RESUMO
Propofol-related infusion syndrome (PRIS) is a rare, yet life-threatening sequelae to prolonged administration of the anesthetic propofol in mechanically intubated patients. The condition is characterized by progressive multi-system organ failure and eventual mortality; of note, the predominant characteristics of PRIS involve but are not limited to cardiovascular impairment and collapse, metabolic and lactic acidosis, rhabdomyolysis, hyperkalemia, and acute renal failure. While potent or extended doses of propofol have been found to be the primary precipitating factor of this condition, others such as age, critical illness, steroid therapy, and hyperlipidemia have been discovered to play a role as well. This bibliometric analysis was done to reflect the current relevance and understanding of PRIS in recent literature. The SCOPUS database was utilized to conduct a search for articles with keywords "propofol infusion syndrome" and "propofol syndrome" from February 24, 2001, until April 16, 2023, with parameters for article title, citation number, citation per year, author, institution, publishing journal, and country of origin. PRIS was first defined in 1990, just a year after its approval by the Food and Drug Administration for use as a sedative-hypnotic. Since then, interest in PRIS slowly rose up to 13 publications per year in 2013. Seven papers on the topic were published in Critical Care Medicine, six in Neurocritical Care, and four in Anesthesia. The most common institutions were Mayo Clinic, Northeastern University, and Tufts Medical Center. To our knowledge, this is the first bibliometric analysis to evaluate the most influential publications about PRIS. A majority of the research is case-based, possibly owing to the rarity of the condition. Our research suggests that confounding factors outside the precipitating dosage of propofol may be implicated in the onset and progression of PRIS. This study could therefore bring renewed interest to the topic and lead to additional research focused on fully understanding the pathophysiology of PRIS in order to promote the development of novel diagnostics and treatment.
RESUMO
The objective of the present study was to examine the idea that the decrease in 50-kHz ultrasonic vocalizations elicited by tickling in juvenile rats following the administration of the psychotomimetic drug phencyclidine (PCP) may represent a valid model of the negative symptoms of schizophrenia. Fifty-kilohertz calls in rodents have been suggested to represent an archaic model of human laughter. Our results showed that daily tickling sessions produced a gradual increase in 50-kHz vocalizations, an effect that reached statistical significance from day 3. Administration of PCP (1 mg/kg, intraperitoneally) attenuated the 50-kHz calls induced by 4 consecutive days of tickling. The ability of several clinically effective or potential antipsychotics to reverse the effects of PCP was investigated. The 5-HT1A receptor partial agonist, buspirone (0.3 and 1 mg/kg, intraperitoneally), the dual D2/5-HT1A receptor ligand, SSR181507 (0.5-0.75 mg/kg, intraperitoneally), but not the atypical antipsychotic, aripiprazole (0.1-1 mg/kg, intraperitoneally), the 5-HT2A receptor antagonist, eplivanserin (0.3-3 mg/kg, intraperitoneally), and the GlyT1 inhibitor, SSR103800 (0.3-3 mg/kg, intraperitoneally) significantly attenuated the effects of PCP on 50-kHz calls. Importantly, in animals not treated with PCP, none of the drugs affected 50-kHz calls elicited by a first handling-tickling session, indicating that the action of buspirone and SSR181507 cannot be explained by an intrinsic effect. To investigate further the specificity of these drug effects, we tested the anxiolytic and antidepressant agents, diazepam (0.1-1 mg/kg, intraperitoneally) and fluoxetine (1-10 mg/kg, intraperitoneally), respectively, in this procedure. Neither drug affected tickling-induced 50-kHz calls in naive or PCP-treated rats. In conclusion, the results of the present study confirm that 50-kHz calls elicited by several tickling sessions in rats can be reduced by acute administration of PCP, and that this effect can be reversed by previous administration of compounds with 5-HT1A receptor agonist properties. As evidence for clinical efficacy of both agents on the negative symptoms of schizophrenia is weak or lacking, the current findings do not allow a definite conclusion to be drawn on the validity of this procedure as a model of this aspect of schizophrenia.
