Changes In Gastric pH Research Articles

Metabolic, Hormonal and Gastric Fluid and pH Changes After Different Preoperative Feeding Regimens

Metabolic, Hormonal and Gastric Fluid and pH Changes After Different Preoperative Feeding Regimens

Review: therapeutic drug monitoring in pediatrics.

Therapeutic drug monitoring (TDM) can be defined as the measurement of drug concentrations in biologic fluids to assess whether they correlate with the patient’s clinical condition and whether the dosage or dosage intervals need to be changed. This is done to optimize the management of patients receiving drug therapy for the alleviation or prevention of disease. Therapeutic drug monitoring is a relatively new service in the clinical pharmacology and toxicology laboratory and has evolved from being a luxury to a necessity. The principles of TDM were developed in the 1960s. Advances in research and knowledge and increasingly sophisticated laboratory methods led to an expansion of TDM (1–3). A drug must meet the following criteria to be eligible for monitoring: There should be a clinically interpretable correlation between the serum drug concentration and its pharmacologic effect. This usually implies a clinically significant correlation between the serum drug concentration and its concentration in the target tissue (1). There should be a better correlation between the plasma drug concentration and the pharmacologic effect than between the drug dosage and the pharmacologic effect. A narrow margin should exist between serum concentrations that cause toxic effects and concentrations that produce therapeutic effects. The serum concentration resulting from a given drug dose is unpredictable as a result of inter- and intraindividual differences in drug absorption, distribution, and elimination. Such poor correlation between serum concentration and drug dosage has been shown with clomipramine used in treatment of enuresis (2). The pharmacologic effects of drugs are not readily measurable (e.g., suppression of seizure activity is difficult to monitor clinically when administering anticonvulsant drugs). There must be a rapid and reliable method for the analysis of the drug. The criteria for monitoring drugs in children are the same as those for adults (6), but several additional factors must be considered. Neonates, infants, and children undergo major and rapid age-related physiologic and biochemical changes, especially during the first year of life, resulting in different clinical pharmacokinetic and pharmacodynamic parameters from adults (Table 1). Recent indications are that approximately 12% of all drugs prescribed in the United States are for children age 9 years and younger (4). Further, review of drug-dosing habits in neonatal intensive care units has shown that the average number of drugs administered to premature infants weighing less than 1,000 g varies from institution to institution but is usually in the range of 15 to 20 drugs; infants weighing more than 2,500 g usually receive 4 to 10 drugs during their hospital stay. Obviously, drug concentrations in many of these patients need to be monitored by the laboratory, and the possibility of drug interactions needs to be considered. Thus, it is important to have a clear understanding of not only the principles of TDM but also the additional factors inherent in and specific to pediatric clinical pharmacology. Table 1 Pharmacokinetic parameters of drugs commonly used in children When administering drugs to children, age-related differences in drug absorption, distribution, metabolism, and clearance should be taken into account to optimize drug efficacy and to avoid toxicity. There are major differences not only between adults and children but also between neonates and pre- and postpubertal children. The following are some important differences between adults and children: Changes in gastric pH and gastric emptying time during the neonatal period lead to variation in the absorption of many drugs. Differences in body composition (neonates are composed of less body fat and more water) lead to differences in the apparent volume of distribution between neonates, children, and adults (Table 2). Table 2 Some factors affecting drug distribution and disposition Slow total drug clearance in premature infants and neonates is due to immature hepatic and renal function. Immaturity of the hepatic microsomal enzyme system produces slow biotransformation of many drugs in premature infants and neonates, requiring a lower mg/kg dosage to achieve therapeutic concentrations. Greater microsomal enzyme activity in prepubertal children than in postpubertal children and adults necessitates a higher mg/kg dosage to achieve similar serum concentrations of some drugs.

