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

The aims of this study were to investigate the effect of changes in arterial blood gases and pH on furosemide pharmacodynamics and kinetics. Five groups of conscious rabbits were used: a control group breathing air with normoxia and normocarbia; a second group with hypercapnia and respiratory acidosis; a third with hypoxemia; a fourth with hypercapnia and respiratory acidosis combined with hypoxemia (HCHO); and the fifth group with metabolic acidosis. All experimental conditions, except hypoxemia, increased sodium tubular reabsorption and therefore, decreased urinary excretion of sodium. Renal blood flow was decreased by HCHO and metabolic acidosis. In response to 5 mg/kv i.v. of furosemide, natriuresis and diuresis were decreased by an average of 44% in animals with HCHO (P less than .05). The kinetics of furosemide were not affected by any of the experimental conditions except HCHO, in which the renal clearance of furosemide was reduced from 7.5 +/- 1.4 ml/min/kg (controls) to 2.7 +/- 0.7 ml/min/kg (P less than .05). The reduction in renal clearance of furosemide was associated with a decrease in urinary excretion of sodium (P less than .05). The reduction in renal clearance of furosemide was probably secondary to the decrease in renal blood flow and an increase in furosemide tubular reabsorption. Finally, HCHO did not decrease plasma volume, suggesting that the reduction in renal blood flow was secondary to blood flow distribution. In conclusion, only hypercapnia and respiratory acidosis combined with hypoxemia decreases the natriuretic and diuretic effect of furosemide.
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PMID:Furosemide pharmacodynamics: effect of respiratory and acid-base disturbances. 308 62

Experiments were performed in isolated non-working guinea pig hearts perfused according to the Langendorff technique (95% O2, 5% CO2), to evaluate the relative contribution of the coronary endothelium to the formation of cardiac adenosine during hypoxia, hypercapnia, and acetylcholine infusion. For this purpose the adenine-nucleotides of the coronary endothelium were prelabeled by perfusion of isolated hearts with 3H-adenosine (10(-8) M) for 35 min. Changes in the relative specific radioactivity (RSA) of adenosine released into the coronary effluent perfusate were used to assess changes in the relative contribution of the coronary endothelium and cardiomyocytes to total cardiac adenosine release. Hypoxic perfusion (15% O2) doubled coronary flow and increased total adenosine release by about two orders of magnitude and in addition, substantially increased the release of 3H-adenosine. The RSA of adenosine, however, was consistently depressed. During hypercapnic acidosis (9% CO2) the increase in coronary flow was associated with only a small and transient rise in cardiac adenosine release, and did not influence the formation of 3H-adenosine. In the unpaced heart, acetylcholine (10(-7) and 2 X 10(-6) M) dose-dependently increased coronary flow and the release of both adenosine and 3H-adenosine. Within the first minute, the RSA of adenosine was increased, but thereafter was decreased relative to control. In the paced heart, the effects of acetylcholine (2 X 10(-6) M) were greatly attenuated. Increasing coronary flow by bradykinin and isosorbide dinitrate or decreasing heart rate by (-)N6-phenylisopropyl-adenosine did not significantly affect effluent perfusate concentration of adenosine or its RSA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of coronary endothelial cells to cardiac adenosine production. 308 33

Experiments were performed to test the possible involvement of arginine vasopressin (AVP) in the systemic cardiovascular responses to acute hypercapnic acidosis in conscious chronically instrumented rats. Exposure to 6% CO2 caused arterial PCO2 to rise from 34 +/- 2 to 53 +/- 1 Torr. This level of hypercapnia was associated with a consistent bradycardia; however, cardiac output, blood pressure, and total peripheral resistance were not significantly affected. Administration of 10 micrograms/kg iv of the specific V1 vasopressinergic antagonist d(CH2)5Tyr(Me)AVP during 6% CO2 had no effect on any of the measured hemodynamic variables. Furthermore, d(CH2)5Tyr(Me)AVP also had no effect in normocapnic control animals. Exposure to a more severe level of hypercapnia (10% CO2, arterial PCO2 = 89 +/- 1 Torr) resulted in marked hemodynamic alterations. Profound bradycardia and decreased cardiac output in addition to increases in mean arterial blood pressure and total peripheral resistance were observed. V1 vasopressinergic antagonism during 10% CO2 had no effect on heart rate but greatly increased cardiac output. In addition, blood pressure fell and resistance was decreased below prehypercapnic levels. These data suggest that a number of the hemodynamic alterations associated with severe hypercapnic acidosis in the conscious rat may be mediated by the peripheral cardiovascular effects of enhanced AVP release.
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PMID:Cardiovascular effect of V1 vasopressinergic blockade during acute hypercapnia in conscious rats. 310 18

