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At least 757 records · Page 42Linked to original sources
PubMed2001

Comparative efficacy of tricaine methanesulfonate and clove oil for use as anesthetics in red pacu (Piaractus brachypomus).

OBJECTIVE: To compare the anesthetic efficacy and physiologic changes associated with exposure to tricaine methanesulfonate and clove oil (100% eugenol). ANIMALS: 15 adult cultured red pacu (Piaractus brachypomus). PROCEDURE: Fish were exposed to each of 6 anesthetic concentrations in a within-subjects complete crossover design. Stages of anesthesia and recovery were measured, and physiologic data were collected before and during anesthesia. RESULTS: Interval to induction was more rapid and recovery more prolonged in fish exposed to eugenol, compared with those exposed to tricaine methanesulfonate. The margin of safety for eugenol was narrow, because at the highest concentration, most fish required resuscitation. Mixed venous-arterial PO2 consistently decreased with anesthesia, while PCO2 consistently increased with anesthesia in all fish regardless of anesthetic agent. The increase in PCO2 was accompanied by a decrease in pH, presumably secondary to respiratory acidosis. Anesthesia was associated with increased blood glucose, potassium, and sodium concentrations as well as Hct and hemoglobin. Fish anesthetized with eugenol were more likely to react to a hypodermic needle puncture than fish anesthetized with tricaine methanesulfonate. CONCLUSIONS AND CLINICAL RELEVANCE: Anesthesia induced with tricaine methanesulfonate or eugenol contributes to hypoxemia, hypercapnia, respiratory acidosis, and hyperglycemia in red pacu. Similar to tricaine methanesulfonate, eugenol appears to be an effective immobilization compound, but eugenol is characterized by more rapid induction, prolonged recovery, and a narrow margin of safety. Care must be taken when using high concentrations of eugenol for induction, because ventilatory failure may occur rapidly. In addition, analgesic properties of eugenol are unknown.

Aminobenzoates↗
PubMed1998

Clinical course of gamma-hydroxybutyrate overdose.

STUDY OBJECTIVE: To describe the clinical characteristics and course of gamma-hydroxybutyrate (GHB) overdose. METHODS: We assembled a retrospective series of all cases of GHB ingestion see in an urban public-hospital emergency department and entered in a computerized database January 1993 through December 1996. From these cases we extracted demographic information, concurrent drug use, vital signs, Glasgow Coma Scale (GCS) score, laboratory values, and clinical course. RESULTS: Sixty-one (69%) of the 88 patients were male. The mean age was 28 years. Thirty-four cases (39%) involved coingestion of ethanol, and 25 (28%) involved coingestion of another drug, most commonly amphetamines. Twenty-five cases (28%) had a GCS score of 3, and 28 (33%) had scores ranging from 4 through 8. The mean time to regained consciousness from initial presentation among nonintubated patients with an initial GCS of 13 or less was 146 minutes (range, 16-389). Twenty-two patients (31%) had an initial temperature of 35 degrees C or less. Thirty-two (36%) had asymptomatic bradycardia; in 29 of these cases, the initial GCS score was 8 or less. Ten patients (11%) presented with hypotension (systolic blood pressure < or = 90 mm Hg); 6 of these patients also demonstrated concurrent bradycardia. Arterial blood gases were measured in 30 patients; 21 had a PCO2 of 45 or greater, with pH ranging from 7.24 to 7.34, consistent with mild acute respiratory acidosis. Twenty-six patients (30%) had an episode of emesis; in 22 of these cases, the initial GCS was 8 or less. CONCLUSION: In our study population, patients who overdosed on GHB presented with a markedly decreased level of consciousness. Coingestion of ethanol or other drugs is common, as are bradycardia, hypothermia, respiratory acidosis, and emesis. Hypotension occurs occasionally. Patients typically regain consciousness spontaneously within 5 hours of the ingestion.

Adjuvants, Anesthesia↗
PubMed2006

Predictors of hospital outcome and intubation in COPD patients admitted to the respiratory ICU for acute hypercapnic respiratory failure.

