Omeprazole reduces preoperative gastric fluid acidity and volume in children

To explore the effects of oral omeprazole on preoperative gastric fluid pH and volume in children, 104 healthy in-patients aged 4–9 yr were randomly allocated to four groups (n = 26). Subjects in the Omeprazole-Omeprazole Group received two doses of omeprazole (20 mg per dose), those in the Placebo-Placebo Group, two doses of placebo, those in the Placebo-Omeprazole and Omeprazole-Placebo Groups, one dose each of the two preparations by mouth. For each treatment regimen, the first medication was administered at 9:00 p.m. on the night before surgery and the second at 5:30 a.m. on the morning of the day of surgery (three hours preoperatively). Children undergoing elective surgery were offered 10 nil · kg^?1 of apple juice three hours before induction of anaesthesia. After induction of anaesthesia and tracheal intubation, gastric fluid was aspirated through a large-bore, multiorifice orogastric tube and analyzed for pH and total fluid volume. The administration of omeprazole at bedtime before surgery increased gastric pH (3.3 ± 1.3 vs 2.0 ± 0.6, P < 0.05) in comparison with placebo, as did two doses of omeprazole (pH = 4.8 ± 1.6, P < 0.05). A single dose of omeprazole administration on the morning of the day of surgery failed to increase gastric pH. There was a reduction in the number of children with a pH < 2.5 and a volume > 0.4 ml · kg^?1 in the Omeprazole-Omeprazole and Omeprazole-Placebo Groups compared with the Placebo-Placebo or Placebo-Omeprazole Groups. Oral omeprazole 20 mg administered on the night prior to surgery will improve the gastric environment at the time of induction of anaesthesia, thus reducing the potential risk of pneumonitis, should the aspiration of gastric contents occur following the induction of anaesthesia. These data also suggest that this drug, when administered in a single dose of approximately 1.0 mg · kg^?1 three hours before surgery, is ineffective in increasing gastric fluid pH to > 2.4.     

Lansoprazole reduces preoperative gastric fluid acidity and volume in children

The purpose of this study was to explore the efficacy of lansoprazole, a proton pump inhibitor, in reducing the acidity and volume of gastric aspirate in children immediately following the induction of anaesthesia. One hundred healthy in-patients aged 3–11 yr undergoing elective surgery were randomly allocated to four groups (n = 25 each): lansoprazole-lansoprazole, placebo-placebo, placebo-lansoprazole, and lansoprazole-placebo. For each treatment regimen, the first medication was administered at 9:00 pm on the night before surgery and the second at 5:30 am on the morning of the day of surgery (three hours preoperatively). The dose of lansoprazole was 30 mg (approximately 1.4 mg · kg^?1 mean). Children were offered 10 ml · kg^?1 apple juice three hours before induction of anaesthesia. After induction of anaesthesia and tracheal intubation, gastric fluid was aspirated through a large-bore, multiorifice orogastric tube and analyzed for pH and total fluid volume. Lansoprazole increased gastric fluid pH and decreased gastric fluid volume regardless of whether it was administered before or after placebo. Two consecutive doses of lansoprazole was the most effective means of increasing the pH and reducing the volume of gastric aspirate; in this group, there were no subjects with gastric aspirate volume >0.4 ml · kg^?1 and pH <2.5. Oral lansoprazole, at least 30 mg, given on the night before surgery or on the morning of surgery will improve the gastric environment at the time of induction of paediatric anaesthesia. The most effective regimen was two doses (at bedtime and on the morning) of lansoprazole.     

Preoperative anxiety and volume and acidity of gastric fluid in children

Forty-three patients aged 3-6 years, undergoing minor surgery were studied. Parents staying with their children were asked to evaluate the anxiety of their children and themselves by a visual-analogue scale the night before surgery (VAS-N) and just before premedication in the morning (VAS-M). After induction, gastric fluid was collected and the volume and pH were measured. Patients with a VAS-M lower than 5 were considered the low-anxiety group (L-group; n=24) and the remainder comprised the high-anxiety group (H-group; n=19). The gastric volume of the H-group was significantly lower than that of the L-group. No difference was found in pH. A significant overall correlation of VAS-N was found between patients and their parents. These results suggest that the low level anxiety of children and their parents could not reduce the volume and acidity of gastric fluid and consequently the risk of aspiration pneumonia.     

Does preoperative anxiety influence gastric fluid volume and acidity?