Gastric tonometry and direct intraabdominal pressure monitoring in abdominal compartment syndrome

Background/Purpose: Abdominal compartment syndrome (ACS) may complicate abdominal closure in patients with abdominal wall defects, abdominal trauma, intraperitoneal bleeding, and infection. Increased intraabdominal pressure (IAP) leads to respiratory compromise, organ hypoperfusion, and a high mortality rate. This study evaluates the efficacy of continuous direct monitoring of IAP and gastric tissue pH in detecting impending ACS. Methods: Ten mongrel puppies weighing 2.8 to 6.4 kg underwent general endotracheal anesthesia, placement of an intraabdominal inflatable balloon to simulate ACS and a Swan-Ganz catheter to measure direct IAP. A gastric tonometer, nasogastric tube, foley catheter, and arterial catheter also were inserted. Half-hourly inflation's of the intraabdominal balloon were used to simulate the development of ACS. Direct intraabdominal (IAP), gastric (GP), bladder (BP), and peak airway pressures (PAP) were measured. Gastric tonometry fluid and arterial blood gas levels were obtained during inflation, and the gastric tissue pH level was calculated. Data were statistically analyzed using Pearson's correlation coefficients. Results: Baseline pressures were 2 to 5 cm H2O in the stomach and bladder catheters, 1 to 3 mm Hg in the intraabdominal catheter, and correlated with a gastric tissue pH level of 7.4. Significantly high correlation coefficients (cc) were observed between IAP versus BP (cc, 0.77; P <.002). IAP versus GP (cc, 0.79; P <.002) and IAP versus PAP (c, 0.83; P <.0004). A high negative correlation coefficient was noted between gastric pH and IAP (cc, 0.61; P <.026). The pH level dropped to 7.0 with BP and GP of 20 cm H2O and IAP of 10 mm Hg, to 6.8 at 30 cm H2O and 20 mm Hg, and 6.5 at 40 cm H2O and 30 mm Hg, respectively. However, correlation coefficients between gastric tissue pH and BP, GP, or PAP were not significant. Conclusions: These data suggest that continuous direct intraabdominal pressure monitoring is a simple and effective method that correlates well with indirect bladder or gastric pressure measurement. Changes in gastric tissue pH in association with increased intraabdominal pressure may be an early indicator of impending abdominal compartment syndrome. These observations indicate that these techniques may be more sensitive than current methods of indirect measurement, which may be associated with delayed recognition of ACS. J Pediatr Surg 37:214-218. Copyright © 2002 by W.B. Saunders Company.

Changes in gastric intramucosal pH and circulating blood volume following coronary artery bypass grafting.

To determine the changes in gastric intramucosal pH (pHi) following coronary artery bypass grafting (CABG) in comparison with systemic hemodynamic variables and circulating blood volume (BVc). Twenty patients who underwent CABG under mild hypothermic cardiopulmonary bypass (CPB) were included. Hemodynamic variables and the values of pHi were obtained at 3,6, 12 and 24 hr after admission to the intensive care unit (ICU). The pHi was measured by gastric tonometric catheter. The BVc was measured by carbon monoxide (CO)-labeled hemoglobin (CO-Hb) dilution method (CO method) at 6 and 24 hr after ICU admission. Systemic vascular resistance index (SVRI) and pulmonary vascular resistance index (PVRI) decreased with time. Systemic oxygen delivery index (DO2I) and systemic oxygen consumption index (VO2I) showed a gradual increase during the study period. By contrast, pHi decreased to the lowest value (7.26+/-0.05) at six hours and returned to normal levels (7.34+/-0.04) at 24 hr after ICU admission. Changes in BVc between six and 24 hr ranged from -242 ml to 978 ml (mean, 334+/-338 ml). The pHi increased in patients whose BVc increased by > 300 ml. Mean fluid balance was negative in this period (-386+/-667 ml; range, -1786 - + 423 ml). The pHi showed the lowest value at six hours and returned to normal at 24 hr after ICU admission. The pHi increased with the decrease in vascular resistance and with the increases in BVc in this period. The improvement of pHi, an indicator of splanchnic perfusion, appears to be related to systemic vasodilatation and an increase in BVc.