BACKGROUND: Mortality rate, the possible factors affecting mortality and intubation in patients with acute exacerbation of chronic obstructive pulmonary diseases (COPD) and hypercapnic respiratory failure (RF) are yet unclear. OBJECTIVE: To identify the possible factors affecting mortality and intubation in COPD patients. DESIGN: A prospective study using data obtained over the first 24h of respiratory intensive care unit (RICU) admission. Consecutive admissions of 656 patients were monitored and 151 of them who had acute exacerbation of COPD and hypercapnic RF were enrolled. SETTING: University hospital, Department of Chest Diseases, RICU. RESULTS: Mean age was 65.1 years. The mean APACHE II score was 23.7. Eighty-seven patients (57.6%) received mechanical ventilation (MV) via an endotracheal tube for more than 24 h. Twenty-two patients received non-invasive ventilation (NIV). Fifty patients died (33.1%) in hospital during the study period. The mortality rate was 52.9% in patients in need of MV. In the multivariate analysis, the need for intubation, inadequate metabolic compensation for respiratory acidosis, and low (=bad) Glasgow Coma Score (GCS) were determined as independent factors associated with mortality. The low GCS (OR: 0.61; CI: 0.48-0.78) and high APACHE II score (OR: 1.24; CI: 1.11-1.38) were determined as factors associated with intubation. CONCLUSION: The most important predictors related to hospital mortality were the need for invasive ventilation and complications to MV. Adequate metabolic compensation for respiratory acidosis at admittance is associated with better survival. A high APACHE II score and loss of consciousness (low GCS) were independent predictors of a need to intubate patients.

Adult↗
PubMed1994

Increased red cell osmotic fragility and hematocrit after hyperbaric O2 exposure are related to acidosis.

Exposure to hyperbaric O2 (0.6 MPa) until convulsion occurred resulted in increased red blood cell osmotic fragility, increased hematocrit, and acidosis. Correction of the mixed metabolic and respiratory acidosis in arterial blood samples completely restored osmotic fragility and lowered hematocrit by 20%. Rats exposed to intermittent hyperbaric O2 (repeated cycles of 7 minutes of O2 and 7 minutes of air) tolerated significantly more O2 time than those exposed continuously. Intermittently exposed animals had smaller increases in osmotic fragility and less-severe acidosis. We verified the influence of pH on osmotic fragility and hematocrit in rats made acutely acidotic and corrected in vivo. Acidosis caused by CO2 inhalation and lactic and hydrochloric acid infusion raised osmotic fragility and hematocrit; these effects were completely reversed in the animal when we restored normal acid-base status. These studies demonstrate that conditions causing acidosis, including hyperbaric O2 exposure, increase red cell fragility and size and increase hematocrit.

Acidosis↗
PubMed1997

In vivo diaphragm metabolism: comparison of paced and inspiratory resistive loaded breathing in piglets.

OBJECTIVE: We hypothesized that spontaneous, loaded diaphragm contractions would lead to diaphragm fatigue, which would correlate with inadequate oxidative metabolism as measured by phosphorus-31 nuclear magnetic resonance spectroscopy. DESIGN: Prospective, randomized, crossover trial. SETTING: University hospital research laboratory. SUBJECTS: Eight piglets, 4 to 6 wks of age. INTERVENTIONS: Each animal underwent, in random order, a 20-min period of diaphragm pacing and a 45-min period of loaded spontaneous breathing, separated by a 20-min recovery period. Mechanical ventilation was used during diaphragm pacing to maintain a PaCO2 of 35 to 45 torr (4.7 to 6.0 kPa) and a PaO2 of > 100 torr (> 13.3 kPa). During spontaneous breathing, inspiratory loading was achieved with a 2.0-mm inner diameter endotracheal tube in the breathing circuit. MEASUREMENTS AND MAIN RESULTS: During pacing, mean transdiaphragmatic pressure decreased by 35%, from 23 +/- 5 (SD) to 15 +/- 3 mm Hg (p < .05), and this decrease correlated with a 335% increase in the ratio of inorganic phosphate to phosphocreatine, from 0.23 +/- 0.1 to 1.0 +/- 0.7 (p < .05). During loaded spontaneous breathing, arterial pH decreased from 7.42 +/- 0.06 to 7.25 +/- 0.05 (p < .05), secondary to an increase in PaCO2 from 41 +/- 4 to 65 +/- 11 torr (5.3 +/- 0.5 to 8.7 +/- 1.5 kPa) (p < .05). Despite respiratory acidosis, there was no decrease in trandiaphragmatic pressure during the period of loaded breathing, nor was any change in the ratio of inorganic phosphate to phosphocreatine seen. CONCLUSIONS: Diaphragm fatigue in a pacing model correlates with inadequate oxidative metabolism. In contrast, severe inspiratory resistive loaded breathing did not result in changes in oxidative metabolism or decreased diaphragm force output, despite hypercapnia and respiratory acidosis.

