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

The ionic compensatory response to CO2 breathing for 3 days was studied on intact and cystectomized turtles at 10 and 20 degrees C. Arterial blood gases, pH, ionized calcium, and the plasma concentrations of Na+, K+, Cl-, total Ca2+, and total Mg2+ were measured periodically. At 20 degrees C, ureteral urine was also collected from bladderless turtles and was analyzed for pH, ions, NH3+, total CO2, osmolality, and titratable acid. When CO2 was breathed there was a compensatory change in the strong-ion difference as manifest by an increase in plasma [HCO3-] that was approximately 10 meq/l both in the 10 and 20 degrees C turtles. The only significant associated strong-ion changes observed consistent with the ionic compensatory response were increases in total and ionized Ca2+ and total Mg2+. These results were unaffected at either temperature by surgical removal of the urinary bladder. Urine collected from cystectomized turtles showed no compensatory increase in acid excretion during hypercapnia; in fact, changes occurred in the opposite direction. Urinary excretion of HCO3- and urine pH increased significantly, whereas titratable acidity decreased significantly. No significant change occurred in ammonia excretion over the three days of hypercapnia. These data argue against compensatory roles for the kidneys and urinary bladder in this species and point to internal ionic exchanges involving bone and shell.
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PMID:Ionic compensation with no renal response to chronic hypercapnia in chrysemys picta bellii. 378 4

An estimate of the total mass of bone in the Channel catfish Ictalurus punctatus Rafinesque, was obtained by dissection. The wet weight of bone constituted 16.3 +/- 1.9% (+/- S.D.) of the total (live) wet weight, and 25.0 +/- 2.1% of the dry weight. Of the dry skeletal material, 66.3 +/- 11.1% was soluble in strong acid. The acid-soluble material was about half mineral salts, consisting of 19.5 +/- 2.21% Ca2+ and 27.6 +/- 3.22% PO4(3-), with minor fractions of Mg2+ (0.33%) and CO3(2-) (1.67%). The pH values of fluid compartments associated with skull and vertebral bone tissues were 7.420 +/- 0.026 and 7.444 +/- 0.017 (+/- S.E.), respectively, at a normocapnic plasma pH of 7.868 +/- 0.020. In response to external hypercapnia (7.5 Torr), the blood response consisted of an immediate decrease in pH, and a subsequent compensatory rise in both pH and [HCO3-]. This compensatory phase was accompanied by a net apparent H+ excretion to the water. The participation of the mineral salts of the bone compartment in compensation appeared to be negligible, since there was no significant change in either blood [Ca2+] or [PO4(3-)], nor any significant increase in calcium efflux to the water. The intracellular pH values of the bone compartments were only slightly higher than other tissues, and the changes in pHi during hypercapnia were similar in bone and white muscle. Thus, the bone compartment in the fish appears to be well regulated, relatively refractory to acute acid-base disturbance, and does not serve as an ion source during acid-base compensation.
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PMID:The bone compartment in a teleost fish, Ictalurus punctatus: size, composition and acid-base response to hypercapnia. 406

Five Merino sheep were dosed 3 g/kg of dry, finely-milled Homeria glauca (Natal yellow tulp) plant material. An electrocardiogram was recorded and the arterial and central venous blood pressure, blood gases, haematological variables, plasma electrolytes (Na+, K+, Ca2+, Mg2+, Cl- and PO4(2-) ) and a variety of serum enzymes and chemical constituents were measured hourly until death (3 sheep) or until sheep were in extremis (2 sheep). Heart rate rose progressively as a result of sinus and, later, ventricular tachycardia. Systolic blood pressure rose, but there was little change in the mean and diastolic arterial pressures and central venous pressure. There was progressive hypoxaemia, hypercarbia and acidaemia with depletion of plasma bicarbonate. Haemoconcentration, hyperkalaemia and hypochloraemia were found along with rising serum creatinine and plasma glucose. Rises in serum enzymes indicated widespread tissue damage. Electrocardiographic recordings were being made at the moment of death in 3 of the 5 sheep. In these 3 sheep the cause of death was ventricular fibrillation.
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PMID:Some physiopathological features of experimental Homeria glauca (Wood & Evans) N. E. Br. poisoning in Merino sheep. 664 61

