Objective:To evaluate the effect of angiotensin-converting enzyme (ACE) gene polymorphism on dexmedetomidine-induced inhibition of responses to endotracheal intubation in the patients with hypertension.Methods:One hundred and eighty patients with essential hypertension, aged 48-61 yr, weighing 51-66 kg, of American Society of Anesthesiologists physical status Ⅱ or Ⅲ, in whom ACE genotype was determined using polymerase chain reaction-restriction fragment length polymorphisms method before operation, were divided into 6 groups ( n=30 each) according to whether dexmedetomidine was applied: DD genotype group (DD group), ID genotype group (ID group), II genotype group (II group), dexmedetomidine plus DD genotype group (DEX+ DD group), dexmedetomidine plus ID genotype group (DEX+ ID group), and dexmedetomidine plus II genotype group (DEX+ II group). Dexmedetomidine 0.8 μg/kg was intravenously infused over 15 min before induction of anesthesia in DEX+ DD group, DEX+ ID group and DEX+ II group.Systolic and diastolic pressure (SP, DP) and heart rate (HR) were measured before dexmedetomidine (T 0), immediately before tracheal intubation (T 1), immediately after tracheal intubation (T 2), and at 1.5 and 5.0 min after tracheal intubation (T 3, 4). The rate-pressure product (RPP) was calculated.The occurrence of myocardial ischemia and cardiovascular responses within 5 min after tracheal intubation was recorded.Blood samples from the internal jugular vein were collected at T 0 and T 2-4, and plasma concentrations of epinephrine (E) and norepinephrine (NE) were determined by high performance liquid chromatography-electrochemical detection assay. Results:Compared with group DD, the SP, DP, HR and RPP were significantly decreased at T 2-4, plasma NE and E concentrations were decreased at T 2, 3, and the incidence of myocardial ischemia and cardiovascular reactions was decreased in group Dex+ DD ( P<0.05). Compared with group ID, SP, DP, HR and RPP were significantly decreased at T 2-4, plasma NE and E concentrations were decreased at T 2, 3, and the incidence of myocardial ischemia and cardiovascular responses were decreased in group Dex+ DD ( P<0.05). Compared with group II, SP, DP, HR and RPP were significantly decreased at T 2, 3, plasma NE and E concentrations were decreased, HR and RPP were decreased at T 4, and the incidence of myocardial ischemia and cardiovascular reactions was decreased in group Dex+ II ( P<0.05). There was no significant difference in the above parameters among group Dex+ DD, group Dex+ ID and group Dex+ II ( P>0.05). Conclusion:ACE gene polymorphism does not affect dexmedetomidine-induced inhibition of responses to endotracheal intubation in the patients with hypertension.

Objective To evaluate the effect of angiotension-converting enzyme (ACE) gene poly-morphism on dexmedetomidine-induced inhibition of responses to extubation in the patients with hyperten-sion. Methods A total of 180 patients with primary hypertension, aged 50-63 yr, weighing 54-69 kg, of American Society of Anesthesiologists physical status Ⅱ or Ⅲ, scheduled for elective abdominal surgery under general anesthesia, in whom ACE genotypes were detected using polymerase chain reaction-restriction fragment length polymorphism, were divided into 6 groups (n = 30 each) according to whether dexmedeto-midine was applied: DD genotype group (DD group), ID genotype group (ID group), Ⅱ genotype group (Ⅱ group), dexmedetomidine +DD genotype group (DEX+DD group), dexmedetomidine +ID genotype group (DEX+ID group) and dexmedetomidine+Ⅱ genotype group ( DEX+Ⅱ group). Dexmedetomidine 0. 5 μg·kg-1 ·h-1 was intravenously infused starting from 30 min before the end of surgery until the end of surgery in DEX+DD, DEX+ID and DEX+Ⅱ groups. Immediately before infusing dexmedetomidine (T1 ), at 30 min of dexmedetomidine infusion (T2 ), immediately after extubation (T3 ) and at 1. 