Gastric mucosal pH and blood flow during weaning from mechanical ventilation in patients with chronic obstructive pulmonary disease.

To determine if gastric intramucosal pH changes during weaning from mechanical ventilation are related to gastric mucosal blood flow modifications, we studied 16 ventilator-supported patients with chronic obstructive pulmonary disease (COPD) who tolerated a 2-h trial of spontaneous breathing with pressure support ventilation and were successfully extubated and 11 patients with COPD who failed such a trial. Gastric mucosal perfusion was assessed using gastric intramucosal pH (pH(i)) by tonometry and laser-Doppler flowmetry. During the weaning attempt, the failure weaning group developed a rapid, shallow breathing pattern with acute respiratory acidosis. The pH(i) was lower and gastric intramucosal PCO(2) (PCO(2)im) was higher in the failure weaning group than in the successful weaning group (p < 0.05). No change in gastric intramucosal-arterial PCO(2) difference was observed and a linear correlation was found between arterial PCO(2) and PCO(2)im (r(2) = 0.70; p < 0.001). Cardiac index increased in the failure group (p < 0.05) and remained stable in the success group whereas gastric mucosal blood flow decreased in the failure group (H(120) (min): -22 +/- 11% from baseline; p < 0.05) and increased in the success group (H(120) (min): 85 +/- 27% from baseline; p < 0.05). We conclude that gastric intramucosal pH changes during a 2-h weaning trial are mainly due to arterial PCO(2) variations. Nevertheless, gastric mucosal blood flow changes do occur and differ according to the weaning success or failure.

Is Pediatric Labeling Really Necessary?

Labeling refers to the label on the drug container and all printed materials, including the package insert, that accompanies the product. Labeling of a drug indicates that there is substantial evidence from adequate and well controlled clinical trials for the safe and effective use of that drug. Labeling provides important information on clinical pharmacology, indications and usage, contraindications, precautions, adverse effects, dosage, and administration. Unfortunately for children, most drug labeling contains the precautionary disclaimer, because safety and efficacy in children have not been established. The availability of safe and effective drugs has been directly responsible for the improvement in health over the past 50 years. Children essentially have been excluded from the benefit of the many therapeutic advances that have marked pharmaceutic drug development. The failure to include children in clinical trials during drug development leads to delay in implementing potentially effective treatment. Most US food and Drug Administration-approved drugs lack approval for use in all children or are restricted to certain pediatric age groups, primarily older children.1 Only a few of the new drugs released in this country each year are approved for use in children. This lack of information on the safe and effective use of drugs in the most vulnerable patients, infants and neonates, is of greatest concern. Only five of the 80 most frequently used drugs have been approved for use in this population. Another problem is that most drugs are not available in suitable pediatric dosage forms. They are not available in appropriate dosage sizes, lack liquid formulation, and taste peculiar to the child, making compliance difficult. Pharmacies extemporaneously prepare many drugs in liquid dosage forms for use in children. These dosage forms are not sufficiently tested to determine stability, efficacy, or expiration dating. For solid dosage forms, parents often must divide adult tablets …

Changes in Gastric Intramucosal pH following Mesenteric Traction in Patients Undergoing Pancreas Surgery

