Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Shifts of Na+, K+, Cl- and HCO3- between the cells and extracellular fluid of nephrectomized mammals in acute response to hypercapnia and to HCl or KCl infusion are simulated in steady state models involving just intracellular buffering and a simply defined interdependence of ionic gradients. Such models integrate diverse kinds of data and suggest new interpretations. In respiratory acidosis K+, HCO3- and water leave some cells and move both to where chemical buffering is least (ECF and other cells) and to cells that regulate pH particularly well by active transport. Buffering by erythrocytes is important, but the effects of distinguishing erythrocytes from other cells in a model is mainly just to emphasize Cl- movements. Effects of departures from the mammalian norm of body composition are explored.
 ...
PMID:The role of intracellular buffers in acid-base disturbances: mathematical modelling. 736 Oct 19

The relaxant effect of hypercapnia (15% CO2) was studied in isolated circular segments of rat basilar arteries with intact endothelium. The nitric oxide synthase inhibitor nitro-L-arginine (L-NOARG) and the cytosolic guanylate cyclase inhibitor methylene blue (MB), significantly reduced this relaxation by 54% and 70%, respectively. The effect of L-NOARG was completely reversed by L-arginine. Blockade of nerve excitation with tetrodotoxin (TTX) had no affect on the 15% CO2 elicited vasodilatation. Measurements of cGMP in vessel segments showed no significant increase in cGMP content in response to hypercapnia. L-NOARG and MB, but not TTX, significantly reduced the basal cGMP content in cerebral vessels. Adding 1.5% halothane to the incubation medium did not result in a significant increase in cGMP content. Lowering the pH by cumulative application of 0.12 M HCl resulted in relaxation identical to that obtained by lowering the pH with 15% CO2. In vessel segments in which the endothelium had been removed beforehand 15% CO2 induced relaxation that was not different from that seen in vessels with intact endothelium. L-NOARG had no affect in endothelium denuded vessels. The results suggest that high CO2 elicits vasodilatation of isolated rat basilar arteries by a mechanism independent of nitric oxide synthase (NOS) activity. The markedly reduced basal cGMP levels in cerebral vessels by L-NOARG and MB suggest that there exists a basal NO formation in the cerebral vessel wall.
 ...
PMID:Hypercapnic vasodilatation in isolated rat basilar arteries is exerted via low pH and does not involve nitric oxide synthase stimulation or cyclic GMP production. 753 5

1. The object of this study was to investigate the effect of central chemoreceptor stimulation on the ventilatory responses to peripheral chemoreceptor stimulation. 2. The level of central chemoreceptor stimulation was varied by performing experiments at two different levels of end-tidal CO2 pressure (PCO2). Variations in peripheral chemoreceptor stimulus were achieved by varying arterial pH (at constant end-tidal PCO2) and by varying end-tidal O2 pressure (PO2). 3. Two protocols were each performed on six human subjects. In one protocol ventilatory measurements were made during eucapnia, when the arterial pH was lowered from 7.4 to 7.3. The variation in pH was achieved by the progressive infusion of acid (0.1 M HCl). In the other protocol ventilatory measurements were made during hypercapnia, when the arterial pH was increased from 7.3 to 7.4. The variation in pH was achieved by the progressive infusion of 1.26% NaHCO3. In each protocol ventilatory responses were measured during euoxia (end-tidal PO2, 100 Torr), hypoxia (end-tidal PO2, 50 Torr) and hyperoxia (end-tidal PO2, 300 Torr), with end-tidal PCO2 held constant. 4. The increase in ventilatory sensitivity to arterial pH induced by hypoxia (50 Torr) was not significantly different between protocols (acid protocol, -104 +/- 31 l min-1 (pH unit)-1 vs. bicarbonate protocol, -60 +/- 44 l min-1 (pH unit)-1; mean +/- S.E.M.; not significant (n.s.)). The ventilatory sensitivity to hypoxia at an arterial pH of 7.35 was not significantly different between protocols (acid protocol, 14.7 +/- 3.3 l min-1 vs. bicarbonate protocol, 15.6 +/- 2.4 l min-1; mean +/- S.E.M.; n.s.). The results provide no evidence to suggest that peripheral chemoreflex ventilatory responses are modulated by central chemoreceptor stimulation.
 ...
PMID:An assessment of central-peripheral ventilatory chemoreflex interaction using acid and bicarbonate infusions in humans. 766 75