Adenosine Triphosphate↗
PubMed1977

Effects of small-particle aerosols of rimantadine and ribavirin on arterial blood pH and gas tensions and lung water content of A2 influenza-infected mice.

The respiratory pathophysiology of A2 influenza infection was studied in mice treated with small-particle aerosols (SPA) of rimantadine or ribavirin. Untreated infections in mice resulted in survival rates of 15% or less and were characterized by (i) severe hypoventilation (decreased P(O2) and increased P(CO2)), (ii) compensated respiratory acidosis (increased P(CO2) and HCO(3) (-), with normal pH), (iii) pneumonia with increased ratio of wet/dry lung weight, and (iv) hypothermia. Treatment with SPA of rimantadine (21 mg/kg per day for 4 days) beginning 72 h after virus challenge significantly improved survival rate (80%) but failed to alter lung pathology from that found in infected, untreated mice. Rimantadine treatment decreased somewhat the severity of hypoventilation, respiratory acidosis, lung wet weight, hypothermia, and lung virus titers from that observed in infected, untreated mice. SPA of ribavirin (26 mg/kg per day for 4 days) initiated 6 h after SPA exposure of mice to virus significantly improved survival rate (95%) and reduced lung virus titers and lung pathology. Gas exchange and pulmonary edema in ribavirin-treated, infected mice were significantly improved over those of infected, untreated controls. The mechanisms for increased survival rates induced by SPA of rimantadine remain uncertain, since increased survival rates could not be ascribed entirely to improvements in lung functions. In contrast, however, ribavirin treatment appeared to improve survival rates by reducing major lung pathology and pulmonary dysfunction. This was probably mediated through the antiviral effects of ribavirin.

Adamantane↗
PubMed1996

Idiopathic pulmonary hemorrhage in infancy. Clinical features and management with high frequency ventilation.

STUDY OBJECTIVES: To describe the clinical characteristics of infants with severe acute pulmonary hemorrhage and the effects of mechanical ventilation on gas exchange. SETTING: Tertiary care pediatric ICU in a university hospital. PATIENTS AND DESIGN: Case records of patients with severe acute pulmonary hemorrhage from January 1992 to July 1995 were reviewed. Acute pulmonary hemorrhage was defined as hemoptysis and/or epistaxis or blood obtained from endotracheal tube which could not be attributed to cardiac or vascular malformation, infectious process, or known trauma. INTERVENTIONS: Patients were initially managed with conventional ventilation. High frequency ventilation (HFV) was utilized when hypoxemia (PaO2/PAO2 < 0.2) and/or respiratory acidosis (PaCO2 > or = 60 mm Hg with pH < 7.25) persisted. MEASUREMENTS AND RESULTS: Six African-American male infants from Detroit, with a median age 2.3 months, presented with severe acute pulmonary hemorrhage. Chest radiographs showed diffuse bilateral infiltrates or opacification with a normal sized heart. All infants were managed with HFV, four by oscillation and two by jet. The indications for HFV were persistent hypoxemia (2), respiratory acidosis (1), and a combination of both (3). There was an improvement in pH and PaCO2, and a decreased need for oxygen 6 and 24 h after initiating HFV. PaO2/PAO2 and oxygenation index showed a tendency toward improvement. All infants survived, and there were no complications. No cause for pulmonary hemorrhage was found in any of the infants. CONCLUSIONS: Idiopathic acute pulmonary hemorrhage is a potentially life-threatening disorder encountered among inner-city infants. HFV is highly effective and safe in rapidly reversing the severe oxygenation and ventilation deficits in this setting.