Background/Aim: During major abdominal surgery, mesenteric traction (MT) may result in hemodynamic instability mainly due to endogenous prostacyclin release. Gastric intramucosal pH (pHi) and PiCO₂ are indicators of splanchnic tissue perfusion with a predictive value for the postoperative outcome. We investigated the influence of MT on gastric pHi and on postoperative outcome in patients undergoing pancreas surgery. Methods: Forty-six consecutive patients scheduled for pancreas surgery were investigated. We registered hemodynamics and pHi by gastric tonometry and documented postoperative outcome (complications, hospital stay). Baseline data (T0) were recorded after skin incision. Further assessments followed 30, 60 and 120 min after intentional MT (T1–3) and at the end of surgery (T4). Results: Thirty-three patients demonstrated a decrease in mean arterial pressure (MAP) following MT, whereas 13 patients showed entirely stable hemodynamics. The significant reduction in MAP in patients with an MT response was not associated with changes in pHi as compared to patients with no response (stable MAP) (T0 7.34 ± 0.08 vs. 7.35 ± 0.06; T1 7.34 ± 0.05 vs. 7.32 ± 0.07; T2 7.32 ± 0.05 vs. 7.31 ± 0.08; T3 7.32 ± 0.05 vs. 7.32 ± 0.07; T4 7.26 ± 0.1 vs. 7.27 ± 0.08; mean ± SD, MT response vs. no response). Neither MT response nor gastric intramucosal acidosis as evidenced by a pHi <7.32 at the end of surgery predicted postoperative complications or longer hospital stay. Conclusion: No deterioration of gastric pHi was found, which could reflect acceptable splanchnic perfusion and oxygenation despite systemic blood pressure reactions in patients experiencing an MT response.

Omeprazole induces altered bile acid metabolism

Background—It has been reported that the acidity of gastric contents could be an important factor in regulating jejunal flora.Aims—To investigate the effects of omeprazole induced changes in gastric pH on...

Effect of ranitidine on gastric intramucosal pH in critically ill patients

To determine whether ranitidine a) increases the values of gastric intramucosal pH (pHi) in critically ill patients, as determined by tonometry; b) reduces the variability of these measurements. Prospective, double blind, randomized, placebo-controlled study. General Intensive Care Unit of a teaching hospital. Twenty-five critically ill, mechanically ventilated patients requiring arterial catheter and nasogastric tube. Tonometer placement; blind, random administration of intravenous ranitidine (50 mg) or placebo. Tonometer saline PCO2 (PCO2i), arterial blood gases, gastric juice pH and pHi were determined immediately before, and 2, 4, 6 and 8 h after, ranitidine (12 patients) or placebo (13 patients). Ranitidine significantly increased gastric juice pH, but did not affect PCO2i or pHi; pHi was 7.34 +/- 0.14 before ranitidine, and 7.30 +/- 0.12, 7.31 +/- 0.11, 7.31 +/- 0.14 and 7.31 +/- 0.12-2, 4, 6 and 8 h, respectively, after ranitidine administration (p = 0.55). Ranitidine did not modify the coefficients of variation of PCO2i or pHi, either. No significant changes in gastric juice pH, PCO2i or pHi were observed in the placebo group. In critically ill patients, ranitidine has no effect on pHi values, and does not increase the reproducibility of pHi measurements.

Gastric intramucosal pH changes after volume replacement with hydroxyethyl starch or crystalloid in patients undergoing elective abdominal aortic aneurysm repair

Purpose : Gastric intramucosal pH (pHi), a surrogate marker of tissue oxygenation, falls following abdominal aorta aneurysm (AAA) repair. We tested the hypothesis that volume replacement with a hydroxyethyl starch solution would result in better preserved splanchnic oxygenation than would volume replacement with crystalloid solutions. Materials and Methods : This was a prospective, randomized, nonblinded study set in a university-affiliated community hospital. Thirty patients undergoing elective AAA repair were studied. Patients were randomly selected to receive intraoperative and postoperative fluid replacement with either hetastarch or crystalloid. According to the study protocol, patients could not receive in excess of 3000 mL of hetastarch. Tissue oxygenation was assessed indirectly by measuring pHi using a nasogastric tonometer. Hemodynamic, oxygenation, and pHi data were collected preoperatively, preclamp, before unclamping, at the end of the procedure and postoperatively for 24 hours. Coagulation parameters were determined preoperatively and postoperatively for 24 hours. Results : Fifteen patients were randomized to each group. There were 18 male and 12 female patients, whose mean age was 66 ± 9 years. The intraoperative fluid balance was significantly greater in the crystalloid compared with the hetastarch group (4194 ± 1500 mL v 2949 ± 1123 mL; P = .05, 95% confidence interval [CI] 23 to 2519 mL). There were no significant differences in the amount of intraoperative blood loss or postoperative transfusion requirements between the two groups. The difference between the preoperative pHi and nadir was 0.07 ± 0.03 in the hetastarch group compared with 0.13 ± 0.04 in the crystalloid group ( P = .001, CI 0.03 to 0.09). By multivariate analysis the only variable that influenced the fall in pHi was the type of resuscitation fluid IF ratio of 7.63; P = .01). There were no significant differences in hemodynamic- and oxygenation-derived variables or coagulation parameters between the two groups of patients. The length of mechanical ventilation, intensive care unit, and hospital stay was comparable between the two groups of patients. Conclusion : In patients undergoing major surgery, volume resuscitation with hydroxyethyl starch solutions may improve microvascular blood flow and tissue oxygenation.