Previously we have shown that hypercarbia produces a larger decrease in agonal glycolytic rate in 1-month-old swine than in newborns. In an effort to understand the mechanism responsible for this difference, we tested the hypothesis that hypercarbia produces age-related changes in the concentration of one or more effectors of phosphofructokinase activity. Specifically, in vivo 31P and 1H NMR spectroscopy was used to compare changes in lactate levels, intracellular pH, free magnesium concentration, and content of phosphorylated metabolites for these two age groups at three intervals during the first 1.5 min of complete ischemia in the presence or absence of hypercarbia (PaCO2 = 102-106 mm Hg). Hypercarbia produced the same drop in intracellular brain pH for both age groups, but the decrease in phosphocreatine level and increase in inorganic phosphate content were greater in 1-month-olds compared with newborns. During ischemia there was no difference between the magnitude of change in intracellular pH and levels of phosphocreatine and inorganic phosphate in hypercarbic 1-month-olds versus newborns. Under control conditions, i.e., normocarbia and normoxia, the free Mg2+ concentration was lower and the fraction of magnesium-free ATP was higher for newborns than 1-month-olds. However, there was no change in these variables for either age group during hypercarbia and early during ischemia. Thus, age-related differences in the relative decrease in agonal glycolytic rate during hypercarbia could not be explained by differences in intracellular pH, inorganic phosphate content, or free magnesium concentration. The [ADP]free at control was higher in newborns compared with 1-month-olds, and there was no age-related difference in [AMP]free. These variables did not change for newborns when exposed to hypercarbia, but for 1-month-olds [ADP]free and [AMP]free increased during hypercarbia relative to control values. High-energy phosphate utilization during ischemia for hypercarbic 1-month-olds was reduced by 74% compared with normocarbic 1-month-olds during ischemia, whereas the reduction in energy utilization (14%) was not significant for hypercarbic versus normocarbic newborns during ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evaluation of potential effectors of agonal glycolytic rate in developing brain measured in vivo by 31P and 1H nuclear magnetic resonance spectroscopy. 779 28

Experiments on rats have shown an important role of hypercapnia in the development of condition of artificial hibernation in combination with influence of hypothermia, hypoxia and hypercapnia. It is proved that the joint action of hypothermia, hypoxia and hypercapnia has induced development of respiratory acidosis and hibernation in animals, while removal of the hypercapnia effect has induced development of acute metabolic acidosis and death of animals. It has been found that animals in the state of artificial hibernation have considerable changes in concentrations of main electrolytes (Na+, K+, Ca+, Mg2+, phosphates, Cl-) and metabolites (NH3, glutamine, urea) in blood as well as in activity of enzymes (glutamaldehydrogenase, glutaminase, arginase) in tissues of the liver and kidneys.
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PMID:[Acid-base equilibrium and nitrogen metabolism in rats in a state of artificial hibernation]. 855 76

1. We investigated the neural mechanisms of the increases in blood flow produced by synaptic activity using the parallel fiber (PF) system of the cerebellum as a model. The midline cerebellum was exposed in anesthetized rats and the PFs were stimulated with tungsten microelectrodes. Cerebellar blood flow (BFcrb) was recorded using a laser-Doppler probe, whereas field potentials were recorded using glass micropipettes. PF stimulation produced increases in BFcrb that were related to the frequency and intensity of stimulation (+60 +/- 9%, mean +/- SE, at 100 microA and 30 Hz; n = 6). The greatest increases were confined to a band stretching along the major axis of the stimulated folium and corresponding to the beam of activated PFs. The increase in evoked by PF stimulation was associated with a corresponding increase in glucose utilization, assessed by the 2-deoxyglucose method. The increases in BFcrb and the field potentials evoked by PF stimulation were abolished by tetrodotoxin (1 microM; n = 6). Ringer solution containing 12 mM Mg2+ and 0 mM Ca2+ blocked synaptic activity in the PFs and abolished the increases in flow (P > 0.05 from baseline; n = 5). The broad-spectrum glutamate receptor antagonist kynurenate (5 mM) prevented depolarization of Purkinje cells and interneurons and abolished the increase in BFcrb evoked by PF stimulation (P > 0.05; n = 6). Treatment with tetrodotoxin, Mg2+, or kynurenate did not affect the increase in BFcrb elicited by systemic hypercapnia or by topical application of the nitric oxide donor 3-morpholino sydnonimine (P > 0.05 from Ringer solution). We conclude that the increases in flow produced by synaptic activity are linked to glutamate-induced depolarization of Purkinje cells and interneurons. These findings provide evidence that activation of glutamate receptors participates in the mechanisms of functional hyperemia, and they support the validity of the PF system as a model for study of the relationship between synaptic activity and blood flow in the CNS.
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PMID:Neural mechanisms of blood flow regulation during synaptic activity in cerebellar cortex. 871 66

