Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of two anaesthetics, sodium pentobarbital and urethane, and the effects of anaesthesia-associated hypothermia on acid-base status and blood gases were studied in rats without assisted ventilation. 2. Manipulation of conscious rats produces a progressive increase in arterial lactate associated with slight hyperventilation. 3. Sodium pentobarbital anaesthesia produces mild respiratory acidosis accompanied by increase in lactate arterial values. Urethane anaesthesia leads to partially compensated metabolic acidosis. 4. Hypothermia reduces metabolic acidosis and hypercapnia induced by sodium pentobarbital anaesthesia. No difference between hypothermic and normothermic values was observed in urethane anaesthesia.
Gen Pharmacol 1992 Jul
PMID:Differential effects of hypothermia upon blood acid-base state and blood gases in sodium pentobarbital and urethane anaesthetised rats. 139 74

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.
Gen Comp Endocrinol 1992 Apr
PMID:Acid-base-electrolyte balance responses of Bufo marinus to aminoglutethimide, corticosterone, and aldosterone during hypercapnia. 150 25

The conductance of the inward-rectifying K+ current (IK1) in isolated cat ventricular myocytes is decreased by reducing the extracellular Na+ concentration. Using a whole-cell patch-clamp technique, possible mechanisms underlying this Na+ dependence were investigated. These included (a) block of inward K+ current by the Na+ substitute, (b) changes in membrane surface charge associated with removal of extracellular Na+, (c) increases of intracellular Ca2+ due to suppression of Na-Ca exchange, (d) reduction of a Na+-dependent K+ conductance due to a subsequent decrease of intracellular Na+, (e) reduction of IK1 conductance (gK1) associated with reduction of intracellular pH due to suppression of Na-proton exchange. The findings support the hypothesis that the effect of removing Na+ is mediated through a decrease in intracellular pH. These include observations that: (a) reducing internal pH by reducing external pH caused a decrease in gK1, and the conductance changes caused by reducing extracellular pH and removing extracellular Na+ were not additive: (b) the effect of reducing pHo was attenuated by dialyzing with a low pH internal solution; (c) gK1 was reduced by exposure to the Na-proton exchange inhibitor dimethylamiloride, and this effect was absent in the absence of Na+. These findings imply that physiological or pathological processes such as ischemia and metabolic or respiratory acidosis which can produce intracellular acidosis should be expected to affect K+ permeation through the IK1 channel.
J Gen Physiol 1989 Aug
PMID:On the role of sodium ions in the regulation of the inward-rectifying potassium conductance in cat ventricular myocytes. 279 68

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.
Gen Comp Endocrinol 1988 Mar
PMID:Metabolic consequences of hypercapnia in the rainbow trout, Salmo gairdneri: beta-adrenergic effects. 283 62

Larval Ambystoma tigrinum (59-199 g) were treated with the drug aminoglutethimide (6 mg/day) in order to abolish steroid hormone synthesis. Steroid deprivation prevented the increase in plasma aldosterone concentration observed in sham-infused larvae during respiratory acidosis. It also blocked the normal compensatory response to respiratory acidosis of elevated plasma [HCO3-] and inhibited cutaneous Na+ transport. Aldosterone (10 micrograms/day) and, to a lesser extent, corticosterone (240 micrograms/day) restored the compensatory response. Aldosterone replacement also stimulated cutaneous Na+ transport in AG-inhibited larvae. The results suggest that aldosterone, at about 1000 pg/ml, supports the compensatory ionic responses to respiratory acidosis in this species.
Gen Comp Endocrinol 1993 Apr
PMID:Interrenal function in larval Ambystoma tigrinum. III. Acid-base balance responses. 850 15

Vanishing lung syndrome is a rare disease that could be treated successfully in selected cases with bullectomy. Protective ventilation is very important during surgery to achieve optimal post-operative results and to prevent complications. Hypercapnia and respiratory acidosis are the main disadvantages of this ventilator strategy. The use of extracorporeal CO2 removal device has been introduced to support protective and ultra-protective ventilation during respiratory failure in complex cases. In thoracic surgery the intraoperative use of this device is still not widespread. We report a successful case of a giant left lung bullectomy with intraoperative support with Pro-Lung CO2 removal device for the management of hypercapnia during single lung ventilation.
Gen Thorac Cardiovasc Surg 2020 Dec
PMID:Intraoperative extracorporeal carbon dioxide removal support for minimally invasive surgical treatment of vanishing lung syndrome. 3182 19