Scorpion venom leads to gastrointestinal ischemia despite increased oxygen delivery in pigs.

Scorpion envenomation may be accompanied by metabolic acidosis even in the absence of hypoxia and cardiovascular derangement. We tested the hypothesis that venom causes ischemia of the gastrointestinal tract rather than failure of delivery of oxygen to the periphery. Repeated measures, prospective study in experimental animals. University-affiliated hospital research laboratory. In ten spontaneously breathing, intubated, sedated pigs, purified dried venom (Leiurus quinquestriatus), 0.05 mg/kg, was administered intravenously. Measurements were obtained before (baseline), and 5, 15, 30, 60, 120, 180, and 240 mins after injection. Variables measured included: mean arterial pressure (MAP), heart rate (HR), mean pulmonary arterial pressure, pulmonary artery occlusion pressure, cardiac output, stroke volume, right ventricular ejection fraction (rapid thermistor), left ventricular dimensions (echocardiography), arterial gas tensions, lactate and catecholamine concentrations, gastric interstitial mucosal pH (tonometry), as well as systemic and pulmonary vascular resistances. Within 5 mins after venom injection, there was a hyperdynamic state accompanied by significantly increased MAP (97 +/- 18 to 136 +/- 47 mm Hg, p < .0003), HR (70 +/- 12 to 121 +/- 24 beats/min, p < .00006), and cardiac output (1.88 +/- 0.35 to 2.95 +/- 0.53 L/min, p < .0003), with no change in stroke volume, or pulmonary artery occlusion pressure. Right ventricular ejection fraction increased from 38.1 +/- 4.3 to 48.6 +/- 9.0% (p < .0009) by 15 mins. No change in left ventricular function was observed. There were significant decreases in systemic vascular resistance and pulmonary vascular resistance following envenomation. Arterial and gastric mucosal pH significantly decreased from 7.40 +/- 0.04 to 7.25 +/- 0.07 (p < .0001) for arterial pH, and 7.33 +/- 0.08 to 7.17 +/- 0.13 (p < .00001) for gastric mucosal pH by 30 mins after envenomation. The decrease in arterial pH was not sufficient to account for the change in gastric mucosal pH, indicating gastric mucosal ischemia. Arterial lactate increased from 2.6 +/- 1.4 to 7.4 +/- 1.9 (p < .05 x 10(-8)). There were significant increases in serum epinephrine and norepinephrine values by 5 mins. All hemodynamic variables and catecholamine concentrations returned to baseline by 4 hrs. However, there was persistent arterial and gastric mucosal acidosis and increased lactate concentrations even at 4 hrs. Oxygen delivery remained normal or supernormal for 4 hrs following envenomation. However, despite this finding, systemic and gastric mucosal pH changes indicate impaired gastrointestinal oxygen delivery. Despite increased peripheral oxygen delivery, scorpion envenomation was associated with evidence of ischemia of the gastrointestinal tract. This association could be due to shunting of blood from metabolically active areas, possibly associated with massive catecholamine release, or a direct toxic effect of the venom on regional oxygen transport at the cellular level.