5, 5 and 15 min after extubation (T4-6 ), systolic blood pressure, diastolic blood pressure, heart rate and ECG were recor-ded, and rate-pressure product was calculated. The development of myocardial ischemia and responses to extubation was recorded within 15 min after extubation. Results Compared with the baseline at T1 , each parameter of hemodynamics was significantly increased at T3-6 in DD, ID and Ⅱ groups (P<0. 05), and no significant change was found in each parameter of hemodynamics at T2-6 in Dex+DD, Dex+ID and Dex+Ⅱ groups (P> 0. 05). Each parameter of hemodynamics was significantly lower at T3-6 , and the inci-dence of myocardial ischemia and responses to extubation was decreased in group Dex+DD than in group DD and in group Dex+ID than in group ID (P<0. 05). Compared with group Ⅱ, each parameter of he-modynamics at T3-6 and incidence of responses to extubation were significantly decreased in group Dex+Ⅱ, and each parameter of hemodynamics was significantly increased at T3-6 , and the incidence of myocardial ischemia and responses to extubation was increased in DD and ID groups (P<0. 05). There was no signif-icant difference in each parameter of hemodynamics or incidence of myocardial ischemia and responses to extubation among group Dex+DD, group Dex+ID and group Dex+I (P>0. 05). Conclusion ACE gene polymorphism does not affect dexmedetomidine-induced inhibition of responses to extubation in the patients with hypertension.

Objective:To evaluate the effect of the positive P-glycoprotein expression on the efficacy of patient-controlled intravenous analgesia (PCIA) with sufentanil or pentazocine in patients with cancer pain.Methods:This was a retrospective cohort study. The medical records of patients with cancer pain of either sex, aged 54-71 yr, weighing 49-67 kg, with TNM stage Ⅱ-Ⅳ, who were treated in People′s Hospital of Lishui from January 2020 to January 2024, were collected. The expression of P-glycoprotein in tumor tissues was determined by the immunohistochemical method. Patients with negative P-glycoprotein expression in tumor tissues were divided into 2 groups: sufentanil group (group S 1) and pentazocine group (group P 1). Patients with positive P-glycoprotein expression in tumor tissues were divided into 2 groups: sufentanil group (group S 2) and pentazocine group (group P 2). The patients in 4 groups received 48 h of PCIA when visual analogue scale > 5 cm. The PCIA solution contained sufentanil 2 μg/kg and tropisetron 10 mg in 100 ml of normal saline in S 1 and S 2 groups or pentazocine 3 mg/kg+ tropisetron 10 mg in 100 ml of normal saline in P 1 and P 2 groups. The PCIA pump was set up to deliver a 1 ml bolus dose with a 10-min lockout interval and background infusion at 2 ml/h after a loading dose of 5 ml. Flurbiprofen 50 mg was intravenously injected when visual analogue scale > 3 cm during analgesia. The consumption of sufentanil, pentazocine and flurbiprofen within 4 h, >4-12 h, > 12-24 h and > 24-48 h of PCIA was recorded. The occurrence of adverse reactions such as respiratory depression (SpO 2<90%), nausea or/and vomiting, pruritus and bradycardia was recorded. Results:One hundred patients were finally included, with 25 in each group. There was no significant difference in the consumption of sufentanil, usage rate of flurbiprofen and incidence of respiratory depression, nausea and vomiting, pruritus and bradycardia during analgesia at each time period during PCIA between group S 1 and group S 2 ( P>0.05). Compared with group P 1, the consumption of pentazocinein was significantly increased within 4 h, > 4-12 h, and > 24-48 h of PCIA ( P<0.05), and no significant change was found in the usage rate of flurbiprofen at each time period and the incidence of respiratory depression, nausea or/and vomiting, pruritus and bradycardia during analgesia in group P 2 ( P>0.05). Conclusions:Positive P-glycoprotein expression may weaken the efficacy of PCIA with pentazocine, but exerts no effect on the efficacy of PCIA with sufentanil in patients with cancer pain.