Acute Disease↗
PubMedDate not supplied

The cardiovascular response of sheep to tiletamine-zolazepam and butorphanol tartrate anesthesia.

Butorphanol tartrate (0.5 mg/kg intravenously [IV]) was administered to six ewes (group 1), 10 minutes before administration of tiletamine-zolazepam (12 mg/kg IV). In six ewes (group 2), butorphanol tartrate and tiletamine-zolazepam were administered simultaneously. Time of administration of butorphanol did not alter hemodynamics or duration of anesthesia significantly. Anesthesia was adequate for 25 to 45 minutes (mean, 31 min) in group 1. The sheep in group 2 were anesthetized effectively for 25 to 50 minutes (mean, 39 min). Neither dosing regimen caused significant changes in right atrial pressure, heart rate, pulmonary vascular resistance, or pulmonary capillary wedge pressure. Mean arterial blood pressure (MABP) decreased an average of 18% from baseline values of 113 mm Hg to a minimum of 84 mm Hg at minute 60 in group 1, and from 111 mm Hg to 92 mm Hg at minute 75 in group 2. The decrease was significant only for group 1. Cardiac output (CO) was significantly decreased 24% from 6.6 L/min at minute 45 in group 1, and 32% from 6.3 L/min at minute 15 in group 2. Systemic vascular resistance (SVR) was increased significantly at minute 15, 11% in group 1 and 37% in group 2. Mild respiratory acidosis was measured by significant decreases in arterial pO2 and pH and a significant increase in pCO2 without significant changes in HCO3-. Results of this study show that (1) tiletamine-zolazepam and butorphanol tartrate produce adequate anesthesia for 25 to 50 minutes; (2) the cardiovascular and anesthetic effects of the dosing schedules were similar; and (3) tiletamine-zolazepam and butorphanol result in decreased CO and MABP with a concomitant increase in SVR, and mild respiratory acidosis.

Anesthesia, Intravenous↗
PubMed1988

Time-course of blood acid-base state during arousal from hibernation in the European hamster.

1. Arterial blood was sampled at 15 min-intervals in European hamsters Cricetus cricetus fitted with indwelling catheters, from deep hibernation to full arousal. Temperature-corrected pH and PCO2, respectively pH* and P*CO2, were directly measured at 37 degrees C. 2. Deep hibernation corresponded to a respiratory acidosis: pH* = 7.01 +/- 0.01 (mean +/- SE), P*CO2 = 160 +/- 4 Torr (n = 9 animals). 3. Three periods could be distinguished in the arousal: (i) a period of hyperventilation (28 +/- 5 min), in which P*CO2 was reduced to 79 +/- 4 Torr, while cheek pouch temperature increased only by 0.9 +/- 0.2 degrees C; (ii) a period of metabolic acidification by lactate accumulation (84 +/- 6 min), corresponding to the period of peak thermogenesis; (iii) a progressive return to euthermic conditions (104 +/- 10 min), by simultaneous respiratory and metabolic alkalinization. 4. Over 60% of the blood CO2 stores accumulated at the beginning of the hibernation bout were released by hyperventilation during the first period, prior to the full development of thermogenesis. This is in agreement with the hypothesis of an inhibitory role of the respiratory acidosis in hibernation.

Acid-Base Equilibrium↗
PubMed1993

Acute asphyxia affects neutrophil number and function in the rat.