The stability of amoxycillin, clarithromycin and metronidazole in gastric juice: relevance to the treatment of Helicobacter pylori infection.

Although omeprazole is an important component in anti-Helicobacter pylori therapeutic regimes using clarithromycin, amoxycillin and metronidazole, the mechanism by which it enhances antimicrobial action is unknown. One potential explanation for this effect is increased antibiotic chemical stability resulting from gastric pH changes induced by co-administration of omeprazole. The chemical stability of clarithromycin, amoxycillin and metronidazole was investigated in aqueous solutions and in human gastric juice collected before and after a 7-day course of omeprazole. Amoxycillin, clarithromycin and metronidazole were prepared in buffered aqueous solutions of pH 1.0 to 8.0 and in gastric juice of pH 2.0 and 7.0. The gastric juice samples were obtained from fasted H. pylori-negative volunteers before and after they had received a 7-day course of omeprazole. All the samples were incubated at 37 degrees C and analysed at intervals by HPLC. Amoxycillin, clarithromycin and metronidazole were stable in aqueous solutions of pH 4.0-7.0, pH 5.0-8.0 and pH 2.0-7.0, respectively. At pH 2.0, the degradation half-lives were 19.0 +/- 0.2 h, 1.3 +/- 0.05 h and 2200 +/- 1100 h, respectively. In gastric juice samples of pH 2.0, the degradation half-lives were 15.2 +/- 0.3 h, 1.0 +/- 0.04 h and > or = 800 h, respectively. The half-lives of the drugs in the gastric juice samples of pH 7.0 were all > 68 h. The co-administration of omeprazole with amoxycillin or clarithromycin is likely to increase the chemical stability of amoxycillin and clarithromycin in gastric juice. Clarithromycin degrades rapidly at normal gastric pH (1.0-2.0) but amoxycillin and metronidazole are sufficiently stable at this pH to maintain an antibacterial concentration in the stomach.

The effect of changes in gastric pH induced by omeprazole on the absorption and respiratory depression of methadone.

The effect of omeprazole (2 mg kg-1 i.v.) on respiratory depression induced in rats by acute oral methadone administration (5 mg kg-1) was examined and compared with control animals that only received methadone. Quantitative assessments of arterial Pco2,Po2, pH, and respiratory rate were employed as criteria for evaluation. Intragastric pH was measured in each rat immediately before and 2 h after methadone. Plasma concentration of methadone was measured for 3 h. The relationship between drug effect and the systemic bioavailability of methadone, measured as the area under the plasma concentration-time curve (AUC0-180), was also evaluated. The intensity of the methadone-induced respiratory depression was significantly greater in the omeprazole group than in control rats. A significant variation (p < 0.01) in all respiratory parameters was detected from 30 to 120 min after methadone. Omeprazole caused a significant increase in methadone levels (Cmax = 156 +/- 6.5 ng mL-1 against 51 +/- 5.8 ng mL-1 in control; p < 0.05). AUC0-180 was higher (p < 0.05) after omeprazole treatment (18.6 +/- 1.4 micrograms mL-1 min) than in control (6.8 +/- 0.6 microgram mL-1 min). Two hours after treatment with omeprazole, intragastric pH values were significantly elevated (4.7 +/- 0.1 against 2.2 +/- 0.04) and continued increasing, being 6.4 +/- 0.1 at the end of the experiment. Correlation was observed between intragastric pH and the area under the effect- (respiratory depression-) time curve (r = 0.74; p < 0.001). A relationship between plasma methadone levels at 120 min and gastric pH (r = 0.92; p < 0.001) was detected. A significant correlation between the area under the effect-time curve (0-120 min) and AUC0-180 has been also observed (r = 0.90; p < 0.01). These pharmacokinetic and pharmacodynamic changes could be gastric pH dependent because they were mimicked when gastric pH was experimentally modified by bicarbonate whereas opposite results were obtained with acidic pH2 solution.