Preoperative anxiety may increase gastric fluid acidity and volume. To pursue this possibility we evaluated the relationship between peroral premedication, preoperative anxiety, and gastric content in 246 consecutive patients presenting for elective gynecologic surgery. All patients fasted overnight and received either flunitrazepam 1 mg, oxazepam 25 mg, or placebo with 20 mL of water on the morning of surgery in a randomized, double-blind fashion. The patients assessed relief of anxiety using a four-graded scale (excellent, good, fair, poor). Both flunitrazepam and oxazepam decreased anxiety (P less than 0.01) compared with placebo. However, no correlations between type of premedication or level of anxiety and gastric contents were found. The proportion of patients with gastric fluid volume greater than 25 mL and pH less than 2.5 was not significantly different in any of the groups studied. These results suggest that neither peroral benzodiazepine premedication nor preoperative anxiety have a clinically important impact on gastric content in patients presenting for elective gynecologic surgery.     

Cardiac apoptosis in burned rats with delayed fluid resuscitation

Clinical and experimental studies have shown that delayed fluid resuscitation postburn decreases heart function. We hypothesized that apoptosis occurs in the cardiomyocyte in this condition. To investigate this hypothesis, rats were burned, fluid resuscitation was delayed, and the integrity of cardiac genomic DNA in the burned rats was determined with an LM-PCR Ladder Assay kit. DNA fragmentation shown as DNA ladders on gels, the hallmark of apoptosis, was found in the heart tissue of these rats. In the early phase of delayed fluid resuscitation, the nuclear factor kappa B (NF-kappa B) was examined using an electrophoretic mobility shift assay and was found to be activated. In comparison with burned rats with immediate fluid resuscitation, nitric oxide levels in hearts from burned rats with delayed fluid resuscitation were significantly lower (P<0.01). These results suggest that apoptosis may be an important pathway for cardiac injury, which may result from the activation of NF-kappa B and decreased nitric oxide levels.     

Effects of pre-anaesthetic glycopyrrolate and cimetidine on gastric fluid acidity and volume in children

The effects of pre-anaesthetic glycopyrrolate and cimetidine on gastric fluid pH and volume were studied in 96 paediatric patients from ages 6 months to 12 years undergoing elective surgery. They were randomly allocated into six groups with 16 patients in each group. Patients in group I received neither glycopyrrolate nor cimetidine and served as controls. Group II patients received glycopyrrolate, 5 micrograms kg-1 intramuscularly in a.m. Patients in group III received cimetidine 5 mg kg-1 orally in a.m. Group IV patients received cimetidine 5 5 mg kg-1 orally in a.m. and glycopyrrolate 5 micrograms kg-1 in a.m. Patients in group V received cimetidine 5 mg kg-1 orally h.s. and a.m. Group VI patients received cimetidine as in group V and also received glycopyrrolate as in group II. Patients with gastric pH 2.5 or less and volume of gastric contents 0.4 ml kg-1 or greater were defined to be at risk of pulmonary damage if aspiration should occur. The patients in the control group had a mean gastric pH of 1.91 +/- 0.074 and mean gastric volumes of 0.52 +/- 0.06 ml kg-1. Ninety-four per cent of patients in this group had gastric pH less than or equal to 2.5 and 69% of patients had gastric volumes greater than or equal to 0.4 ml kg-1. Glycopyrrolate (group II) reduced patients with pH less than or equal to 2.5 to 50% and volumes greater than or equal to 0.4 ml kg-1 to 44%. Cimetidine markedly reduced both gastric acidity (gastric pH less than or equal to 2.5 in 0-13% of patients in groups III-VI) and gastric volume (greater than or equal to 0.4 ml kg-1 in 19-38% of patients in groups III-VI). Only a maximum of 13% of the patients presented with combination of both risk factors in groups III-VI.(ABSTRACT TRUNCATED AT 250 WORDS)     

胆汁内引流对梗阻性黄疸大鼠胃黏膜的保护作用及机制

目的：探讨不同胆汁引流方式对梗阻性黄疸（OJ）大鼠肠黏膜的影响及机制。 方法：将80只SD大鼠随机均分为假手术组、OJ模型组（模型组）、OJ模型+胆汁内引流组（内引流组）;OJ模型+胆汁外引流组（外引流组）。实验共2周,结束时,处死各组大鼠,观察胃黏膜形态学变化,检测血清内毒素、内皮素1（ET-1）,胃黏膜ET-1、内皮素受体A（ET-A）mRNA表达。 结果：除假手术组外,各组大鼠均有不同程度的胃黏膜损伤,但内引流组的损伤情况明显较模型组与外引流组为轻;与假手术组比较,模型组和外引流组大鼠血清内毒素、ET-1和胃黏膜ET-1水平和ET-A mRNA表达明显升高,差异均有统计学意义（均P<0.05）,内引流组以上指标轻度升高,差异无统计学意义（均P>0.05）。 结论：胆汁内引流对OJ大鼠胃黏膜有保护作用,机制可能与其降低ET-1水平和ET-A的表达有关。

     