Somatolactin is a putative pituitary hormone of the growth hormone/prolactin family in fish. Its function is still unknown. The effects of environmental hypercapnia and hypoxia, acid (HCl) infusion and exhaustive exercise on plasma somatolactin levels were examined in the chronically cannulated rainbow trout to study the possible physiological roles of somatolactin. Respiratory acidosis induced by hypercapnia (2% CO2) did not affect plasma somatolactin level. In contrast, metabolic acidosis induced by acid infusion and exercise increased plasma somatolactin level. Blood pH was depressed to a similar extent by both types of acidosis, whereas plasma [HCO3-] was elevated by respiratory acidosis but reduced by metabolic acidosis. A moderate hypoxia (water PO2 9.3kPa) affected neither acid­base status nor plasma somatolactin level. A more severe hypoxia (water PO2 6.1kPa) resulted in metabolic acidosis accompanied by an apparent rise in plasma somatolactin level, although the difference in somatolactin level from the control value was not statistically significant. Somatolactin immunoneutralization retarded recovery of plasma [HCO3-] following acid infusion. These results indicate that somatolactin is involved in the retention of HCO3- during metabolic acidosis but not in the active accumulation of HCO3- for acid­base compensation of respiratory acidosis in rainbow trout Oncorhynchus mykiss.
 ...
PMID:Possible involvement of somatolactin in the regulation of plasma bicarbonate for the compensation of acidosis in rainbow trout 932 95

To elucidate the differential reactivity of pulmonary microvessels in the acini to hypoxia, excessive CO2, and increased H+, we investigated changes in the diameter of precapillary arterioles, postcapillary venules, and capillaries in isolated rat lungs on exposure to normocapnic hypoxia (2% O2), normoxic hypercapnia (15% CO2), and isocapnic acidosis (0.01 mol/L HCl). Microvascular diameters were precisely examined using a real-time confocal laser scanning luminescence microscope coupled to a high-sensitivity camera with an image intensifier. Measurements were made under conditions with and without indomethacin or N(omega)-nitro-L-arginine methyl ester to assess the importance of vasoactive substances produced by cyclooxygenase (COX) or NO synthase (NOS) as it relates to the reactivity of pulmonary microvessels to physiological stimuli. We found that acute hypoxia contracted precapillary arterioles that had diameters of 20 to 30 microm but did not constrict postcapillary venules of similar size. COX- and NOS-related vasoactive substances did not modulate hypoxia-elicited arteriolar constriction. Hypercapnia induced a distinct venular dilatation closely associated with vasodilators produced by COX but not by NOS. Arterioles were appreciably constricted in isocapnic acidosis when NOS, but not COX, was suppressed, whereas venules showed no constrictive response even when both enzymes were inhibited. Capillaries were neither constricted nor dilated under any experimental conditions. These findings suggest that reactivity to hypoxia, CO2, and H+ is not qualitatively similar among intra-acinar microvessels, in which COX- and NOS-associated vasoactive substances function differently.
 ...
PMID:Response of intra-acinar pulmonary microvessels to hypoxia, hypercapnic acidosis, and isocapnic acidosis. 954 81

We investigated the effects of repeated hypercapnic episodes (inspired CO2 fraction = 0.10) on posthypercapnic respiratory nerve discharge. Anesthetized (urethan), vagotomized, and artificially ventilated rats were presented with three consecutive 5-min episodes of hyperoxic hypercapnia, separated by 5 min of hyperoxic normocapnia (inspired O2 fraction = 0.5). Respiratory nerve discharge and blood gases were recorded before and 30 and 60 min after the final hypercapnic episode. Posthypercapnia, arterial PCO2 was maintained within 1 Torr of initial baseline values. Integrated phrenic and hypoglossal burst amplitudes decreased posthypercapnia by up to 46 +/- 17 and 55 +/- 13% of baseline values, respectively, and remained reduced for at least 1 h [long-term depression (LTD)]. The protocol was repeated in rats pretreated with the alpha2-adrenergic antagonists yohimbine HCl (0.5 mg/kg; n = 7) or 2-[2-(2-methoxy-1,4-benzodioanyl)]imidazoline (RX-821002) HCl (0.25 mg/kg; n = 3). Both drugs attenuated LTD in the phrenic and hypoglossal neurograms. Results indicate that episodic hypercapnia elicits a yohimbine- and RX-821002-sensitive LTD of respiratory nerve activity in rats, suggesting that LTD requires alpha2-receptor activation.
 ...
PMID:Hypercapnia-induced long-term depression of respiratory activity requires alpha2-adrenergic receptors. 960 5

In order to evaluate the effect of brain acidosis on neuronal functions as assessed by the in vivo studies, changes of cerebral blood flow (CBF), brain pH ([pH]o) and brain amino acid levels in the same brain region of the two different acidosis model rats were measured under isoflurane anesthesia. Three micro probes to measure CBF, [pH]o and amino acids, respectively, were implanted into the frontal cortex, and these parameters were recorded simultaneously. In the metabolic acidosis rats, the sustained decrease of [pH]o and amino acid levels, particularly Glu, were detected after the treatment with 10 min-i.v. infusion of 1 N HCl, although the significant changes of CBF did not appear because of the respiratory management. In the respiratory acidosis model, however, transient and significant increase of CBF and decrease of Glu and [pH]o were recorded after 10 min-exposure to about 30% CO2 (N2O:O2:CO2 = 2:5:3). The levels of Gly and Gln were reduced after acute exposure to hypercapnia, but these levels recovered to the control level in 20-30 min after hypercapnia exposure. In both animals, the amounts of Tau was gradually reduced after the treatment with 1 N HCl and hypercapnia, and these levels did not return to the control level when other amino acid levels had recovered. These differences of brain amino acid levels in the two different types of acidosis model rats may be related to the brain amino acid metabolic pathway. Thus, during brain acidosis induced by 1 N HCl and hypercapnia, the amount of extracellular Glu in the brain was reduced, and this reduction may contribute to the neuroprotective effects.
 ...
PMID:[Acidosis and neuroprotection in two types of acidosis model rats under isoflurane anesthesia: evaluation of blood flow, pH and amino acid levels in the cortex]. 983 87

