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PubMed1997

The optimum pneumoperitoneum pressure for laparoscopic surgery in the rat model. A detailed cardiorespiratory study.

BACKGROUND: There is increasing interest in the rat model of laparoscopic surgery. This study evaluates the cardiorespiratory effects of increasing CO2 pneumoperitoneum (PP) in the rat. METHODS: Nine Sprague-Dawley rats were subjected to CO2 PP at pressures of 2, 5, 10, and 15 mmHg or control (no PP) under anesthesia. Catheters were placed in the femoral artery and the jugular vein to measure heart rate (HR), blood pressure (MAP), and arterial pH, PCO2, PO2, and HCO3. A thermistor probe in the aortic arch measured cardiac output (CO) and blood temperature (BT). RESULTS: CO2 PP had no effect on CO, MAP, or BT at any pressure. CO2 PP greater than 5 mmHg caused significant bradycardia and CO2 PP greater than 10 mmHg caused significant respiratory acidosis. CONCLUSIONS: CO2 PP pressures above 10 mmHg in rat should be avoided when performing laparoscopic surgery in the rat model.

Analysis of Variance↗
PubMed1999

Prematurity-associated nephrocalcinosis and kidney function in early childhood.

To assess the impact of prematurity-associated nephrocalcinosis on kidney function later in life, 20 premature children with neonatal nephrocalcinosis and 20 controls, matched for birth weight and postnatal age but without nephrocalcinosis, were examined (birth weight 905+/-209 vs. 957+/-226 g; study age 4.7+/-1.1 vs. 4.6+/-0.9 years). Distal tubular acidification capacity was measured with the oral acetazolamide test, in which the response was abnormal in 1 out of the 20 children with a history of nephrocalcinosis, but in none of the controls. Urinary calcium and beta(2)-microglobulin excretion were higher in the children with nephrocalcinosis, but no differences were found in fractional excretion of sodium and potassium or tubular reabsorption of phosphate. Estimated creatinine clearance was not different between the groups. Of the 6 children with nephrocalcinosis lasting beyond 2 years of age, 5 had had chronic lung disease neonatally and exhibited a tendency for compensated respiratory acidosis at the time of the examination. Neonatal nephrocalcinosis seems to lead to some signs of renal tubular dysfunction in early childhood of preterm infants. Glomerular function, however, appears not to be specifically disturbed by nephrocalcinosis.

Calcium↗
PubMed1998

Potential pitfalls in apnea testing.

To determine the influence of baseline paCO2 on the results of apnea testing in the diagnosis of brain death, we performed an open prospective study on 36 patients fulfilling all other criteria for the diagnosis of brain death according to the criteria proposed by the Advisory Board of the German Federal Chamber of Physicians. For testing of apnea, patients underwent hypoventilation with 100% oxygen supply until a baseline paCO2 of 40 torr (5.3 kPa, n = 24, group 1) or 60 torr (8.0 kPa, n = 12, group 2) was reached. Then, patients were disconnected from the ventilator and apneic oxygenation with insufflation of 61 O2/min into the tracheal cannula was performed for five minutes. Arterial blood gas samples were obtained every minute during the testing period. In parallel, patients were observed for signs of spontaneous breathing. All patients remained apneic during the five minute test period. No relevant hypoxia (paO2 < 80 torr [10.6 kPa]) was observed in either group. In group 1, a mean baseline paCO2 of 45 torr (6.0 kPa) was registered, mean end-paCO2 was 75 torr (10.0 kPa). In group 2, paCO2 values were 66 torr (8.8 kPa) and 90 torr (12 kPa), respectively. Baseline pH in group 1 (7.32) decreased to 7.18 at the end of testing and from 7.23 to 7.13 in group 2. Patients in group 2 were in possible danger of developing a CO2-induced narcosis mimicking apnea. Secondary organ damage due to severe respiratory acidosis could not be excluded in the patients of group 2. As no complications were observed in group 1 and apnea was evident in all these patients, we consider a baseline paCO2 of 40 torr (5.3 kPa) sufficient to establish apnea after five minutes of apneic oxygenation if an increase of baseline paCO2 of at least 20 mmHg is documented by arterial blood gas sampling. A higher baseline paCO2 may endanger patients without yielding more specific testing results.