Specimens of Bufo marinus were exposed to aerial and aquatic hypercapnia (5% CO2) in a closed, water recirculation system to evaluate mechanisms involved in the compensation of a respiratory acidosis in these animals. Arterial PCO2 was elevated from about 9 mmHg (1 mmHg = 133.3 Pa) to 35 (1 h) and 37 mmHg (2 h), and gradually approached about 40 mmHg (24 h of hypercapnia). The typical hypercapnia-induced reduction in plasma pH from about 7.9 to below 7.4 was partially offset, at least during the first hours of hypercapnia, by a reduction in the inspired/arterial PCO2 difference, presumably brought about by pulmonary hyperventilation. The predominant contributor to extracellular pH compensation, however, was a net gain of bicarbonate from the environment, mainly facilitated by ammonia excretion. Bicarbonate originating from the environment was accumulated in the body fluids, increasing the plasma concentration from the control of about 9 to 36 mmol l-1 after 24 h. Extracellular pH was compensated to only about 30% of the shift expected at constant bicarbonate level and, according to the steady reduction of pH, non-bicarbonate buffering of CO2 also contributed significantly to the elevation of bicarbonate. This relatively poor pH compensation (compared with fishes) could not be improved either by direct administration of bicarbonate into the bloodstream or by increased environmental ion concentrations. It is concluded that the availability of bicarbonate is not a limiting factor for pH compensation during hypercapnia, and that the inability of Bufo to accumulate bicarbonate to concentrations sufficient for better hypercapnia compensation is based on a constitutional 'bicarbonate threshold' of the resorbing and retaining structures for acid-base-relevant ions.
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PMID:Acid-base regulation and blood gases in the anuran amphibian, Bufo marinus, during environmental hypercapnia. 312 28

Anesthesia induced by use of a combination of xylazine, ketamine, and halothane, under conditions of spontaneous and mechanically controlled ventilation, was evaluated in 5 llamas positioned in dorsal recumbency. Using chronically implanted catheters, systemic arterial blood pressure, pulmonary arterial pressure, right atrial pressure, heart rate and rhythm, cardiac output, blood pH and gas tensions, body temperature, and respiratory rate were measured before anesthesia induction (baseline), throughout the anesthetic period, and for 1 hour into the recovery period. During anesthesia, llamas undergoing spontaneous ventilation developed hypercapnia and respiratory acidosis. Cardiovascular function was decreased during both types of ventilation. The combination of xylazine, ketamine, and halothane in various doses and 2 ventilation procedures (spontaneous and controlled) provided a reliable method for general anesthesia in llamas, but marked cardiovascular depression developed during anesthesia maintenance with halothane. Spontaneous ventilation resulted in potentially clinically important respiratory acidosis.
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PMID:Evaluation of a combination of xylazine, ketamine, and halothane for anesthesia in llamas. 323 40

Papillary muscle preparations from rats with normal arterial oxygen and carbon dioxide tensions and from rats which had been maintained with normal oxygen tension but with hypercapnia for 28 days (FICO2 = 5%) were subjected to acute hypercapnia with or without amiloride, a competitive inhibitor of the Na+/H+ pump. Acclimatisation to hypercapnia reduced the slope of the line relating log tension against the extracellular pH from 0.96(SEM0.06) to 0.71(0.07) (p less than 0.02). Amiloride increased the slope in unacclimatised muscle to 1.39(0.09), p less than 0.001 and in muscles acclimatised to hypercapnia to 1.03(0.13), p less than 0.05. The slope in acclimatised muscles was significantly less steep than in unacclimatised muscle (p less than 0.05). The sarcolemmal Na+H+ exchanger is important in the protection of rat cardiac muscle against acute respiratory acidosis.
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PMID:Effect of amiloride on contractility of rat cardiac muscle exposed to chronic hypercapnia and acute acidosis. 325 18

Blood gas and haemodynamic changes caused by chronic respiratory insufficiency affect the right ventricle and produce chronic cor pulmonale. Equally important but less well known modifications affect the left ventricle and the general circulation and are the subject of the present report. Hypoxemia, hypercapnia and acidosis caused by severe hypoxia create functional disturbances in both ventricles that are manifested in a volume overload that added to other major malfunctions provoke congestive heart failure. The coronary circulation is affected by metabolic factors, perfusion alterations, right ventricular hypertrophy and concomitant coronary lesions. Advanced respiratory insufficiency caused by poorly compensated respiratory acidosis and metabolic acidosis reduces cardiac output and frequency so that tissue perfusion is compromised. Furthermore alterations in transmembrane electrolytic concentrations produce repeated multifocal ventricular arrhythmias that expose the patient to the risk of sudden death. Cardiac failure is reflected in other organs like the kidney and the central nervous system and also contributes to tissue and cerebral hypoxia. The later depresses the respiratory centres and develops into often irreversible coma. A better knowledge of these elements may contribute to the development of appropriate treatment.
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PMID:[General cardiocirculatory effects in chronic respiratory insufficiency]. 354 42