不同营养支持途径对烧伤大鼠肠黏膜损伤和修复的影响

目的 探讨不同营养支持途径对大鼠烧伤后肠黏膜损伤和修复的影响及其可能的机制。方法 采用30％TBSAⅢ度烧伤大鼠模型,随机分成伤前对照组(C),静脉营养组(PN)及肠道营养组(EN)。EN和PN组给予等氮、等热卡、等体积的营养液,观察肠组织中肠三叶因子(intestinal trefoil factor,ITF)含量、血浆二胺氧化酶(DAO)活性、肠黏膜跨膜电位差(PD)及增殖细胞核抗原(PCNA)的变化,并进行相关分析。结果 烧伤后肠黏膜组织结构受损,血浆DAO活性明显高于伤前,而PD、PCNA值及ITF含量均明显低于伤前。两组相比,EN组大鼠肠道受损程度明显低于PN组,同时其ITF含量、PD、PCNA值均高于PN组,而DAO活性显低于PN组。相关分析显示,ITF含量同血浆DAO活性呈显负相关,而与PCNA及PD值呈显正相关。结论 严重烧伤后肠黏膜结构受损与肠道合成和分泌ITF的能力大幅下降有关,肠道营养减轻伤后ITF的程度可能是在减轻肠黏膜损伤,促进肠黏膜修复方面优于静脉营养。     

Fluoride absorption: the influence of gastric acidity

The influence of gastric acidity on the absorption of intragastrically administered fluoride was investigated in rats. Intact animals were pretreated with atropine or cimetidine to reduce gastric acid secretion or were given fluoride in NaHCO3 to reduce the acidity of the gastric contents. Compared with pentagastrin-treated animals or animals that received fluoride in 0.1 N HCl, their rate of fluoride absorption was markedly reduced as judged by lower plasma fluoride concentrations and areas under the time-plasma concentration curves, especially during the first hour after dosing. In crossover studies with the stomachs isolated in situ, fluoride absorption was at least 50% faster from a pH 2.1 buffer compared with its absorption from a pH 7.1 buffer. The findings are consistent with the hypothesis that fluoride is absorbed from the gastric lumen principally as the undissociated molecule, HF. The results may contribute to a more complete understanding of acute fluoride toxicity, the development of dental fluorosis and, perhaps, the use of fluoride in the treatment of osteoporosis.     

Effects of cerebrospinal fluid acidity on cerebral blood flow and autoregulation in rats

Using a ventriculocisternal perfusion method, the effects of cerebrospinal fluid (CSF) acidity of nonrespiratory origin on cerebral blood flow (CBF) and autoregulation of CBF were investigated. Three groups (six rats each) were studied: one group of sham operated rats, one control group with ventriculocisternal perfusion at normal pH (mean inflow pH +/- SD, 7.42 +/- 0.02), and one experimental group with ventriculocisternal perfusion at low pH (mean inflow pH +/- SD, 6.81 +/- 0.01). CBF was measured by the intracarotid xenon 133 method. Autoregulation was studied by repetitive measurements of CBF during an initial increase and then stepwise reduction of mean arterial blood pressure (MABP). No difference in CBF was found between sham operated and control rats with unperturbed pH (mean cisternal outflow pH +/- SD, 7.42 +/- 0.03) of CSF), and autoregulation was intact in both groups. In the experimental group, the mean CBF +/- SD was increased by 58%, from 127 +/- 33 mL/(100 g.min) before ventriculocisternal perfusion to 201 +/- 54 mL/(100 g.min) (P <.00001) during perfusion with acid CSF (mean cisternal outflow pH +/- SD, 7.23 +/- 0.04). In this group, the relationship between CBF and MABP was linear, thus indicating disrupted autoregulation. In conclusion, CSF acidity significantly increases CBF and impairs autoregulation of CBF.     

Protective effect of pentoxifylline on gastric mucosa

Pentoxifylline (PF) has been shown to increase tissue oxygen tension. This study was performed to determine if PF has a protective effect on the gastric mucosa against alcohol (EtOH)-induced injury. Fasted Sprague-Dawley rats were pretreated with randomized test solution (control, normal saline, or PF, 75 mg/kg) intraperitoneally (ip). At 30 min, 100% EtOH (pH 8.5) was given intragastric. At 90 min, laparotomy was performed and gastric serosal stomach surface oxygen tensions (pO2) were measured. Stomachs were excised and opened and pH was measured. Photographs were taken and sections were obtained for histologic analysis to determine mucosal injury. The PF-pretreated rats had significantly higher serosal pO2 and significantly lower intragastric pH than control animals. There was significantly less gross and histologic mucosal injury in PF-treated animals. We conclude that PF is protective against EtOH gastric mucosal injury. This effect correlates with increased gastric serosal pO2 and is likely due to improved microcirculatory blood flow following PF administration.     

