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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study analyzes the changes in cardiopulmonary parameters of patients undergoing laparoscopic cholecystectomy. Six healthy females with normal preoperative cardiopulmonary status were selected for laparoscopic surgery using the same criteria as for traditional cholecystectomy. Respiratory and cardiovascular parameters were collected and compared prior to peritoneal insufflation and just before desufflation. Patients experienced significant elevations of arterial and end-tidal CO2, accompanied by decreased pH. Bicarbonate concentration, blood pressure and pulse rate remained constant. Based on these results, and on our laboratory investigations, we have introduced helium as an alternate agent for insufflation, and present the data from the first two patients so managed. No change was observed in EtCO2, PaCO2 or pH in either of these two patients during the course of surgery. We conclude that hypercarbia occurs in those undergoing laparoscopic cholecystectomy with CO2 insufflation. This acidosis requires compensation by increased minute ventilation to prevent decline in pH. In our initial experience, helium did not produce these changes, and therefore merits further investigation as an alternate agent for abdominal insufflation.
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PMID:Laparoscopic surgery with carbon dioxide insufflation causes respiratory acidosis. 134 70

1. Regulation of intracellular and extracellular pH may conflict in their requirements for movement of acid or base. 2. Cells make a positive or a negative contribution to 'tissue buffering' of extracellular fluid (ECF), depending on their internal buffer value, on the tightness of their internal pH control by membrane mechanisms, and on the nature of the acid-base disturbance. 3. A role is suggested for electrogenic Na-HCO3 co-transport in some of the ion shifts that occur in acid-base disturbances. 4. The time course of 'tissue buffering' in nephrectomized mammals in hypercapnia is variable, and it is far from clear in intact, unanaesthetized mammals. 5. Buffering of ECF by Ca salts of bone mineral in acidosis can only be substantial if accompanied by Ca excretion; the release of HCO3 with Na and K is more significant. 6. The relative importance of cells and of bone mineral in the buffering of ECF is unclear.
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PMID:The roles of intracellular buffers and bone mineral in the regulation of acid-base balance in mammals. 135 35

Experiments were conducted to test the hypothesis that one or more interrenal steroids are active in regulatory responses to respiratory acidosis in the toad, Bufo marinus. Toads were divided into four experimental groups. The first group received sham injections. The second group received 1-3 mg of aminoglutethimide (AG) every 8 hr. AG inhibits the conversion of cholesterol to pregnenolone, thus inhibiting all steroid hormone synthesis. The third group received AG + 5 micrograms of aldosterone on the same schedule. The fourth group received AG + 25 micrograms of corticosterone on the same schedule as the other groups. All four groups were subjected to hypercapnia using 5% CO2 to induce a respiratory acidosis. The sham-operated animals displayed the normal compensatory pattern of producing a metabolic alkalosis (elevated plasma HCO3-) after 24 hr. AG-treated toads failed to elevate plasma HCO3-. Administration of interrenal steroids produced compensation in varying degrees. Aldosterone produced a small compensation while corticosterone produced a compensation similar to that seen in sham-operated animals. Analysis of steroid titers in toad plasma during hypercapnia showed that Bufo marinus does not elevate aldosterone during respiratory acidosis, but that corticosterone is elevated. AG blocked the corticosterone elevation, however. AG also produced a hyponatremia that was corrected with aldosterone or corticosterone. Normocapnic controls showed that AG does not produce deleterious effects on pH or blood gases in toads in the absence of a respiratory acidosis. We conclude that corticosterone is important in acid-base regulatory responses to respiratory acidosis in this amphibian.
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PMID:Acid-base-electrolyte balance responses of Bufo marinus to aminoglutethimide, corticosterone, and aldosterone during hypercapnia. 150 25

Exposure of adult brown bullheads Ictalurus nebulosus (120-450 g) to environmental hypercapnia (2% carbon dioxide in air) and subsequent recovery caused transient changes in whole body net sodium flux (JnetNa+) and net chloride flux (JnetCl-) resulting largely from changes in whole body sodium influx (JNa+in) and chloride influx (JinCl-). Scanning electron microscopy (SEM) revealed that the fractional area of chloride cells (CCs) on the interlamellar regions was reduced by 95% during environmental hypercapnia. During post-hypercapnic recovery, gill filament CC fractional area increased. The changes in JinCl- during and after environmental hypercapnia were closely associated with the changes in CC fractional area while the changes in JinNa+ did not correspond to the changes in CC fractional area. Transmission electron microscopy (TEM) supported the SEM observations of CC surface area changes and demonstrated that these changes were caused by covering/uncovering by adjacent pavement cells (PVCs). Lamellar and filament PVC microvilli density increased during hypercapnia while there was a subsequent reduction in the posthypercapnic period. These data suggest that an important mechanism of acid-base regulation during hypercapnic acidosis is modification of the chloride cell-associated Cl-/HCO3- exchange mechanism. We suggest that bullheads vary availability, and thus functional activity, of this transporter via reversible morphological alterations of the gill epithelium. The increase in density of PVC microvilli may be associated with sodium uptake and/or acidic equivalent excretion during acidosis.
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PMID:Evidence for a morphological component in acid-base regulation during environmental hypercapnia in the brown bullhead (Ictalurus nebulosus). 162 10

