Summary

Background and objective: The intravenous anaesthetic propofol has been reported to exert neuroprotective actions by several mechanisms. This study has been designed to investigate the effects of propofol on intracellular calcium increase in cultured cerebrocortical neurons after exposure to pathological concentrations of N-methyl-d-aspartate (NMDA) mediated by potential direct interactions of propofol with NMDA receptors.

Methods: The effects of propofol (0.1–100 μmol) on intracellular calcium increase induced by 300 μmol NMDA (180 s) were measured in cultured cerebrocortical neurons using the calcium-sensitive fluorochrome calcium green-5N-acetoxymethylester with confocal laser scanning microscopy.

Results: The intraneuronal calcium increase after exposure to 300 μmol NMDA depended on extracellular calcium concentration. Propofol reduced the increase of NMDA receptor-induced intraneuronal calcium concentration dependently with a threshold concentration for a significant effect of 10 μmol. The overall effect was small, since even high concentrations of propofol (100 μmol) diminished intraneuronal calcium rise by only 50%.

Conclusions: The threshold concentration for significant effects of propofol on the NMDA-induced increase of intraneuronal calcium turned out to be in the upper limit of propofol concentrations that are considered to be clinically relevant. However, in the presence of high propofol concentrations, inhibition of NMDA receptor-mediated calcium increase might contribute to neuroprotective effects observed with propofol.

Summary

Background and objective: Target-controlled infusions (TCIs) of remifentanil and fentanyl in conscious sedation regimes for extra-corporeal shock-wave lithotripsy have not been reported. We estimated the effect site concentrations of remifentanil and fentanyl needed to obtain adequate analgesia in 50% of patients (EC50) and compared both drugs in terms of intra- and post-procedure complications.

Methods: Forty-four adult patients were randomly distributed into two groups: Group R received remifentanil and Group F received fentanyl TCI with initial effect site concentrations of 1.5 and 2 ng mL−1, respectively. Pain was assessed using a 10-point verbal analogue scale and <3 was considered adequate analgesia. Increments or decrements of 0.5 ng mL−1 were then introduced for subsequent patients according to Dixon's up and down method. During the rest of the procedure, TCI was adjusted to maintain verbal analogue scale <3.

Results: Remifentanil and fentanyl EC50 were 2.8 ng mL−1 (95% confidence interval (CI): 1.8–3.7 ng mL−1) and 2.9 ng mL−1 (95% CI: 1.7–4.1 ng mL−1), respectively (n.s.). At EC50, the probability of having a respiratory rate <10 was 4% (95% CI: 0–57%) for remifentanil and 56% (95% CI: 13–92%) for fentanyl. Hypoxaemia, vomiting and sedation were more frequent in Group F during and after the procedure (P < 0.05).

Conclusions: A similar EC50 but more respiratory depression, sedation and PONV were found with fentanyl TCI than with remifentanil TCI.

Summary

Background and objective: The aim of this study was to investigate the effect of ketamine on the endocrine and lipid metabolic status of the renal-banded animals. Methods: Forty male rats were randomly divided into four groups. Group A served as control, Group B animals received ketamine intraperitoneally at a dose of 100 mg kg−1, Group C was submitted to 2-kidney 1-clip experimental hypertension and Group D received ketamine as above, as well as being submitted to renal artery clipping. Atrial natriuretic peptide, angiotensin II and free fatty acid concentrations were measured in serum. In addition, adipose tissue lipoprotein lipase activity and angiotensin II content were determined, while the left ventricular weight relative to body weight was used as a cardiac hypertrophy index. Results: In renal-banded rats (Groups C and D) serum atrial natriuretic peptide, free fatty acid and angiotensin II concentrations as well as ventricular weight were increased, while adipose tissue lipoprotein lipase activity was lower than in control animals (Groups A and B). Ketamine administration did not influence angiotensin II concentrations either in normal (Group B) or banded rats (Group D). Ketamine increased serum atrial natriuretic peptide and free fatty acid concentrations only in normal animals (Group B). It had no influence on adipose tissue lipoprotein lipase activity either in normal (Group B) or banded animals (Group D). Adipose angiotensin II content did not differ between the four groups. Conclusion: Ketamine increased the atrial natriuretic peptide and free fatty acid concentration in normal rats. In 2-kidney 1-clip animals, ketamine did not elicit an additional response of serum atrial natriuretic peptide or free fatty acids levels. Its contribution to these factors was not significant.