A.48 Gastric and colonic mucosal pH changes during abdominal aortic surgery — correlation with oxygen delivery and consumption

A.48 Gastric and colonic mucosal pH changes during abdominal aortic surgery — correlation with oxygen delivery and consumption

The Time Course of Gastric pH Changes Induced by Omeprazole and Ranitidine

The Time Course of Gastric pH Changes Induced by Omeprazole and Ranitidine

Gastric pH Change according to the Administration Methods of Preanesthetic Ranitidine in Surgical Patient

Gastric pH Change according to the Administration Methods of Preanesthetic Ranitidine in Surgical Patient

Measurement of gastric mucosal pH by tonometry in major abdominal surgery

To investigate whether changes in gastric intramucosal pH (pHim) occur during major abdominal surgery, and if so, to determine the relationship between classic global indices of tissue perfusion such as mean arterial blood pressure (MAP), heart rate (HR), central venous pressure (CVP), urine flow (UF) and arterial pH (pHa). Prospective descriptive study. Seven ASA2 patients undergoing major abdominal surgery. After induction of anaesthesia and endotracheal intubation, a tonometer nasogastric tube was positioned in the stomach. Measurements of tonometric PCO2 (PCO2ss), end-tidal PCO2 (PETCO2), PaCO2, bicarbonates [bicarb], pHa, MAP, HR, CVP and UF were collected at baseline (HO), and one, two, three, and 24 hours (H1, H2, H3, and H24) after the beginning of surgery. Haemodynamics did not significantly change during anaesthesia. During recovery HR increased and CVP decreased significantly. The pHim decreased significantly from 7.42 +/- 0.03 at H0 to 7.30 +/- 0.02 at H3. This was associated with a significant decrease in pHa (from 7.43 +/- 0.02 at H0 to 7.33 +/- 0.02 at H3) and in [bicarbo] from 22 +/- 1 mmol at H0 to 20 +/- 1 mmol at H3). The PaCO2 increased significantly from 33.5 +/- 1.5 mmHg at H0 to 39.5 +/- 2.8 at H3. On the other hand, pHimcorr (7.40- (pHa-pHim) and delta CO2 (PCO2ss-PETCO2) did not vary during anaesthesia. Postoperative organ failure did not occur in these patients. The pHim may decrease during anaesthesia without evidence of abnormal tissue perfusion. In order to avoid.

Comparative Effects of Liquid Antacids on Esophageal and Gastric pH in Patients with Heartburn.

This double-blind crossover trial compared the postmeal effects of single doses of liquid antacids on esophageal and gastric pH in patients with a history of heartburn. Treatment consisted of one of two antacids containing the same active components---aluminum and magnesium hydroxide---but different in vitro acid-neutralizing capacities (ANCs). The pH was assessed continually from 1 h before a refluxogenic meal to 4 h after its completion in 24 subjects who received 20 ml of Mylanta((R)) Double Strength (MYL-20: ANC = 101.6 mEq), 20 or 30 ml of Extra-Strength Maalox((R)) Plus (MA-20, MA-30: ANC = 116.2 and 174.3 mEq, respectively), or placebo (ANC = 0) in random order. Esophageal pH increased rapidly and significantly (p < 0.05) to peak values of 7.0--7.4 with antacid. The increase in mean esophageal pH values was significantly higher (p < 0.05) than placebo for 30 min with MA-20 and for at least 70 min with MYL-20 and MA-30. In contrast, gastric pH rose slowly to mean peaks of 2.9--3.1 with antacid. During this interval, only MYL-20 was associated with significant improvements (p < 0.05 versus placebo) in total number of reflux episodes and total time that esophageal pH measured >4. Thus, ANC alone is not a useful guide in predicting in vivo antacid behavior, as in this study where the antacid dose with the lowest ANC demonstrated a duration of action as long or longer than that of antacid doses with higher ANC values. The rapid, prolonged increases in esophageal pH that preceded modest changes in gastric pH strongly suggest that the lower esophagus is the primary site of antacid action for heartburn relief.