Carotid body (CB) chemosensory responses to natural and pharmacological stimuli were studied in vitro in the presence and nominal absence of CO2-HCO3- in the perfusion-superfusion media. The CBs obtained from cats (n = 10), anesthetized with sodium pentobarbitone, were simultaneously perfused and superfused with a modified Tyrode solution at 36.5 +/- 0.5 degrees C, equilibrated respectively with PO2 of 120 and less than 20 Torr. The Tyrode, nominally free of CO2-HCO3- (HEPES-NaOH, pH 7.38, 310 mOsm), was used first. Subsequently the Tyrode containing HEPES-HCO3-, equilibrated with PCO2 of 36.8 Torr (pH 7.38) was used. Chemosensory discharges were recorded from the carotid sinus nerve. Both hypoxia (PO2 = 20-25 Torr) and ischemic hypoxia stimulated the discharge in the absence and presence of CO2-HCO3-. However, the presence of CO2-HCO3- significantly raised the baseline activity, augmented the speed, sensitivity and the maximal responses to both types of hypoxia. Hypercapnic perfusate (PCO2 = 65 Torr at pH 7.17) produced a peak response equally promptly in the absence and presence of CO2-HCO3- in the ongoing perfusate but generated a larger and more sustained response. Presence of CO2-HCO3- strongly potentiated the responses to cyanide (10(-10)-10(-7) mol) but less strikingly the responses to nicotine (10(-11)-10(-8) mol). Thus, the extracellular CO2-HCO3- significantly improved the response to hypoxia but was not essential for O2 chemoreception. The underlying mechanisms of the effect of CO2-HCO3- is likely to be mediated by the Cl(-)-HCO3- anion exchanger in the pH regulation of glomus cells.
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PMID:Carotid body chemoreception in the absence and presence of CO2-HCO3-. 166 17

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
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PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56

We superimposed extreme hypercapnia (arterial Pco2 400-450 mmHg) immediately before and during incomplete cerebral ischemia to distinguish the role of intracellular pH (pHi) and bicarbonate [( HCO3-]i) in postischemic metabolic and electrophysiological recovery. Incomplete global ischemia was produced in seven anesthetized dogs by 30 min of intracranial hypertension followed by 4 h of reperfusion. ATP, phosphocreatine (PCr), and pHi were measured with 31P magnetic resonance spectroscopy, and [HCO3-]i was calculated from the Henderson-Hasselbalch equation using the measured pHi and sagittal sinus Pco2. Cerebral blood flow was reduced to 7 +/- 1 ml.min-1.100 g-1 (+/- SE) during ischemia with extreme hypercapnia, and pHi decreased to 5.72 +/- 0.09. During normocapnic reperfusion, pHi rapidly returned to near baseline values by 14 min. [HCO3-]i fell from 12.1 +/- 0.9 to 6.0 +/- 1.2 mM by the midpoint of ischemia and recovered by 30 min of reperfusion. ATP, PCr, and O2 consumption also recovered rapidly and completely. Somatosensory-evoked potentials (SEP) recovered to 43 +/- 10% of control amplitude. These results are in marked contrast to the poor metabolic and SEP recovery previously observed in hyperglycemic dogs in which pHi decreased to the same range as with hypercapnic ischemia, but in which [HCO3-]i was much lower (1.1 +/- 0.5 mM). Therefore, [HCO3-]i depletion during hyperglycemic ischemia may be a more important factor in recovery than end-ischemic pHi per se. We speculate that higher [HCO3-]i may improve glial cell buffering capacity or decrease iron availability for hydroxyl radical production.
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PMID:Bicarbonate conservation during incomplete cerebral ischemia with superimposed hypercapnia. 190 5

The Na(+)-H+ antiporter of renal brush-border membranes has been well characterized and plays a role in adaptation to acidosis. Na(+)-H+ antiporter activity has been described in other renal regions, but its kinetics as well as its role in adaptation to acidosis are unclear. Thus we measured Na(+)-H+ antiporter activity in membrane vesicles of outer and inner stripes of outer medulla (OSOM and ISOM, respectively) and in plasma membranes from papilla and compared it to Na(+)-H+ antiporter activity of the cortex in control and hypercapnic rabbits. Chronic hypercapnia (induced by exposure to CO2 for 48 h) was associated with significantly higher PCO2 and plasma HCO3- and lower urine pH than controls. In control animals, magnitude of Vmax of amiloride-sensitive component of Na(+)-H+ antiporter (expressed as fluorescence units.300 micrograms protein-1.min-1) was 392.2 +/- 32 in cortex, 115 +/- 9.7 in OSOM, 66.1 +/- 9.4 in 15-25% (F1) fraction and 118.7 +/- 16.8 in 25-40% (F2) fraction of ISOM, respectively, and 79.3 +/- 5.2 in papilla. These values were significantly different from each other except between F1 and papilla and F2 and OSOM. The Km for Na, however, was not different, suggesting that the renal Na(+)-H+ antiporter is basically the same in different renal regions but displays different activity. Hypercapnia for 48 h increased significantly the amiloride-sensitive component of Na(+)-H+ antiporter by 60% in cortex, 43% in F1, and 29% in papilla but failed to alter Vmax in OSOM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional localization of renal Na(+)-H+ antiporter: response to respiratory acidosis. 197 34

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.
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PMID:Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis. 199 47

Toads (Bufo marinus L.) and bullfrogs (Rana catesbeiana Shaw) were subjected to a series of 24 h step increases in aerial CO2 (2, 4, 6 and 8%) to assess the degree of extracellular pH compensation at each CO2 level and to ascertain the importance of cutaneous ion transport in this process. Elevation of plasma [HCO3-] occurs during the 24 h period, with the bullfrogs showing a greater ability to compensate at each step. There was no indication that a [HCO3-] threshold of 30 mmol l-1 existed in either species, although bullfrogs appeared to have a greater compensatory potential when exposed to the higher levels of CO2. The results of the ion flux experiments suggest that neither the terrestrial Bufo nor the semi-aquatic Rana use their skin to any great extent for acid-base balance during hypercapnia.
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PMID:Compensation of progressive hypercapnia in the toad (Bufo marinus) and the bullfrog (Rana catesbeiana). 210 65


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