Apnea↗
PubMed1978

Evaluation of continuous monitoring of tissue pH in cats.

An improved continuous tissue pH monitoring system, designed for human subcutaneous fetal scalp tissue, was evaluated in 10 cats for total of 60 hours. Respiratory acidosis was induced with and without hypoxia to model the pathology of human clinical fetal distress. Arterial and venous pH were sampled every 15 minutes and the values were compared to those from the pH monitor system. The values paralleled arterial and venous blood pH, with correlation coefficients up to 0.98 under various pathologic acidotic conditions.

Animals↗
PubMed1981

Malignant hyperthermia syndrome.

Malignant hyperthermia is a pharmacogenetic disease involving uninhibited flow of calcium ion into the muscle substance. This leads to a combined metabolic and respiratory acidosis and the liberation of heat. If not immediately controlled, cellular death results. We treated a 4-year-old girl who suffered a malignant hyperthermia crisis during strabismus surgery. Hyperventilation with 100% oxygen and intravenously administered dantrolene sodium, furosemide, and fluids controlled the attack and the child recovered completely.

Calcium↗
PubMed1989

Cerebral vasoreactivity to carbon dioxide during cardiopulmonary perfusion at normothermia and hypothermia.

With the pH-stat acid-base regulation strategy during hypothermic cardiopulmonary bypass (CPB), carbon dioxide (CO2) is generally administered to maintain the partial pressure of arterial CO2 at a higher level than with the alpha-stat method. With preserved CO2 vasoreactivity during CPB, this induction of "respiratory acidosis" can lead to a much higher cerebral blood flow level than is motivated metabolically. To evaluate CO2 vasoreactivity, cerebral blood flow was measured using a xenon 133 washout technique before, during, and after CPB at different CO2 levels in patients who were undergoing coronary artery bypass grafting with perfusion at either hypothermia or normothermia. The overall CO2 reactivity was 1.2 mL/100 g/min/mm Hg. There was no difference between the groups. The CO2 reactivity was not affected by temperature or CPB. The induced hemodilution resulted in higher cerebral blood flow levels during CPB, although this was counteracted by the temperature-dependent decrease in the hypothermia group. After CPB, a transient increase in cerebral blood flow was noted in the hypothermia group, the reason for which remains unclear. The study shows that manipulation of the CO2 level at different temperatures results in similar changes in cerebral blood flow irrespective of the estimated metabolic demand. This finding further elucidates the question of whether alpha-stat or pH-stat is the most physiological way to regulate the acid-base balance during hypothermic CPB.

Acid-Base Equilibrium↗
PubMed1988

Panic attacks during sleep: a hyperventilation-probability model.

Panic attacks during sleep are analysed in terms of a hyperventilation theory of panic disorder. The theory assumes that panic attacks during sleep are a manifestation of severe chronic hyperventilation, a dysfunctional state in which renal compensation has led to a relatively steady state of diminished bicarbonate. Reductions in respiration during deep non-REM sleep lead to respiratory acidosis which triggers hyperventilatory hypocapnea and subsequent panic. A probability model designed to predict when during sleep panic attacks are likely to occur is supported by relevant data from studies of sleep and panic attacks. Implications for treatment are discussed.

Carbon Dioxide↗
PubMedDate not supplied

Relationships between acid-base balance, serum composition and colostrum absorption in newborn calves.

Twenty-seven newborn Holstein bull calves were bottle-fed 2 litres of pooled colostrum which had been stored at -20 degrees C. Blood gas analysis before feeding showed a partially compensated respiratory acidosis in most of the calves, although they all appeared to be clinically normal. Mean venous blood pH was 7.346, carbon dioxide tension (PCO2) was 57.5 mmHg (7.6 kPa), bicarbonate was 30.6 mmol/l and base excess was 3.82 mmol/l. Mean serum IgG1 increased to 8.1 g/l after feeding colostrum. Several significant positive correlations were observed between post-absorptive serum protein, IgG1, IgM, gamma-glutamyltransferase (gamma GT) and D-xylose. Calves with either low serum albumin, high serum CK or low serum gamma GT before feeding tended to have less absorption of colostral protein. It was concluded that reduced absorption of IgG1 from colostrum is associated with hypercapnia in apparently healthy newborn calves.