Summary

Background and objective: Clonidine, which is used for induction of sympatholysis and prevention or treatment of alcohol withdrawal in anaesthesia and intensive care medicine, may have deleterious effects on intestinal mucosal perfusion. This study was designed to investigate the effects of clonidine on intestinal perfusion and oxygenation. Methods: Following ethical approval 17 anaesthetized, and acutely instrumented pigs were randomly assigned to two groups: eight animals received intravenous clonidine (2 μg kg−1 bolus and 2 μg kg−1 h−1), nine animals served as a control group. Measurement points for systemic and regional haemodynamic and oxygenation parameters were 135 and 315 min after starting the clonidine application. Results: Clonidine elicited systemic haemodynamic changes (median [25–75th interquartile range]): heart rate (106 [91, 126] to 84 [71, 90] beats min−1) cardiac output (147 [123, 193] to 90 [87, 107] mL min−1 kg−1) and mean arterial pressure (77 [72, 93] to 69 [61, 78] mmHg) decreased. Despite systemic haemodynamic changes, the superior mesenteric artery blood flow did not change in the clonidine group. The vascular resistance of the superior mesenteric artery decreased. The small intestinal oxygen supply, the mucosal and the serosal tissue oxygen partial pressure did not change. Conclusions: Systemic sympatholysis induced by intravenously applied clonidine in addition to basic intravenous anaesthesia elicited a decrease in cardiac output and mean arterial pressure. However, regional macrohaemodynamic perfusion was maintained and intestinal oxygenation did not change. Clonidine does not impair intestinal mucosal and serosal oxygenation under physiological conditions.

Summary

Background and objective: The aim of the present study was to investigate the impact of arginine vasopressin (AVP), a drug currently under investigation for use during cardiopulmonary resuscitation, on cerebral oxygenation and cerebral blood volume (CBV) in pigs with intact systemic circulation using near infrared spectroscopy.

Methods: Nine healthy pigs were anaesthetized and subjected to invasive haemodynamic monitoring as well as to non-invasive determination (with near infrared spectroscopy) of changes in the Tissue Oxygenation Index (TOI is the ratio of oxygenated to total tissue haemoglobin), Tissue Haemoglobin Index (THI, representing CBV) and cytochrome oxidase (ΔCytOx, representing the balance of intracellular oxygen supply).

Results: At both 3 and 5 min after AVP administration, TOI, THI and ΔCytOx were significantly (P < 0.001) reduced compared to baseline, while cerebral perfusion pressure increased significantly (P < 0.001). The effects of AVP on TOI and THI lasted longer than on ΔCytOx. There were no significant changes with respect to the intracranial pressure throughout the study period.

Conclusions: No improvement of cerebral oxygenation was detected after AVP administration in swine with an intact systemic circulation. In contrast to recently published investigations, AVP provoked a sustained drop in indices of cerebral oxygenation and CBV.

Summary

Background and objective: This prospective, randomized, double-blind, controlled study was designed to test the effect of pre-anaesthetic administration of dexmedetomidine, given as a single intravenous (i.v.) dose, on postoperative pain scores and morphine consumption in patients receiving patient-controlled morphine after abdominal surgery.

Methods: Sixty patients were randomly allocated to receive dexmedetomidine (1 μg kg−1) or saline 10 min before induction of anaesthesia. Twenty minutes before the end of surgery, all patients received a standardized (0.1 mg kg−1) loading dose of morphine. They were then allowed to use a patient-controlled analgesia (PCA) device giving bolus doses of morphine (0.02 mg kg−1). Pain, discomfort and sedation scores; cumulative morphine consumption; time to extubation; time to recovery; and any side-effects were recorded after recovery and at 1, 2, 6, 12 and 24 h after the start of PCA.

Results: The mean time to extubation at the end of anaesthesia and recovery time were similar in both groups. There were no significant differences between groups with regard to mean pain, discomfort, sedation and nausea scores. Cumulative morphine consumption was significantly lower in the dexmedetomidine group at 6, 12 and 24 h (P < 0.05). The incidence of side-effects did not differ between the groups.

Conclusions: A single i.v. dose of dexmedetomidine (1 μg kg−1) given 10 min before induction of anaesthesia significantly reduced postoperative morphine consumption at identical pain scores compared to control, but had no effect on postoperative recovery time.