This study was designed to evaluate 2 combinations for immobilization of bison. Seven wood bison received 1.5 mg/kg body weight (BW) of xylazine HCl + 1.5 mg/kg BW of zolazepam HCl and 1.5 mg/kg BW of tiletamine HCl on one occasion. The bison received 60 micrograms/kg BW of medetomidine HCl + 0.6 mg/kg BW of zolazepam HCl and 0.6 mg/kg BW of tiletamine HCL on another occasion. Xylazine was antagonized with 3 mg/kg BW of tolazoline HCl and medetomidine HCl was antagonized with 180 micrograms/kg (BW) of atipamezole HCl. Temporal characteristics of immobilization and physiological effects (acid-base status, thermoregulatory, cardiovascular, and respiratory effects) of the drug combinations were compared. Induction was significantly faster with xylazine HCl-zolazepam HCl/tiletamine HCl. Recovery following antagonist administration was significantly faster with medetomidine HCl-zolazepam HCl/tiletamine HCl. The average drug volumes required were 7.00 mL of xylazine HCl-zolazepam HCl/tiletamine HCL and 2.78 mL of medetomidine HCl-zolazepam HCl/tiletamine HCl. Hypoxemia, hypercarbia, and rumenal tympany were the major adverse effects with both drug combinations.
 ...
PMID:Anesthesia of wood bison with medetomidine-zolazepam/tiletamine and xylazine-zolazepam/tiletamine combinations. 1064 72

To examine the distribution and physiological role of CO2/pH-sensitive chemoreceptors in the gills of the tropical fish, traira (Hoplias malabaricus), fish were exposed to acute environmental hypercarbia (1.25, 2.5 and 5.0% CO2 in air) and subjected to injections of HCl into the ventral aorta and buccal cavity. This was done before and after selective denervation of branchial branches of the IXth and Xth cranial nerves to various gills arches. Hypercarbia produced a significant decrease in heart rate, a mild hypotension as well as increases in both ventilation rate and ventilation amplitude. The data suggest that the hypercarbic bradycardia and increase in ventilation frequency arise from receptors exclusively within the gills but present on more than the first gill arch, while extra-branchial receptors may also be involved in controlling the increase in ventilation amplitude. With the exception of a decrease in heart rate in response to HCl injected into the ventral aorta, the acid injections (internal and external) did not mimic the cardiorespiratory responses observed during hypercarbia suggesting that changes in CO2 are more important than changes in pH in producing cardiorespiratory responses. Finally, the data indicate that chemoreceptors sensitive to CO2/pH and to O2 in the gills of this species involved in producing ventilatory responses are distributed in a similar fashion, but that those involved in producing the bradycardia are not.
 ...
PMID:Cardiovascular and respiratory reflexes in the tropical fish, traira (Hoplias malabaricus): CO2/pH chemoresponses. 1078 44

It has been suggested that pulmonary injury and inflammation-induced histamine release from airway mast cells may contribute to exercise-induced arterial hypoxemia (EIAH). Because stress failure of pulmonary capillaries and EIAH are routinely observed in exercising horses, we examined whether preexercise administration of an H1-receptor antagonist may mitigate EIAH. Two sets of experiments, placebo (saline) and antihistaminic (tripelennamine HCl at 1.10 mg/kg iv, 15 min preexercise) studies, were carried out on seven healthy, exercise-trained Thoroughbred horses in random order 7 days apart. Arterial and mixed venous blood-gas and pH measurements were made at rest before and after saline or drug administration and during incremental exercise leading to maximal exertion at 14 m/s on 3.5% uphill grade for 120 s. Galloping at this workload elicited maximal heart rate and induced exercise-induced pulmonary hemorrhage in all horses in both treatments, thereby indicating that capillary stress failure-related pulmonary injury had occurred. In both treatments, EIAH, desaturation of hemoglobin, hypercapnia, and acidosis of a similar magnitude developed during maximal exertion, and statistically significant differences between the placebo and antihistaminic studies could not be demonstrated. The failure of the H1-receptor antagonist to modify EIAH significantly suggests that pulmonary injury-induced histamine release may not play a major role in bringing about EIAH in Thoroughbred horses.
 ...
PMID:H1-receptor antagonist, tripelennamine, does not affect arterial hypoxemia in exercising Thoroughbreds. 1189 18


<< Previous 1 2 3 4 Next >>