The interactions between the acid-base variables that contribute to exudate acidosis were studied in the subcutaneous air-pouch after carrageenan injection in rats. We studied the concurrent changes of exudate gases (PCO2 and PO2), main ions ([Na+], [K+], [Ca2+], [Mg2+], [Cl-] and [Lac-]), inorganic phosphate (P(i)) and albumin in acutely inflamed rats (4, 8, 12, 24 and 48 h of inflammation). A notable hypercapnia was found in the exudate after only 8 h (exudate PCO2 = 64.3 +/- 2.9 mm Hg) but this hypercapnia decreased after 48 h (32.9 +/- 12.7 mm Hg), coincident with the greatest increase in exudate cells. With respect to the metabolic acid-base variables, the most important changes found were a parallel decrease in the strong ion difference ([SID]) and exudate pH, as well as increases in the exudate weak acid buffers ([ATOT]) due to albumin and inorganic phosphate (P(i)) increases. However, after 12 h, the exudate acidosis was stable at around pH 7. A similar acid pH was obtained after 24 h of inflammation when the carrageenan solution injected was previously adjusted to a physiological pH (7.4). This pH, analogous to that of the exudate, was the result of compensation by the acid-base independent variables, a fact which suggests that acid pH may be a beneficial condition for cells taking part in inflammatory processes.
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PMID:Factors influencing the acid-base changes in the air-pouch exudate following carrageenan induced inflammation in rats. 887 14

The neurotransmitter mechanisms that process acid hypercapnia in the mammalian carotid body (CB) are poorly understood. Using a co-culture model containing rat CB chemoreceptor (type 1 cell) clusters and petrosal neurons (PN), we tested the hypothesis that co-released ACh and ATP was an important mechanism. Sensory transmission from type I clusters to PN in co-culture occurred at chemical synapses via co-release of ATP and ACh because isohydric hypercapnia depolarized and/or increased firing in co-cultured PN, but not in PN cultured alone; PN chemoexcitatory responses were inhibited by decreasing the extracellular Ca(2+):Mg2+ ratio; partial inhibition of these responses occurred during separate perfusion of cholinergic (hexamethonium or mecamylamine) and P2X (suramin) receptor blockers, although inhibition was often complete with both blockers present; and rapid chemoexcitatory responses to hypercapnia were inhibited by acetazolamide (10 microM), an inhibitor of carbonic anhydrase, localized in type I cells. Acidosis (pH = 7.0, 7.2) enhanced the ATP-induced whole cell current in functional PN relative to that at physiologic pH (7.4), suggesting that increased sensitivity of postsynaptic P2X receptors may contribute to acid chemotransmission. Type I cells in CB tissue sections expressed vesicular acetylcholine transporter (VAChT), a cholinergic marker, as revealed by confocal immunofluorescence. Thus co-release of ACh and ATP is an important neurotransmitter mechanism for processing isohydric and acidic hypercapnia in the rat carotid body.
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PMID:CO2/pH chemosensory signaling in co-cultures of rat carotid body receptors and petrosal neurons: role of ATP and ACh. 1505 81