Background: An accurate estimation of resources use by individual patients is crucial in hospital management. Aim: To measure financial costs of health care actions in intensive care units of two public regional hospitals in Chile. Material and Methods: Prospective follow up of 716 patients admitted to two intensive care units during 2011. The financial costs of health care activities was calculated using the Activity-Based Costing methodology. The main activities recorded were procedures and treatments, monitoring, response to patient needs, patient maintenance and coordination. Results: Activity-Based Costs, including human resources and assorted indirect costs correspond to 81 to 88% of costs per disease in one hospital and 69 to 80% in the other. The costs associated to procedures and treatments are the most significant and are approximately $100,000 (Chilean pesos) per day of hospitalization. The second most significant cost corresponds to coordination activities, which fluctuates between $86,000 and 122,000 (Chilean pesos). Conclusions: There are significant differences in resources use between the two hospitals studied. Therefore cost estimation methodologies should be incorporated in the management of these clinical services.

Intensive care medicine in Chile is still in its dawn. It has experienced a progressive growth in the last decade, but continues to be weak. Although investments in the discipline have increased fivefold, there is still a severe deficiency of intensive care specialists. This issue will represent a serious problem in the near future. The Ministry of Health gathered an expert committee to study the problem and propose solutions for the future development of the discipline.

Background: Intensive medicine is especially expensive and requires an efficient management. Aim: To measure the real costs of diseases treated in an intensive care unit and compare them with the costs assigned by the Chilean National Health Fund (FONASA) for 2008. Material and Methods: Retrospective review of 225 patients, representing 82% of discharges from an intensive care unit during 2008. Patients were classified according to their medical conditions as having sepsis, trauma, cardiovascular, respiratory or neurological diseases. Costs were calculated using the cost per activity system. Results: Trauma, sepsis and cardiovascular diseases had the greatest cost per inpatient day, corresponding to 294,779; 253,513 and 244,713 Chilean pesos, respectively. Seventy percent of costs correspond to human resources followed by complementary examinations, that represent up to 15% of costs. Patients with sepsis and cardiovascular diseases absorbed 28 and 26% of intensive care unit resources, respectively. Patients who died with these diseases absorbed 35 and 16% of resources, respectively. Conclusions: All diseases studied had significantly higher costs than those assigned by the National Health Fund.

Nitric oxide synthase (NOS)-containing neurons have been localized in various parts of the CNS. These neurons occur in the hypothalamus, mostly in the paraventricular and supraoptic nuclei and their axons project to the neural lobe of the pituitary gland. We have found that nitric oxide (NO) controls luteinizing hormone-releasing hormone (LHRH) release from the hypothalamus acting as a signal transducer in norepinephrine (NE)-induced LHRH release. LHRH not only releases LH from the pituitary but also induces sexual behavior. On the other hand, it is known that oxytocin also stimulates mating behavior and there is some evidence that oxytocin can increase NE release. Therefore, it occurred to us that oxytocin may also stimulate LHRH release via NE and NO. To test this hypothesis, we incubated medial basal hypothalamic (MBH) explants from adult male rats in vitro. Following a preincubation period of 30 min, MBH fragments were incubated in Krebs-Ringer bicarbonate buffer in the presence of various concentrations of oxytocin. Oxytocin released LHRH at concentrations ranging from 0.1 nM to 1 µM with a maximal stimulatory effect (P<0.001) at 0.1 µM, but with no stimulatory effect at 10 µM. That these effects were mediated by NO was shown by the fact that incubation of the tissues with NG-monomethyl-L-arginine (NMMA), a competitive inhibitor of NOS, blocked the stimulatory effects. Furthermore, the release of LHRH by oxytocin was also blocked by prazocin, an <FONT FACE="Symbol">a</font>1-adrenergic receptor antagonist, indicating that NE mediated this effect. Oxytocin at the same concentrations also increased the activity of NOS (P<0.01) as measured by the conversion of [14C]arginine to citrulline, which is produced in equimolar amounts with NO by the action of NOS. The release of LHRH induced by oxytocin was also accompanied by a significant (P<0.02) increase in the release of prostaglandin E2 (PGE2), a mediator of LHRH release that is released by NO. On the other hand, incubation of neural lobes with various concentrations of sodium nitroprusside (NP) (300 or 600 µM), a releaser of NO, revealed that NO acts to suppress (P<0.01) the release of oxytocin. Therefore, our results indicate that oxytocin releases LHRH by stimulating NOS via NE, resulting in an increased release of NO, which increases PGE2 release that in turn induces LHRH release. Furthermore, the released NO can act back on oxytocinergic terminals to suppress the release of oxytocin in an ultrashort-loop negative feedback