is the renin-angiotensin and adrenalin system influence on the changes of cerebral blood flow during the general hypoxic hypoxia and cephalic ischemia. Experiments were performed in 10 dogs anaesthetised with a mixture of chloralose, urethan and morphine. Hypoxic hypoxia was obtained by breathing a mixture of 11% oxygen in nitrogen, in a closed system and cerebral ischemic hypoxia by partial compression of the carotid arteries, after the ligation of the vertebral and thyroid arteries. The arterial blood pressure and the cerebral and hypothalamic blood flow, measured with the heated thermoelement, were registered. The plasma renin activity was tested radioimmunologically before, at 1.5 min, 5, 10 and 15 min, after the beginning of hypoxia. In ischemic hypoxia the experiment was repeated after venous perfusion with propranolol (0.6 mg/kg/h). The systemic blood pressure increased in both forms of hypoxia. The cortical and hypothalamic blood flow increased with the systemic arterial blood pressure. The hypothalamic blood flow remained stable or diminished a little. Propranolol increased the cerebral blood flow during ischemic hypoxia up to 300%. The i.v. administration of angiotensin (1-5 mg/kg) increased the cortical flow, while the hypothalamic flow remained self-regulated. Plasma renin activity increased more in general hypoxic hypoxia, than in cephalic ischemic hypoxia. After propranolol the increase was higher in this hypoxia. Propranolol produced a major activation of the renin-angiotensin system and of the cortical blood flow in ischemic cephalic hypoxia, the renin-angiotensin system being located in the cerebral structure. As well high doses of angiotensin produced cerebral vasodilatation in small cerebral vessels. This effect was found in our experiments in the cortical blood flow too. Our results indicate a beneficial propranolol effect on cortical circulation in ischemic hypoxia.

Influence of some inhibitors and activators of fibrinolysis on transcapillary transport of macromolecules.

The RISA transcapillary transport in the posterior paw was followed up under the influence of some substances inhibiting and activating fibrinolysis (Trasylol, EACA and Streptokinase and Salyrgan, respectively) in 11 dogs under narcosis with chloralose and the cannulation of the lymphatics in the popliteal space. It was found that EACA inhibits the transcapillary RISA transport and streptokinase activates it. Trasylol and Salyrgan produced no changes, the slope of the vanishing curve of the tracer being identical with that of the controls.

Effects of some m-cholinomimetics and alpha- and beta-adrenomimetics on cyclic-AMP content of the rat submaxillary gland.

The experiments were performed on four groups of rats of both sexes, anesthetized with pentobarbital: one control and three experimental groups. The experimental group was treated with carbachol 50 micrograms/100 g, isoprenaline 10 micrograms/100 g and phenylephrine 10 micrograms/100 g, respectively. The cyclic AMP was assayed by a R.I.A. method, at 4-6 min after administration of the drugs. The salivary secretion was estimated semiquantitatively by qualifying adjectives: very copious, copious and absent. In the control group the concentration of cAMP was 699 +/- 212 p.mol/g of wet tissue; carbachol administration resulted in an important and statistically significant increase (1030 +/- 205 p.mol/g; P less than 0.001) and isoprenaline increased the cAMP concentration more than twice (1414 +/- 368 p.mol/g, P less than 0.001). Phenylephrine decreased the level of cAMP to 481 +/- 79 p.mol/g, the decrease being statistically significant (0.02 less than p less than 0.05).

Reflex and neuro-humoral pressor action of the hypertonic solutions.

The intraarterial injections of 50% urea or 20% NaCl induced a rise of the systemic arterial blood pressure simultaneously with a constriction of the vessels of the legs. The mechanism which is responsible for these phenomena is very complex. It includes a reflex arising from the arterial wall, which is mediated through the spinal cord, the release of catecholamines and of some still nonidentified pressor substances and a central component which is normally masked by the depressor sinus reflex.

The influence of bradykinin on carotid baroreceptors in vitro.

The actions of bradykinin on isolated and superfused carotid baroreceptors have been examined. Bradykinin was applied either locally, in the organ bath, in doses of 9 microng, or by superfusion in doses of 0.8 - 0.9 microng/ml saline. The results have shown that bradykinin has no effects upon the activity of baroreceptors.