Acid-Base Equilibrium↗
PubMed1987

Effect of methadone on plasma arginine vasopressin level and urine production in conscious dogs.

The aim of this study was to examine the effect of i.v. methadone on the plasma arginine-vasopressin (AVP) levels and urine production in 9 conscious dogs. A highly significant increase from the baseline plasma AVP values of below 3 pg/ml occurred within 5 min following methadone administration. Maximum levels were reached within 30-50 min post-injection and varied from 18.5 to 100 pg/ml. A significant decrease in urine production was not seen under these experimental conditions. Mean arterial blood pressure did not change significantly during the experiment. Apart from the partial influence of the methadone-induced respiratory acidosis, we postulate a direct relationship between i.v. administration of methadone and the increased plasma AVP levels in dogs.

Animals↗
PubMed1989

Effect of systemic pH on models of altered ileal transport in the rat.

Decreases in arterial pH markedly increase sodium, chloride, and water absorption in the normal ileum and can reverse ongoing cholera toxin-induced secretion. In the current study we examined whether these effects of pH are evident in other models of ileal secretion, and in a model of increased absorption. Rats were anesthetized and transport was measured in ileal loops during respiratory acidosis and alkalosis. Decreases in arterial pH increased absorption equally in control loops and in adjacent loops perfused with a Ringer's solution containing ST toxin (cyclic guanosine monophosphate-mediated secretion), hypertonic mannitol (passive, osmotically mediated secretion), or glucose. Decreases in arterial pH increased absorption in a similar way in loops exposed to cholera toxin (cyclic adenosine monophosphate-mediated secretion) that were then perfused with glucose-Ringer's solution. Alterations in arterial and luminal pH did not affect glucose absorption. These results suggest that the effect of arterial pH on ileal absorption occurs by a mechanism that is independent of these various means of altering transport.

Absorption↗
PubMed1988

Metabolic consequences of hypercapnia in the rainbow trout, Salmo gairdneri: beta-adrenergic effects.

The metabolic consequences of external hypercapnia (1% CO2) were assessed in rainbow trout (Salmo gairdneri) in the presence or absence of circulating levels of the beta adrenoceptor antagonist, propranolol. External hypercapnia caused a severe extracellular respiratory acidosis and a less pronounced reduction of hepatic intracellular pH (pHi). pHi was restored to prehypercapnic values after 48 hr of continuous hypercapnia due to elevation of bicarbonate levels. In the presence of propranolol, hypercapnia elicited a pronounced activation of pyruvate kinase (PyK) (measured at both low and high phosphoenolpyruvate (PEP) concentrations) and inactivation of both total glycogen phosphorylase (GPase) and glycogen phosphorylase a (GPase a). In the absence of propranolol, the changes in enzyme activities were significantly reduced (low PEP PyK activity) or totally absent (GPase inactivation). These results suggest that beta adrenoceptor-mediated phenomena offset disruptive effects of hypercapnia on PyK and GPase activities and may be important in the control of gluconeogenesis and glycogenolysis during this acid-base disturbance. The adrenergic effects were not related to modification of hepatic intracellular acid-base status. Hypercapnia induced a rapid depletion of liver glycogen and concomitant hyperglycemia. These effects were not prevented by pretreating fish with propranolol and appeared to be unrelated to changes in GPase a activity. These results suggest that factors other than adrenergic activation of GPase a are involved in the enhancement of liver glycogenolysis.

Acid-Base Equilibrium↗
PubMed1988

Effect of some recent analgesics on labor pain and maternal and fetal blood gases and pH.

This study attempts to determine the analgesic properties of nalbuphine, pentazocine and butorphanol during labor and their potential effects on maternal and fetal blood gases and pH. Butorphanol analgesia was superior to either nalbuphine or pentazocine in relieving labor pain. The studied analgesics caused significant maternal respiratory acidosis and fetal metabolic acidosis. These acidotic changes were most marked with pentazocine, moderate with nalbuphine and minimal with butorphanol.

