Incidence of perioperative hypotension in patients undergoing transurethral resection of bladder tumor after oral 5-aminolevulinic acid administration: a retrospective multicenter cohort study.

PURPOSE: Tumors can be visualized using 5-Aminolevulinic acid hydrochloride (5-ALA) during transurethral resection of bladder tumors (TURBT). Hypotension is an adverse effect of 5-ALA; however, its incidence and morbidity rates are unknown. This study aimed to describe the incidence of perioperative hypotension and identify risk factors for hypotension among patients after 5-ALA administration in TURBT. METHODS: This retrospective multicenter cohort study was conducted at three general hospitals in Japan. Adult patients who underwent elective TURBT after 5-ALA administration between April 2018 and August 2020 were included. The primary outcome was the incidence of perioperative hypotension (mean blood pressure < 65 mmHg). The secondary outcomes were the use of vasoactive agents and adverse events, including urgent intensive care unit (ICU) admission. Multivariate logistic regression analysis was performed to investigate risk factors of the incidence of intraoperative hypotension. RESULTS: The median age of 261 patients was 73 years. General anesthesia was induced in 252 patients. The intraoperative hypotension was observed in 246 (94.3%) patients. Three patients (1.1%) were urgently admitted to the ICU for continued vasoactive agent use after surgery. All three patients had renal dysfunction. Multivariate logistic regression analysis revealed that general anesthesia was significantly associated with intraoperative hypotension (adjusted odds ratio, 17.94; 95% confidence interval, 3.21-100.81). CONCLUSION: The incidence of hypotension in patients undergoing TURBT after 5-ALA administration was 94.3%. The incidence of urgent ICU admission with prolonged hypotension was 1.1% in all patients with renal dysfunction. General anesthesia was significantly associated with intraoperative hypotension.

Intraocular pressure during robotic-assisted laparoscopic prostatectomy: a prospective observational study.

BACKGROUND AND OBJECTIVES: Although previous reports have shown intraocular pressure changes during robotic-assisted laparoscopic prostatectomy, they did not discuss the time course of changes or the timing of the largest change. We conducted this study to quantify pressure changes over time in patients assuming the steep Trendelenburg position during robotic-assisted laparoscopic prostatectomy. METHODS: Twenty-one men were enrolled. Intraocular pressure was measured before anesthesia induction in the supine position (T0); 30 (T1), 90 (T2), and 150 minutes after assuming the Trendelenburg position (T3); and 30 minutes after reassuming the supine position (T4). End-tidal carbon dioxide and blood pressure were also recorded. To compare intraocular pressure between the time points, we performed repeated-measures analysis of variance. A mixed-effects multivariate regression analysis was conducted to adjust for confounding factors. RESULTS: The mean (standard deviation) intraocular pressure was 18.3 (2.4), 23.6 (3.0), 25.1 (3.1), 25.3 (2.2), and 18.1 (5.0) mmHg at T0, T1, T2, T3, and T4, respectively. The mean intraocular pressure was higher at T1, T2, and T3 than at T0 (p < 0.0001 for all). There was no significant difference between T0 and T4, and between T3 and T2 (p > 0.99 for both). CONCLUSIONS: The Trendelenburg position during robotic-assisted laparoscopic prostatectomy increased intraocular pressure. The increase was moderate at 90 minutes after the position was assumed, with the value being approximately 7 mmHg higher than the baseline value. The baseline intraocular pressure was restored at 30 minutes after the supine position was reassumed. TRIAL REGISTRATION: UMIN ID 000014973 DATE OF REGISTRATION: August 27, 2014.

[Airway Management in a Patient with Forestier's Disease].

Airway management in a patient with Forestier's disease can be challenging clinically because this disease may cause not only dysphagia but also airway obstruction due to the compression of the pharynx and esophagus caused by the ossification of anterior longitudinal ligament. We report our anesthetic management in a patient with Forestier's disease. Meanwhile, we studied the causes of difficult airway and the most suitable airway device for a patient with this disease from a standpoint of anatomy of upper airway. Our study indicated the possibility that the most suitable airway device differed depending on the actual location of the ossification of anterior longitudinal ligament in the cervical spine and that more prudent airway management would be required if its lesion location extended to upper cervical spine.

Effects of erythropoietin on intracellular calcium concentration of rat primary cortical neurons.