OBJECTIVES: Previous studies in adults suggest that various types of physiologic stress appear to decrease phagocytic cell function. Adherence and chemotaxis of, and phagocytosis and bacterial killing by, neonatal neutrophils are altered compared with adult neutrophil function. Stresses encountered by the fetus and neonate, such as asphyxia, were hypothesized to further alter neonatal neutrophil function. To investigate the impact of asphyxia on systemic immunity, we developed a rat model of acute asphyxia and evaluated the effect of asphyxia on neutrophil number and function. DESIGN: Prospective, laboratory study. SETTING: Research laboratory. SUBJECTS: Adult female Wistar rats. INTERVENTIONS: Exposure to CO2 and cold stress. MEASUREMENTS AND MAIN RESULTS: Arterial blood gas, blood glucose, neutrophil number, neutrophil-mediated, complement-dependent bacterial phagocytosis and killing were determined. After a 20-sec exposure to CO2 and cold stress (dry ice vapors), adult rats developed acute respiratory acidosis (pH 6.89 +/- 0.26, PaCO2 220 +/- 183 torr [29.3 +/- 24.3 kPa]), and mild hypoxia (60 +/- 20 torr [8.0 +/- 2.7 kPa]) followed by significant metabolic acidosis (base deficit = -12.0 +/- 1.5). Neutrophil number slowly increased and reached statistical significance by 72 hrs (5.0 +/- 1.5 x 10(3)/mm3) compared to controls (2.9 +/- 1.6 x 10(3)/mm3) (p = .03). Phagocytosis and killing of group B streptococci by neutrophils isolated immediately after asphyxia were significantly impaired (p = .03), and this decrease in function lasted for 24 hrs after asphyxia (p = .04), as measured by two different in vitro complement and antibody-mediated functional assays. CONCLUSIONS: After brief exposure to CO2 and cold stress, rats developed an acute respiratory acidosis and subsequent metabolic acidosis similar to acute asphyxia. Neutrophil number did not increase until 72 hrs after asphyxia. However, neutrophil-mediated phagocytosis and killing of bacteria were immediately impaired. We speculate that asphyxia may increase the risk for sepsis secondary to altered neutrophil function.

Acidosis↗
PubMed2005

Blood gas and acid-base status during tiletamine/zolazepam anaesthesia in dogs.

OBJECTIVE: To evaluate the effect of the tiletamine/zolazepam (TZ) combination (Zoletil 100; Virbac, Carros, France) with and without atropine on blood gas values and acid-base status in dogs. STUDY DESIGN: Randomized cross-over experimental study. ANIMALS: Six healthy adult cross-bred dogs, weighing 11.0-18.5 kg. MATERIALS AND METHODS: Each dog received four different drug treatments at intervals of at least 15 days: (i) 5 mg kg(-1) intravenous (IV) TZ (TZ.IV); (ii) 10 mg kg(-1) intramuscular (IM) TZ (TZ.IM); (iii) atropine, 20 microg kg(-1) IV, followed 5 minutes later by 5 mg kg(-1) TZ IV (A.TZ.IV); and (IV) atropine (same dose) given 5 minutes before 10 mg kg(-1) TZ IM (A.TZ.IM). Arterial blood samples were collected from each dog before drug administration (baseline) at induction of anaesthesia (time 0) and 2, 5, 10 and 30 minutes thereafter. RESULTS: Transient hypoxaemia and respiratory acidosis were observed just after induction. PaO(2) and SaO(2) dropped, while H(+) concentration and PaCO(2) rose significantly above baseline values. In groups TZ.IV and A.TZ.IV, PaO(2) values as low as 6.0-6.4 kPa (45-48 mm Hg) were recorded. However, there was no significant difference in blood gas variables among the groups encountered during the evaluation period. The overall change in [HCO(3) (-)] and base excess (BE) was not significant among groups. Atropine did not affect the above variables. CONCLUSIONS AND CLINICAL RELEVANCE: Tiletamine/zolazepam injection may induce transient hypoxaemia and respiratory acidosis, but acid-base status changes are clinically unimportant. Particularly, close observation of dogs is recommended during the first 5-10 minutes after induction with TZ, especially in animals with cardiopulmonary disease. TZ should perhaps not be used in animals intolerant of tachycardia.

Acidosis↗
PubMed1978

The effect of dibutyryl cyclic AMP and glucagon on the myocardial cell pH1.

DBcAMP or crystalline glucagon was utilized to elevate the intracellular cyclic AMP concentration in isolated rat hearts. Butyric acid, a metabolite of DBcAMP, was also investigated. Their effect on the intracellular pH (pHi) as determined by the distribution of [14C]DMO was investigated. Rat hearts, perfused with a recirculated modified Krebs-Henseleit solution maintained at 30 degrees C, were exposed to respiratory acidosis by bubbling the perfusate with 20% CO2. alpha- and beta-receptor antagonists were used to block the effects of endogenous catecholamines. Hypercapnia decreased the pHi from 7.09 to 6.82. A similar degree of hypercapnia decreased the pHi to only 6.95 in the presence of DBcAMP and to only 6.96 in the presence of glucagon. The effective buffer values (delta[HCO-3]i/deltapHi) were: control, 19; butyric acid, 16; DBcAMP, 139; glucagon, 148. These data suggest that cAMP mediates the effect of norepinephrine, which has been shown to diminish the change in pHi accompanying respiratory acidosis.

