Doxapram alleviates low SpO2 induced by the combination of propofol and fentanyl during painless gastrointestinal endoscopy.

BACKGROUND: Painless gastrointestinal endoscopy under intravenous propofol anesthesia is widely applied in the clinical scenario. Despite the good sedation and elimination of anxiety that propofol provides, low SpO2 may also result. Doxapram is a respiratory stimulant with a short half-life. The primary aim of this study was to investigate the effects of doxapram on alleviating low SpO2 induced by the combination of propofol and fentanyl during painless gastrointestinal endoscopy. METHODS: In this prospective study, patients scheduled for painless gastrointestinal endoscopy were randomly assigned to group D or S with 55 patients per group. Initially, both groups received a combination of propofol and fentanyl. Patients in group D received 50 mg doxapram after propofol injection, while patients in group S received an equal volume of saline. Vital signs of the patients, propofol dose, examination duration, and incidences of low SpO2 were recorded. RESULTS: There were no statistical differences in propofol consumption and examination duration between the two groups. Twenty-six patients in group S experienced low SpO2 versus 10 in group D (P = 0.001). Nineteen patients in group S underwent oxygenation with a face mask in contrast to 8 in group D (P = 0.015). Eighteen patients in group S were treated with jaw lifting compared to 5 in group D (P = 0.002). Four patients in group S underwent assisted respiration compared to 2 in group D (without statistical difference). The average oxygen saturation in group S was significantly lower than that in group D at 1, 2 and 3 min after propofol injection (P < 0.001, P = 0.001 and P = 0.020, respectively). There were no statistical differences in oxygen saturation at other time points. There were no statistical differences in MAP and HR (except for the time point of 1 min after the induction) between the two groups. CONCLUSIONS: Low dose of doxapram can effectively alleviate low SpO2 in painless gastrointestinal endoscopy with intravenous propofol, without affecting propofol consumption, examination duration, MAP, or HR. TRAIL REGISTRATION: The study was approved by the Institutional Ethics Committee of Clinical and New Technology of Wuxi People's Hospital on 20th July, 2018 (KYLLH2018029) and registered in the Chinese Clinical Trial Register on 16th August, 2018 (ChiCTR1800017832).

The effect of angiotensin-converting enzyme polymorphism on hemodynamic response to endotracheal intubation in hypertensive patients.

Endotracheal intubation elicits a hemodynamic response associated with increased heart rate and blood pressure that is influenced by the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) genetic polymorphism which may be of importance also for the pressure response to anesthesia. A total of 337 patients underwent abdominal surgery in general anesthesia and 16% were D/D-homozygotes, 45% were I/D heterozygotes and 39% of the patients were I/I homozygotes. Before surgery most patients were in treatment for arterial hypertension. Systolic and diastolic pressure, heart rate and concentrations of catecholamines in blood were determined before and after induction of anesthesia and for up to 10 minutes following endotracheal intubation. Anesthesia decreased blood pressure and for patients presenting ID and DD, blood pressure and heart rate reached similar levels but compared to II-homozygotes, D-carriers demonstrated significantly higher levels for systolic pressure and heart rate before and after intubation (p < 0.05). The blood levels of catercholamines were similar in the three genotype groups. The incidence of ECG-determined myocardial ischemia was higher in D-allele carriers compared to I-allele homozygotes (DD 22%, ID 25% vs. II 5%). In response to anesthesia and intubation and independent of sympathetic nervous activity, D-allele carriers for ACE polymorphism increased blood pressure response and higher risk for development of cardiovascular complications compared to patients homozygous for the I-allele.

[The effect of propofol preconditioning on cytochrome C release from mitochondria after mild hypothermic ischemia/reperfusion in isolated rat hearts].

AIM: To explore the effect of propofol preconditioning on cardiomyocyte apoptosis and cytochrome C release from mitochondria during mild hypothermic ischemia/reperfusion in isolated rat hearts. METHODS: 50 isolated SD rat hearts perfused on Langendorff apparatus were randomly divided into 5 groups (n=10): control group (C), DMSO group (D), 3 different concentrations of propofol groups of 25 micromol x L(-1) (P1), 50 micromol x L(-1) (P2), 100 micromol x L(-1) (P3) propofol respectively. All of the isolated rat hearts were subjected to 31 degrees C mild hypothermic ischemia for 55 min followed by 60 min reperfusion. The D, P1, P2, P3 groups were preconditioned by perfusing with K-H solution containing 20 micromol x L(-1) DMSO and 25, 50, 100 micromol x L(-1) propofol respectively for 10 min and then followed by 5 min K-H solution washing out before ischemia. The preconditioning procedure was repeated twice. Hemodynamics of the hearts was recorded after equilibration(baseline values) immediately before ischemia, 30 min and 60 min after reperfusion respectively. Cardiomyocyte apoptosis rate and contents of cytosolic and mitochondrial cytochrome C were measured at the end of reperfusion. RESULTS: After 30 min and 60 min reperfusion, LVEDP was significantly lower and LVDP was significantly higher in P3 group than those in C group ( P < 0.05, P < 0.01). Compared with C group, cardiomyocyte apoptosis rate of the hearts decreased significantly in P2,P3 groups at the end of reperfusion (P < 0.05, P < 0.01). Cytochrome C level increased significantly in mitochondria but decreased significantly in cytosol in P2, P3 groups as compared with C group (P < 0.05, P < 0.01). CONCLUSION: Propofol preconditioning decreased cardiomyocyte apoptosis, protected the heart against 31 degrees C mild hypothermic ischemia/reperfusion injury by attenuation of the release of cytochrome C from mitochondria to cytosol.