Healthcare workers in Saudi Arabia (KSA) perceive stress differently according to gender but not in cortisol levels - an immunoassay study

Background: Working in the healthcare sector is generally regarded as stress inductive, which hampers performance, yet one demanding constant accuracy. This dichotomy has led to numerous investigations on the impact from perceived stress on hospital workers but focused primarily on employing psychological methods to determine perceived stress. This study sought to employ an arguably more objective measure of chronic stress on female healthcare professionals in Saudi Arabia, by assaying the concentration of hair cortisol (HCC) in parallel with stress questionnaires. Methods: Pharmacists, nurses and lab workers participated in providing hair samples. Cortisol levels were subsequently quantified using immunoassay methods. Investigations considered the variables of age, gender, and smoking, hair coloring or bleaching or working in shifts on both stress perception and HCC. Results: On average chronic stress was perceived comparably between the different healthcare professions and not differ significantly against the female control group. However, chronic stress differed significantly between genders within the healthcare profession. In contrast, HCC levels showed no direct relation to stress perception with respect to either gender or profession. HCC did, however, show steady decreases with respect to age, as an indirect measure of experience, that contrasted against the identical scores for stress perception. Finally, night shifts, smoking or hair colouring did not produce a significant change on HCC in the healthcare cohorts. Conclusions: Women in the healthcare profession perceive stress higher irrespective of profession compared to men. Also show a pattern of decreasing levels of cortisol with increasing age despite reporting similar stress perception against younger participants

Opioids depress cortical centers responsible for the volitional control of respiration

Respiratory depression limits provision of safe opioid analgesia and is the main cause of death in drug addicts. Although opioids are known to inhibit brainstem respiratory activity, their effects on cortical areas that mediate respiration are less well understood. Here, functional magnetic resonance imaging was used to examine how brainstem and cortical activity related to a short breath hold is modulated by the opioid remifentanil. We hypothesized that remifentanil would differentially depress brain areas that mediate sensory-affective components of respiration over those that mediate volitional motor control. Quantitative measures of cerebral blood flow were used to control for hypercapnia-induced changes in blood oxygen level-dependent (BOLD) signal. Awareness of respiration, reflected by an urge-to-breathe score, was profoundly reduced with remifentanil. Urge to breathe was associated with activity in the bilateral insula, frontal operculum, and secondary somatosensory cortex. Localized remifentanil-induced decreases in breath hold-related activity were observed in the left anterior insula and operculum. We also observed remifentanil-induced decreases in the BOLD response to breath holding in the left dorsolateral prefrontal cortex, anterior cingulate, the cerebellum, and periaqueductal gray, brain areas that mediate task performance. Activity in areas mediating motor control (putamen, motor cortex) and sensory-motor integration (supramarginal gyrus) were unaffected by remifentanil. Breath hold-related activity was observed in the medulla. These findings highlight the importance of higher cortical centers in providing contextual awareness of respiration that leads to appropriate modulation of respiratory control. Opioids have profound effects on the cortical centers that control breathing, which potentiates their actions in the brainstem

Control of glutamatergic neurotransmission in the rat spinal dorsal horn by the nucleoside transporter ENT1

Adenosine modulates nociceptive processing in the superficial dorsal horn of the spinal cord. In other tissues, membrane transporters influence profoundly the extracellular levels of adenosine. To investigate the putative role of nucleoside transporters in the regulation of excitatory synaptic transmission in the dorsal horn, we employed immunohistochemistry and whole-cell patch-clamp recording of substantia gelatinosa neurons in slices of rat spinal cord in vitro. The rat equilibrative nucleoside transporter (rENT1) was revealed by antibody staining to be abundant in neonatal and mature dorsal horn, especially within laminae I-III. This was confirmed by immunoblots of dorsal horn homogenate. Nitrobenzylthioinosine (NBMPR), a potent non-transportable inhibitor of rENT1, attenuated synaptically evoked EPSCs onto lamina II neurons in a concentration-dependent manner. Application of an adenosine A1 antagonist 1,3-dipropyl-8-cyclopentylxanthine produced a parallel rightward shift in the NBMPR concentration-effect curve. The effects of NBMPR were partially reversed by adenosine deaminase, which facilitates the metabolic degradation of adenosine. The modulation by NBMPR of evoked EPSCs was mimicked by exogenous adenosine or the selective A1 receptor agonist, 2-chloro-N6-cyclopentyl adenosine. NBMPR reduced the frequency but not the amplitude of spontaneous miniature EPSCs and increased the paired-pulse ratio of evoked currents, an effect that is consistent with presynaptic modulation. These data provide the first direct evidence that nucleoside transporters are able to critically modulate glutamatergic synaptic transmission