The Time Course of Gastric pH Changes Induced by Omeprazole and Ranitidine

The time-course of the effects of single-dose acid-reducing therapy in surgical patients is not known. Therefore, a prospective, randomized trial compared the effects of single-dose administration of omeprazole or ranitidine on gastric pH in 52 patients undergoing lower abdominal surgery. The two drugs were administered intravenously in random fashion after placement of a gastric electrode for continuous 24-h pH monitoring. In patients receiving omeprazole 20 mg (n = 13) and 40 mg (n = 13), gastric pH >or=to 2.5 was achieved after a median of 80 (range 15-269) min and 40 (6-102) min (P = not significant [NS]), whereas in those receiving ranitidine 25 mg (n = 13) and 50 mg (n = 13), this pH was reached after a median of 32 (15-82) and 44 (16-84) min, respectively (P = NS). Over the first 24 h postoperatively, gastric pH remained less than 2.5 for a significantly longer time (1060 min vs 611 min), and more than 4.0 for a significantly shorter time (240 min vs 780 min) after omeprazole 20 mg than after ranitidine 50 mg. There were no other significant differences among treatment groups regarding the duration of gastric pH less than 2.5, between 2.5 and 4.0, and more than 4.0. In all treatment groups, the gastric pH returned to the baseline value of < 2.0 within 18 h. We conclude that when it is desired that gastric pH be more than 4.0 for at least 3 h, a single dose of ranitidine 25 mg or 50 mg should be administered 30-45 min prior to induction of anesthesia. (Anesth Analg 1995;80:975-9)

Dobutamine-induced dissociation between changes in splanchnic blood flow and gastric intramucosal pH after cardiac surgery

Gastric intramucosal acidosis, a sign of splanchnic tissue hypoxia, is common after cardiac surgery. We tested the hypothesis that an increase in splanchnic blood flow induced by dobutamine improves splanchnic tissue oxygenation after cardiac surgery. We measured changes in gastric intramucosal pH, splanchnic blood flow and oxygen transport in response to increased systemic flow induced by dobutamine (mean 4.4 (range 3.0-7.0) micrograms kg-1 min-1) after coronary artery bypass. We studied 22 stable postoperative patients who were allocated randomly to receive dobutamine (n = 11) or to serve as controls (n = 11). Dobutamine was given also to a separate group with a low cardiac index after operation (n = 6). The end-point was to increase cardiac index by at least 25% and to exceed 2 litre min-1 m-2. Dobutamine consistently increased mean splanchnic blood flow (control 0.6 (SD 0.2) vs 0.7 (0.2) litre min-1 m-2 (P < 0.05); normal cardiac output and dobutamine 0.7 (0.2) vs 1.1 (0.4) litre min-1 m-2 (P < 0.01); low cardiac output and dobutamine 0.4 (0.1) vs 0.7 (0.1) litre min-1 m-2 (P < 0.05)) and oxygen delivery (control 102 (29) vs 111 (28) ml min-1 m-2 (ns); normal cardiac output and dobutamine 106 (27) vs 156 (47) ml min-1 m-2 (P < 0.01); low cardiac output and dobutamine 75 (21) vs 110 (26) ml min-1 m-2 (P < 0.05)) but had no effect on splanchnic oxygen consumption (control 44 (10) vs 49 (10) ml min-1 m-2 (ns); normal cardiac output and dobutamine 45 (12) vs 51 (17) ml min-1 m-2 (ns); low cardiac output and dobutamine 37 (9) vs 40 (9) ml min-1 m-2 (ns)).(ABSTRACT TRUNCATED AT 250 WORDS)