术前静脉输注不同剂量泮托拉唑钠对患者术中胃液酸度的影响

目的 评价术前静脉输注不同剂量泮托拉唑钠对患者术中胃液酸度的影响.方法 择期外科手术患者60例,随机分为3组(n=20),生理盐水组(N组)入室后于15 min内静脉输注生理盐水100ml,P1组和P2组分别静脉输注泮托拉唑钠40和80 mg(用生理盐水稀释至100 ml).给药后15 min进行麻醉诱导.分别于给药前(基础状态)、给药后1 h、2 h和术毕时抽取胃液,测定pH值.记录术后24 h内头晕、恶心、呕吐和腹泻等不良反应的发生情况.记录术后2周内应激性溃疡的发生情况.结果 与N组比较,P1组和P2组胃液pH值升高,P2组胃液pH值≤2.5发生率和应激性溃疡发生率降低(P＜0.05).各组间不良反应发生率差异无统计学意义(P＞0.05).结论 术前静脉输注泮托拉唑钠40 mg可提高术中胃液的pH值,有助于降低应激性溃疡的发生和误吸导致肺损伤的危险.     

Omeprazole-induced hypergastrinemia: role of gastric acidity

The increase in gastrin caused by the gastric proton pump inhibitor, omeprazole, is presumably related to inhibition of gastric acid secretion (GAS). We investigated omeprazole's effect on gastrin release by studying two doses of omeprazole which produced marked acid suppression. Six gastric fistula dogs received omeprazole, 3 mumole/kg, daily for 20 days and, after a rest interval of 2 months, omeprazole, 10 mumole/kg again for 20 days. Both doses of omeprazole increased gastrin levels and produced a decrease in GAS which was still significant (P less than 0.05) 3 days postfinal dose. The increase in the integrated gastrin response by omeprazole, 10 mumole, was greater than by omeprazole, 3 mumole. Omeprazole, 10 mumole, also reduced GAS and gastric acidity, and increased gastric pH more consistently than omeprazole, 3 mumole. The magnitude of the gastrin response corresponded with the degree of acid inhibition and pH increase. Therefore, the data support the hypothesis that the hypergastrinemia caused by omeprazole is dependent on gastric pH and GAS suppression.     

The acidity of the gastric juice

Data concerning the activity of the “mucoid cells” of the gastric glands were considered, and the possible influence of their secretion on the acidity of the gastric juice was discussed.     

Effect of obstructive jaundice on the electrophysiological characteristics of the gastric mucosa and gastric acid secretion in rats

To elucidate the effect of jaundice on the electrophysiological characteristics of the gastric mucosa and gastric acid secretion, gastric mucosal potential difference (PD) and gastric acid secretion were measured in rats with obstructive jaundice. Also transepithelial potential difference (TEPD), short circuit current (Isc) and transepithelial electrical resistance (Rt) were measured in the isolated gastric mucosa of rats with obstructive jaundice. Secondly, to confirm whether the alteration of these parameters were induced by jaundice and increased serum bile acids in the jaundiced rats, the effects of biliary drainage on the electrophysiological characteristics and gastric acid secretion, and the effects of bile acid (TCA) on TEPD, Isc, Rt were evaluated. PD, TEPD, Isc and gastric acid secretion were reduced in the jaundiced rats, and tended to recover after biliary drainage. TEPD and Isc were reduced significantly by TCA administration. These results suggest that active ion transport in the gastric mucosal cells and gastric acid secretion are impaired in jaundiced rats and the increased serum bile acid in jaundiced rats may cause these dysfunctions and the impaired active ionic transport function is improved by biliary drainage.     

Septic induced acute gastric erosions: the role of cimetidine.

A reproducible septic canine model closely akin to the clinical situation has been developed. Intraperitoneal instillation of four different bacteria plus canine gall bladder bile led to bacterial peritonitis, septicemia, and bleeding acute fundic gastric mucosal erosions. Intraperitoneal instillation of normal saline did not cause septicemia and acute gastric erosions did not develop. In this model oral cimetidine prevented the development of septic induced acute erosions, even though in these animals blood cultures were positive and bacterial peritonitis was present.     

The effect of laser photocoagulation on the gastric mucosa and bleeding gastric lesions: an experimental study.

An argon ion laser beam was tested experimentally with regard to its histological effect on and penetration of the gastric mucosa of the rat and man and its ability to induce haemostasis in traumatically produced gastric lesions and transected small blood vessels. Localized laser photocoagulation for periods of up to 5 minutes at 1 watt produced a coagulative necrosis of the gastric mucosa and half of the muscularis propria, but transmural necrosis required prolonged exposure. Laser phototherapy markedly reduced the bleeding time in experimental ulcers and small blood vessels, provided the superficial blood could be adequately dispersed from the direct beam of the laser.