We tested the hypothesis that nitric oxide (NO) arising from the action of inducible nitric oxide synthase (iNOS) is responsible for the deficiency in vasopressin (AVP) release and consequent hypotension during endotoxaemic shock. Wild-type (WT) and iNOS knockout mice (iNOS(-/-)) were given either saline or Escherichia coli lipopolysaccharide (LPS, 1.0 mg/kg i.v., final volume 0.03 ml). Mean arterial blood pressure (MAP) was measured and plasma AVP levels determined before and after LPS or saline injection. In WT mice, MAP was significantly lower 2 h after LPS administration and remained low for the remainder of the 6-h observation period. AVP plasma levels were increased at the 2nd and 4th h of the experiment, returning thereafter to basal levels. Conversely, LPS injection in iNOS iNOS(-/-) mice elicited a sustained increase in plasma AVP concentration and attenuated the fall in blood pressure. These data indicate that NO arising from the iNOS plays an important inhibitory role in AVP release during endotoxaemia and may be responsible for the hypotension occurring during this vasodilatory shock.

Previous studies have shown that immunological challenges as lipopolysaccharide (LPS) administration increases plasma oxytocin (OT) concentration. Nitric oxide (NO), a free radical gas directly related to the immune system has been implicated in the central modulation of neuroendocrine adaptive responses to immunological stress. This study aimed to test the hypothesis that the NO pathway participates in the control of OT release induced by LPS injection. For this purpose, adult male Wistar rats received bolus intravenous (i.v.) injection of LPS, preceded or not by i.v. or intracerebroventricular (i.c.v.) injections of aminoguanidine (AG), a selective inducible nitric oxide synthase (iNOS) inhibitor. Rats were decapitated after 2, 4 and 6h of treatment, for measurement of OT by radioimmunoassay. In a separate set of experiments, mean arterial pressure (MAP) and heart rate (HR) were measured every 15 min over 6h, using a polygraph. These studies revealed that LPS reduced MAP and increased HR at 4 and 6h post-injection. LPS significantly increased plasma OT concentration at 2 and 4h post-injection. Pre-treatment with i.c.v. AG further increased plasma OT concentration and attenuated the LPS-induced decrease in MAP, however, i.v. AG failed to show similar effects. Thus, iNOS pathway may activate a central inhibitory control mechanism that attenuates OT secretion during endotoxemic shock.

O objetivo deste estudo foi identificar os diagnósticos de enfermagem prevalentes nos pacientesinternados com sepse, sepse grave ou choque séptico em um Centro de Terapia Intensiva. A população foiconstituída pelos pacientes com idade superior a 18 anos, internados no Centro de Terapia Intensiva, dejaneiro a dezembro de 2010. As informações foram coletadas do prontuário, de acordo com as característicassociodemográficas e clínicas e diagnósticos de enfermagem registrados. No período estudado, foram internados103 pacientes, sendo que 79,4% foram a óbito. Os diagnósticos de enfermagem identificados foram: risco deinfecção, risco de aspiração, risco para integridade da pele prejudicada, ventilação espontânea prejudicada,troca de gases prejudicada, perfusão tissular ineficaz cardiopulmonar e integridade da pele prejudicada. Emconclusão, espera-se que a identificação dos diagnósticos, presentes nos prontuários de pacientes com sepse,possam contribuir para a assistência de enfermagem a essa clientela.

To evaluate the effect of an educational intervention on knowledge about hand hygiene in nursing students. Method: Quasi-experimental study of the pre-and post-intervention type, carried out with 23 nursing students. Knowledge about hand hygiene was evaluated using a form containing questions about the subject. In addition, a theoretical and practical 1. er Trimestre 2019 • Año XXIII-N.° 53 Conclusions: The educational intervention performed in this study proved to be efficient in improving knowledge about hand hygiene.

BACKGROUND AND PURPOSE Regression of left ventricular hypertrophy by moxonidine, a centrally acting sympatholytic imidazoline compound, results from a sustained reduction of DNA synthesis and transient stimulation of DNA fragmentation. Because apoptosis of cardiomyocytes may lead to contractile dysfunction, we investigated in spontaneously hypertensive rats (SHR), time‐ and dose‐dependent effects of in vivo moxonidine treatment on cardiac structure and function as well as on the inflammatory process and signalling proteins involved in cardiac cell survival/death. EXPERIMENTAL APPROACH 12 week old SHR received moxonidine at 0, 100 and 400 µg·kg−1·h−1, s.c., for 1 and 4 weeks. Cardiac function was evaluated by echocardiography; plasma cytokines were measured by elisa and hearts were collected for histological assessment of fibrosis and measurement of cardiac proteins by Western blotting. Direct effects of moxonidine on cardiac cell death and underlying mechanisms were investigated in vitro by flow cytometry and Western blotting. KEY RESULTS After 4 weeks, the sub‐hypotensive dose of moxonidine (100 µg) reduced heart rate and improved global cardiac performance, reduced collagen deposition, regressed left ventricular hypertrophy, inhibited Akt and p38 MAPK phosphorylation, and attenuated circulating and cardiac cytokines. The 400 µg dose resulted in similar effects but of a greater magnitude, associated with blood pressure reduction. In vitro, moxonidine inhibited norepinephrine‐induced neonatal cardiomyocyte mortality but increased fibroblast mortality, through I1‐receptor activation and differential effects on downstream Akt and p38 MAPK. CONCLUSIONS AND IMPLICATIONS While the antihypertensive action of centrally acting imidazoline compounds is appreciated, new cardiac‐selective I1‐receptor agonists may confer additional benefit.