Erythropoietin (Epo) has been shown to afford neuroprotection in many experimental models. Although the cytosolic Ca(2+) concentration ([Ca(2+)](i)) is an important factor regulating cell survival, the effects of Epo on [Ca(2+)](i) in neurons are not fully elucidated. We studied the effects of human recombinant Epo on [Ca(2+)](i) of rat primary cortical neurons in normal and excitotoxic conditions. Changes in [Ca(2+)](i) were measured using fura-2 microfluorometry in rat primary cortical cultures. In the control condition with 2mM Mg(2+) in the bath solution, Epo at 4 u/ml significantly increased the fluorescence ratio, but the Epo-induced increase in the fluorescence ratio was abolished by omission of Ca(2+) from the bath solution and by the addition of cadmium. Omission of Mg(2+) and supplementation with glycine resulted in basal and periodic increases in the fluorescence ratio, due to sustained activation of N-methyl-d-asparate (NMDA) receptors. Epo at 0.4 and 4 u/ml significantly decreased the fluorescence ratio in this condition, and this effect was attenuated by the phosphoinositide 3-kinase (PI3K) inhibitors, LY 294002 and wortmannin, and the Ca-activated K channel blocker, iberiotoxin. In the presence of Mg(2+) and exogenous glutamate, 4 but not 0.4 u/ml Epo slightly but significantly reduced the [Ca(2+)](i) elevation. These results suggest that Epo increased [Ca(2+)](i) in cortical neurons by inducing Ca(2+) entry in the control condition but decreased [Ca(2+)](i) in the Mg(2+)-free excitotoxic condition, at least in part via PI3K-dependent activation of Ca-activated K channels. Reduction of [Ca(2+)](i) by Epo in the excitotoxic condition may contribute to neuroprotection.

A1 adenosine receptor-mediated modulation of neuronal ATP-sensitive K channels in rat substantia nigra.

ATP-sensitive K (K(ATP)) channels, widely expressed in cytoplasmic membranes of neurons, couple cell metabolism to excitability. They are considered to play important roles in controlling seizure activity during hypoxia and in neuroprotection against cell damage during hypoxia, ischemia and excitotoxicity. It is known that adenosine augments the opening of cardiac surface K(ATP) channels by reducing the sensitivity of these channels to ATP blockade. We investigated whether a similar modulation occurs in neuronal channels. Whole cell voltage-clamp recordings were made using rat midbrain slices to record the membrane current and conductance in principal neurons of the substantia nigra pars compacta (SNc). When the pipette solution contained 1 mM ATP, the membrane current at -60 mV and cellular conductance remained stable for at least 15 min. When slices were treated with (-)-N(6)-2-phenylisopropyl adenosine (R-PIA), a selective agonist for A(1) adenosine receptors, in the same condition, the outward current developed slowly to the amplitude of 109.9+/-26.6 pA, and conductance increased to 229+/-50% of the baseline. These changes were strongly inhibited by 200 microM tolbutamide, a K(ATP) channel blocker, suggesting that opening of K(ATP) channels mediated these changes. Pretreatment with 8-cyclopentyltheophylline (CPT), a selective A(1) adenosine receptor antagonist, abolished the outward current and conductance increases. Treatment of adenosine resulted in the similar changes sensitive to tolbutamide. These changes were abolished by CPT. These results suggest that activation of A(1) adenosine receptors promotes the opening of K(ATP) channels in principal neurons of the SNc by removing the blockade by ATP.

The sympathomimetic actions of l-ephedrine and d-pseudoephedrine: direct receptor activation or norepinephrine release?

UNLABELLED: The basic mechanisms by which ephedrine is preferred over other vasopressors in obstetric anesthesia have not been clearly defined. We examined the sympathomimetic effects of l-ephedrine, currently used as a vasopressor, and d-pseudoephedrine, currently used as a decongestant. In anesthetized rats, l-ephedrine and d-pseudoephedrine caused dose-dependent increases in arterial blood pressure and heart rate, and these effects disappeared after destruction of the sympathetic nerve terminals with 6-hydroxydopamine (6-OHDA) pretreatment. The two ephedrine isomers produced concentration-dependent increases in tension of anococcygeal muscle and sinus rate of right atrium from rats. However, the anococcygeal and atrial responses to d-pseudoephedrine were abolished after 6-OHDA pretreatment, whereas approximately 50% of the responses to l-ephedrine were 6-OHDA-resistant. In human umbilical artery and vein, the two isomers failed to generate any contraction when given at the concentration that is capable of producing significant effects on anococcygeal and atrial tissues. Although direct adrenoceptor activation with l-ephedrine was detectable at tissue levels, the pressor response in vivo was entirely attributable to norepinephrine release from sympathetic nerves. This indirect mechanism could partly explain why l-ephedrine is better at increasing maternal arterial blood pressure while preserving the uteroplacental blood flow that is devoid of the involvement of the sympathetic innervation. IMPLICATIONS: The indirectly sympathomimetic property of l-ephedrine may be one of the mechanisms to explain why ephedrine is preferred over alpha-adrenergic agonists as a vasopressor for treatment of intraspinal anesthesia-induced hypotension in obstetrics.