An 87-year-old female, with a history of hypertension controlled with hydrochlorothiazide, was scheduled for excision of a cystic mass of the left lobe of the thyroid. In the course of the anaesthetic, she developed partial airway obstruction that resulted in respiratory acidosis (PaCO2 108 mmHg, pH 7.06), developed premature ventricular contractions and experienced a reduction in plasma potassium concentration from 3.9 to 2.9 mmole X L-1. We interpret this hypokalaemia as a consequence of the epinephrine discharge due to hypercapnia. The case is reported to emphasize the importance of minimizing the sympathetic response to induction of anaesthesia, intubation and surgery in patients with marginal potassium stores.
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PMID:Hypokalaemia and respiratory acidosis following partial obstruction of the airway. 360 55

Necrotizing tracheobronchitis (NTB) is an acute inflammatory lesion of the lower airway which can result in total airway obstruction. While potentially treatable, this lesion has been described predominantly in autopsy or animal studies. We observed clinical symptoms which reflect development of this lesion. Symptoms of acute airway obstruction (hypercarbia, respiratory acidosis, decreased chest wall movement) occurred in eight neonates undergoing treatment with high-frequency jet ventilation; five patients treated with HFJV were studied without signs of obstruction. Emergency bronchoscopy using a rigid bronchoscope was performed in the intensive care unit. The diagnosis of NTB was made by the observation of hyperemia, intraluminal debris, or the appearance of eschar formation. Necrotic debris was removed using forceps and/or suction as necessary. All patients survived treatment. Seven were long-term survivors, all with bronchopulmonary dysplasia. In patients who died, autopsy evaluation of the airway revealed a characteristic picture consisting of necrosis, neutrophil infiltration, epithelial erosion, and intraluminal obstruction.
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PMID:Necrotizing tracheobronchitis: a newly recognized cause of acute obstruction in mechanically ventilated neonates. 362 23

The intrinsic processes involved in the initiation and arrest of seizures are not completely understood. Cortical and cerebellar inhibitory mechanisms, accumulation of metabolic products, and glial uptake of extracellular potassium (K+o), anions, and released neurotransmitters are all important processes that limit focal firing and terminate a seizure once it has been initiated. Of these, the intrinsic cortical inhibitory mechanisms--i.e., recurrent and surround inhibition--appear to be the most important. Active cation and anion transport processes are two metabolic events that have yet to be elucidated but clearly could be involved in terminating a seizure discharge. For example, without an active mechanism to transport chloride, opening of the chloride channel by the inhibitory transmitter GABA would not result in increased chloride permeability. The transient hypoxia and hypercapnia and lactic acidosis that follows a severe tonic-clonic seizure produces a mixed systemic metabolic and respiratory acidosis. In experimental animals, the hypercapnia that results is sufficient to block seizure discharges. Increasing the CO2 concentration significantly reduces the extension to flexion (E/F) ratio of mice given maximal electroshock seizures (MES) and increases the time required for 50% of the animals to recover sufficiently from a first MES to be able to have another MES. The decreased E/F ratio and the increased recovery time (RT50) are both indicative of a decrease in seizure activity. Since the extent to which CO2 is allowed to accumulate in the brain is regulated by the glial specific enzyme carbonic anhydrase (CA), it follows that the glial cell has an integral role in the mechanisms involved in arresting seizure activity. In contrast, hypoxia increased the E/F ratio and decreased the RT50, evidence that seizure activity was enhanced. Another metabolic factor affecting duration of seizure activity, susceptibility to seizures, and recovery from seizures is glucose. Recovery from seizures depends in part on an adequate supply of this energy source. An inverse correlation (R = 0.95) between RT50 and blood sugar was found when the blood sugar was altered experimentally by treatments that altered the endocrine status (pancreatectomy, treatment with alloxan, cortisol, insulin, glucagon, and dextrose). Since glial cells contain (as glycogen) the small amount of glucose present in the brain, they probably hasten the ability of the brain to recover normal function following a seizure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of glial cation and anion transport mechanisms in etiology and arrest of seizures. 370 23


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