Acid-Base Equilibrium↗
PubMed2005

Enhancement of indomethacin-induced gastric damage by mouth breathing in rabbits.

Previous studies have reported that mouth breathing is associated with respiratory acidosis. Regarding to the reports that renal elimination of weak acids such as indomethacin is pH dependent, this study was carried out to evaluate the role of mouth breathing on plasma level of indomethacin and indomethacin-induced gastric damage in rabbits. Mouth breathing was induced by surgical ligation of nostrils under general anesthesia. One day after the operation, arterial blood samples were collected for acid-base balance analysis and indomethacin was administered intraperitoneally in a single dose of 40mg/kg. The animals were killed 4h after indomethacin administration and blood samples were collected for spectrofluorometric determination of indomethacin in plasma. The results showed that indomethacin induces more severe gastric damage in nose obstructed rabbits compared with sham and unoperated (UNOP) animals. Acid-base analysis revealed a respiratory acidosis in nose obstructed rabbits and indomethacin level of plasma was significantly higher in nose obstructed animals in comparison with control rabbits. The study shows that mouth breathing can increase the potentiation of indomethacin-induced gastric mucosal damage that may be due to higher level of indomethacin in plasma of nose obstructed animals.

Journal Article↗
PubMed2000

Heliox improves ventilation during high-frequency oscillatory ventilation in pediatric patients.

OBJECTIVE: To describe improved ventilation during high-frequency oscillatory ventilation when a nitrogen-oxygen gas mixture is replaced by a helium-oxygen gas mixture. DESIGN: Case series. SETTING: A tertiary pediatric intensive care unit. PATIENTS: Five patients with hypoxemic respiratory failure who developed persistent respiratory acidosis during treatment with high-frequency oscillatory ventilation. INTERVENTIONS: Introduction of helium-oxygen into a conventional high-frequency oscillatory ventilation circuit. MEASUREMENTS AND MAIN RESULTS: Blood gas values (pH, Pco2, and Po2) were compared in these patients during treatment with high-frequency oscillatory ventilation with nitrogen-oxygen gas flow and then for several hours after a change in treatment to helium-oxygen gas flow. An initial 24% decrease in Pco2 was documented, and an ultimate 43% decrease in Pco2 was observed. The mechanism for this improved ventilation may be related to improved gas flow properties as well as increased CO2 diffusion resulting from helium's low-mass density. Oxygenation was not adversely affected in any way. CONCLUSION: In patients with hypoxemic respiratory failure and in whom respiratory acidosis develops during high-frequency oscillatory ventilation, the use of helium-oxygen rather than nitrogen-oxygen may improve ventilation and decrease ventilator-related trauma. Further investigation is needed to validate these findings and to elucidate the mechanisms of improved ventilation.

Journal Article↗
PubMed1988

The distribution of branchial carbonic anhydrase and the effects of gill and erythrocyte carbonic anhydrase inhibition in the channel catfish Ictalurus punctatus.

Carbonic anhydrase (CA) activity was assayed in lysed erythrocytes and in branchial cytoplasm, mitochondria and microsomes of the channel catfish, Ictalurus punctatus. Branchial CA activity was highest in the cytoplasmic fraction, but activity was very low in mitochondria and microsomes. Erythrocyte CA activity was over four-fold greater than that in the gills. Intact animals were injected with the CA inhibitors acetazolamide and benzolamide. Slow, intra-arterial injection of both inhibitors elicited transient side effects of apnoea, bradycardia and hypoxaemia. Acetazolamide and benzolamide induced a mixed but primarily respiratory acidosis. The onset and the time course of the acidosis were correlated with the inhibition of erythrocyte CA; acetazolamide acted faster because it is more freely diffusible than benzolamide. The acid-base disturbance in the blood reached its maximum after 2 h; compensation was delayed until 24 h, when CA inhibition began to disappear. We conclude from these results that there is very little, if any, membrane-associated CA in the gill, and that the branchial enzyme is not quantitatively important in directly converting plasma HCO3- to CO2 for excretion. Rather, CO2 excretion is accomplished via the traditional chloride shift, followed by intracellular dehydration of HCO3- by erythrocyte CA. These results also suggest that branchial cytoplasmic CA inhibition might impair ion transport processes that are used to compensate blood acid-base disturbances and thus delay compensation of the respiratory acidosis.