Adult↗
PubMed1989

Developmental changes of sarcolemmal Na+-H+ exchange.

We previously demonstrated that the effect of respiratory acidosis on cardiac contractility in the newborn was less than in the adult rabbit, and these data suggested a higher [Na+]i and [Na+]i-[Ca2+]o exchange in the newborn as compared to the adult. In this study, we investigated developmental changes of Na+-H+ exchange in isolated sarcolemmal vesicles. Sarcolemmal purification for Na+-K ATPase was 61.9 and 67.1 fold in the newborn and the adult rabbit heart, respectively. In the presence of an outwardly directed proton gradient across the vesicular membrane, sarcolemmal 22Na uptake rate in the newborn (0.22 +/- 0.01 nmol Na+/mg prot/s) was significantly higher than than in the adult (0.16 +/- 0.01 nmol Na+/mg prot/s). 1.0 mM amiloride inhibited 22Na uptake by 75% and 80% in the newborn and the adult, respectively. In the absence of a pH gradient, vesicular 22Na uptake in the newborn and the adult were not significantly different. In conclusion, the higher Na+-H+ exchange in the newborn may lead to a higher [Na+]i and subsequent calcium influx via Na+-Ca2+ exchange as compared with the adult during acidosis. This may explain the greater recovery of mechanical function in the newborn heart as compared to the adult heart during acidosis.

4-Nitrophenylphosphatase↗
PubMed1995

The relation between extracellular potassium concentration and pH in the border zone during regional ischemia in isolated porcine hearts.

During regional ischemia gradients of extracellular potassium concentration ([K+]o) and extracellular pH (pHo) exist. In globally ischemic papillary muscles increased PCO2 causes a rise in [K+]o. We studied whether pHo and [K+]o are causally related during acute regional ischemia in the isolated blood-perfused pig heart. Multiple pH- or K(+)-sensitive electrodes were inserted in the left ventricular midmyocardium. Local electrograms and ionic data were simultaneously acquired. Regional ischemia was produced by interrupting left anterior descending (LAD) artery flow (10 min). Up to 5 mm from the electrophysiological border the pH-K relation deviated from that in the central ischemic zone. Respiratory acidosis (pH about 7.10) of the perfusate in the presence of LAD-ischemia caused acidification of the ischemic border zone without a local change in [K+]o. We conclude that pHo changes are not related to changes of intramural [K+]o in the lateral border zone during regional ischemia.

Animals↗
PubMed1986

Fetal carbon dioxide tension during human labour.

Fetal carbon dioxide tension during labour is elevated in both metabolic and respiratory acidosis, but intermittent fetal blood analyses often fail to detect PCO2 changes during acute complications. Transcutaneous carbon dioxide monitoring is continuous and the possibility of diagnosing PCO2 changes is therefore better. The theoretical background for transcutaneous measurements and methods for clinical monitoring are described. Close correlations with capillary and arterial blood values have been found, and the atraumatic principle with a simple electrode application indicates a promising new method for acid-base assessment during human labour.

Acidosis↗
PubMed1975

Blood acid-base changes during experimental emersion and reimmersion of the intertidal crab Carcinus maenas (L.).

The time course of blood acid-base changes was studied in Carcinus maenas during experimental emersion and reimmersion at 15 degrees C by measuring pH and PCO2 and calculating bicarbonate concentration. During the first 4 hr of the emersion period, a marked rise of PCO2 entails a respiratory acidosis which is progressively compensated by a slow increase of the bicarbonate concentration; this compensation is completed after about 100 hr and the steady state mean pH value approximates that found for the immersed controls. Return to aquatic conditions is characterized by a rapid decrease of both PCO2 and blood bicarbonate concentration. During the first 2 hr of the reimmersion period, the decrease of blood bicarbonate concentration is accompanied by excretion of a significant amount of base in water, thus suggesting that readjustments of acid-base balance take place at least in part by ionic exchanges between the blood and the external milieu. Initial status was restored after 9 hr. These finding agree with the general views concerning the blood acid-base changes which must occur at transition from water-to air-breathing.

Acid-Base Equilibrium↗
PubMed1976

The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain.

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.

Acetazolamide↗