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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Laparoscopic surgery has been termed minimally invasive surgery by advocates of this technology. It has been demonstrated previously that using carbon dioxide for insufflation produces a respiratory acidosis due to transperitoneal absorption of gas. Insufflation with helium does not create this acidosis. We questioned whether laparoscopic surgery would elicit a stress response and whether the absence of acidosis with helium might prevent or reduce the levels of stress hormones. Sixteen female patients undergoing laparoscopic cholecystectomy were randomly assigned to helium (n = 8) or CO2 (n = 8) insufflation. Serum cortisol, epinephrine, and norepinephrine were measured preoperatively, after induction of anesthesia but before insufflation, at 45 min of surgery, and after desufflation. There were increases in epinephrine, norepinephrine, plasma cortisol, and urine cortisol at 45 min and at the conclusion of the procedure over the preoperative value. With ANOVA, each variable showed significant increases from preoperative values, at 45 min, and at the end of the case. Except for the increased epinephrine when helium was used, there were no significant differences in the other variables between helium and CO2. Laparoscopic cholecystectomy produces significant increases in stress hormone levels. Prevention of acidosis with helium insufflation does not appear to protect against increases in stress hormones. Epinephrine levels with helium insufflation are higher than with CO2, and elevations in stress hormones suggest that laparoscopic cholecystectomy is not physiologically minimally invasive.
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PMID:Comparative stress hormone changes during helium versus carbon dioxide laparoscopic cholecystectomy. 873 46

Long-term exposure to elevated ambient CO2-levels is a common condition for living in a closed environment such as a spacecraft. In this study, the cardio-respiratory system response to CO2-levels of 0.7% and 1.2% was assessed. The response was investigated during non-REM sleep when the sensitivity of the respiratory system to ambient CO2 is low and only subject to the metabolic respiratory drive. Four subjects were exposed to 0.7% and 1.2% CO2 for 23 d each. Respiration rate and heart rate were determined for the first two phases of slow wave sleep. In addition, the occurrence of central apneas was assessed. Data were analyzed by a repeated measure ANOVA. As a response to CO2 exposure two dynamic effects were observed. Heart rate increased initially with a peak between the second and the sixth night. Over the period of the exposure, respiration rate and heart rate decreased steadily. At least two mechanisms with different time constants must be considered for this dynamic behavior: an uncompensated respiratory acidosis, followed by a phase of relative compensation. At the end of the 23-d exposure, equilibrium in the physiological state had not been reached. Though the experiment did not show severe effects from CO2, it is too early to state that a long-term exposure does not have any consequences for health and well-being.
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PMID:Joint NASA-ESA-DARA Study. Part three: cardiorespiratory response to elevated CO2 levels during sleep. 959 21

The aim of this study was to determine whether respiratory acidosis favors the cerebral distribution of cyanide, and conversely, if respiratory alkalosis limits its distribution. The pharmacokinetics of a nontoxic dose of cyanide were first studied in a group of 7 rats in order to determine the distribution phase. The pharmacokinetics were found to best fit a 3-compartment model with very rapid distribution (whole blood T(1/2)alpha = 21.6 +/- 3.3 s). Then the effects of the modulation of arterial pH on the distribution of a nontoxic dose of intravenously administered cyanide into the brains of rats were studied by means of the determination of the permeability-area product (PA). The modulation of arterial blood pH was performed by variation of arterial carbon dioxide tension (PaCO2) in 3 groups of 8 anesthetized mechanically ventilated rats. The mean arterial pH measured 20 min after the start of mechanical ventilation in the acidotic, physiologic, and alkalotic groups were 7.07 +/- 0.03, 7.41 +/- 0.01, and 7.58 +/- 0.01, respectively. The mean PAs in the acidotic, physiologic, and alkalotic groups, determined 30 s after the intravenous administration of cyanide, were 0.015 +/- 0.002, 0.011 +/- 0.001, and 0.008 +/- 0.001 s(-1), respectively (one-way ANOVA; p < 0.0087). At alkalotic pH the mean permeability-area product was 43% of that measured at acidotic pH. This effect of pH on the rapidity of cyanide distribution does not appear to be limited to specific areas of the brain. We conclude that modulation of arterial pH by altering PaCO2 may induce significant effects on the brain uptake of cyanide.
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PMID:Effects of respiratory acidosis and alkalosis on the distribution of cyanide into the rat brain. 1135 36