Acetazolamide↗
PubMed1994

CARBONIC ANHYDRASE INJECTION PROVIDES EVIDENCE FOR THE ROLE OF BLOOD ACID-BASE STATUS IN STIMULATING VENTILATION AFTER EXHAUSTIVE EXERCISE IN RAINBOW TROUT

This study tests the hypothesis that the increase in blood PCO2 and associated respiratory acidosis after exhaustive exercise play an important role in stimulating ventilation during post-exercise recovery in fish. Injection of bovine carbonic anhydrase (10 mg kg-1) into the bloodstream of rainbow trout caused a persistent 40 % increase in the HCO3- dehydration capacity of the blood. The treatment was designed to increase CO2 excretion and therefore to reduce PCO2 build-up and acidosis after exercise. Aerobic and anaerobic swimming performance were not affected by carbonic anhydrase, and there were only very minor effects on arterial blood acid&shy;base status in resting fish. However, carbonic anhydrase attenuated post-exercise increases in PaCO2 and decreases in pHa by about 50 % without altering arterial O2 variables, red cell swelling or the intracellular pH of the brain or muscle tissues. The effects on arterial pH (pHa) resulted largely from alleviation of the increase in PaCO2. In accordance with the original hypothesis, normal post-exercise hyperventilation was greatly attenuated, through reductions in both ventilatory stroke volume and frequency, and excess post-exercise O2 consumption was reduced. Post-exercise increases in plasma levels of adrenaline and noradrenaline were also reduced by the carbonic anhydrase treatment. Overall, there was a strong correlation between increases in relative ventilation and decreases in pHa after exhaustive exercise. The results provide functional significance for the phenomenon of PaCO2 elevation and associated respiratory acidosis after exercise and are consistent with other recent studies indicating an important secondary drive to ventilation in fish based on arterial acid&shy;base status, in addition to the primary drive based on arterial O2 levels.

Journal Article↗
PubMed2000

Arterial to end-tidal carbon dioxide pressure difference during laparoscopic surgery in pregnancy.

BACKGROUND: There is controversy about whether capnography is adequate to monitor pulmonary ventilation to reduce the risk of significant respiratory acidosis in pregnant patients undergoing laparoscopic surgery. In this prospective study, changes in arterial to end-tidal carbon dioxide pressure difference (PaCO2--PetCO2), induced by carbon dioxide pneumoperitoneum, were determined in pregnant patients undergoing laparoscopic cholecystectomy. METHODS: Eight pregnant women underwent general anesthesia at 17-30 weeks of gestation. Carbon dioxide pnueumoperitoneum was initiated after obtaining arterial blood for gas analysis. Pulmonary ventilation was adjusted to maintain PetCO2 around 32 mmHg during the procedure. Arterial blood gas analysis was performed during insufflation, after the termination of insufflation, after extubation, and in the postoperative period. RESULTS: The mean +/- SD for PaCO2--PetCO2 was 2.4 +/- 1.5 before carbon dioxide pneumoperitoneum, 2.6 +/- 1.2 during, and 1.9 +/- 1.4 mmHg after termination of pneumoperitoneum. PaCO2 and pH during pneumoperitoneum were 35 +/- 1.7 mmHg and 7.41 +/- 0.02, respectively. There were no significant differences in either mean PaCO2--PetCO2 or PaCO2 and pH during various phases of laparoscopy. CONCLUSIONS: Capnography is adequate to guide ventilation during laparoscopic surgery in pregnant patients. Respiratory acidosis did not occur when PetCO2 was maintained at 32 mmHg during carbon dioxide pneumoperitoneum.

Analysis of Variance↗