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

Intravenous infusion of salbutamol 10 mug/min in seven healthy subjects significantly increased their ventilatory responses to inhaled CO2 in both hypoxia and hyperoxia. These changes in chemical control of breathing are unlikely to be significant when the drug is used in severe asthma but may benefit patients with acute exacerbations of chronic ventilatory failure. The infusion also increased heart rate, which was most pronounced when hypoxia was combined with hypercapnia. The infusion produced an average fall in plasma potassium from 3-99 to 3-10 mmol/l, which was associated with an increase in plasma glucose and serum insulin, suggesting that this arose from a shift of potassium from the extracellular to the intracellular space. Routine monitoring of plasma potassium and the electrocardiogram is indicated when an intravenous salbutamol infusion is used to treat severe asthma as the drug may predispose to cardiac dysrhythmias.
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PMID:Effect of intravenous infusion of salbutamol on ventilatory response to carbon dioxide and hypoxia and on heart rate and plasma potassium in normal men. 124 57

The influence of a anesthetic, ethyl-ether, on arterial plasma levels of glucose, insulin and lipids was studied in starved Wistar rats. Ethyl-ether increased significantly (P < 0.05) glucose plasma levels, as a result not only of stress and of the release of catecholamines and glucocorticoids, but also of the decrease in the use of glucose by the tissues. Ethyl-ether did not change significantly the level of triglycerides, cholesterol and phospholipids. Insulin concentration was not increased, even when hyperglycemia was established. Ketonuria, acidosis and hypercapnia were increased. In these rats the administration of insulin produced a diminution in glycemia. The findings suggest that, under anesthesia with ether, the endocrine pancreas is incapable of recognizing glucose as a specific stimulus to promote the release of insulin.
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PMID:Effects of inhalation of ethyl-ether on glycemia and on some variables of intermediate metabolism in rats. 128 85

The oxygenation and metabolism in appropriate (AGA) and small for gestational age (SGA) fetuses has been investigated by cordocentesis. The umbilical venous and arterial pO2 and pH decrease with gestational age while pCO2 increases and blood lactate concentration does not change. The mean umbilical venous blood glucose concentration is higher than in the umbilical artery indicating that there is fetal glucose uptake from the placenta. Similarly, the maternal glucose concentration is higher than the fetal and the levels in the two compartments are significantly correlated. The plasma insulin concentration increases exponentially with gestation reflecting the progressive maturation of the fetal pancreas. The fetal plasma cortisol does not change but the fetal plasma ACTH increases with gestation. Fetal plasma triglyceride concentration decreases exponentially with gestation and this is likely to be the result of increased utilization by the fetus for deposition into adipose tissue. There is a high correlation between fetal and maternal levels for individual amino acids and the concentration in the fetus is higher than in the mother, supporting the active transport of amino acids by the placenta. Some SGA fetuses are compromised by hypoxemia, hypercapnia, hyperlacticemia and acidosis, are starved of glucose and amino acids, and are hypertriglyceridemic. Furthermore, some of these fetuses are hypoinsulinemic and the degree of hypoinsulinemia is disproportional to the degree of hypoglycemia suggesting pancreatic dysfunction. In SGA fetuses the plasma cortisol is increased and the plasma ACTH decreased. Knowledge of human fetal oxygenation and metabolism may help in deciding the optional timing of delivery but may also constitute a basis for future fetal therapy in the form of oxygen and nutrient supplementation.
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PMID:Metabolic and endocrine findings in appropriate and small for gestational age fetuses. 165 88

The health risks of obesity increase with its severity and reach significance at a weight greater than 20% above optimal, by using life insurance tables, or at a body mass index greater than 27. Risks include hypertension, insulin resistance and diabetes mellitus, cardiovascular disease, hypertriglyceridemia, low high-density-lipoprotein cholesterol, and, in some studies, high total-and low-density-lipoprotein cholesterol. There is an increased mortality from endometrial cancer in women and from colorectal cancer in men. Chronic hypoxia and hypercapnia, sleep apnea, gout, and degenerative joint disease can occur with more severe obesity. The distribution of body fat is directly related to these health risks. Abdominal obesity is more dangerous than gluteal-femoral obesity because the amount of intraabdominal fat seems to determine much of the increased peril; therefore, risks of cardiovascular disease, stroke, hypertension, and diabetes increase with abdominal obesity, even independently of total fat mass.
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PMID:Health implications of obesity. 203 92

This study examined the effects of hypoglycemia (HG) on cerebral metabolism and cerebrovascular reactivity to carbon dioxide. Cerebral blood flow (CBF) was determined using radiolabeled microspheres in pentobarbital-anesthetized dogs. Cerebral oxygen, glucose, lactate, pyruvate, acetoacetate, and beta-hydroxybutyrate uptakes were calculated using the respective concentrations measured in arterial and sagittal sinus blood samples. EEG was recorded throughout each experiment. HG was induced with insulin to obtain a blood glucose less than 30 mg/100 ml. Hypercapnia was studied in 10 animals (3 control, 7 HG) by increasing arterial carbon dioxide tension (PaCO2) from control (35 +/- 4; mean +/- SE) to 54 +/- 2 Torr during normoglycemia (NG) and HG. Hypocapnia was studied in 11 animals (3 control, 8 HG) by decreasing PaCO2 from control (39 +/- 1) to 14 +/- 1 Torr in NG and HG. Measurements were taken after reaching steady-state PaCO2 in both groups at each control and altered PaCO2 state. In the hypercapnic group, glucose decreased from 71 +/- 3 to 28 +/- 3 mg/100 ml. CBF increased with hypercapnia to 175% of control in both NG and HG. Cerebral metabolic rate of oxygen and electroencephalogram (EEG) did not change in the hypercapnic group. In the hypocapnic group glucose decreased from 71 +/- 3 to 19 +/- 2 mg/100 ml. CBF decreased with hypocapnia to 62 +/- 5% of control in NG but remained at control in HG. This was not accompanied by changes in cerebral oxygen consumption; however, a flat EEG occurred in all HG hypocapnic animals. No change occurred in uptake of the other cerebral metabolites measured in any group. This study shows that the CBF hypercapnic response remains intact during HG; however, hypocapnia causes severe EEG disturbances and impairs the cerebral vasoconstriction response.
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PMID:Effect of hypoglycemia on cerebral metabolism and carbon dioxide responsivity. 249 46

Cardiorespiratory reflexes (CRRs) were studied by measuring heart-rate (HR) variation during 6 breaths/min respiration (delta R6) and Valsalva maneuver (VR) in 145 healthy and 417 type I (insulin-dependent) diabetic subjects. HR variation with breathing at 12 breaths/min and ventilatory response to hypercapnia/hypoxia were measured in fewer subjects. CRR results were compared with symptoms of autonomic dysfunction, the neurological examination, nerve conduction studies, and quantitative sweat testing. The objective was to compare the sensitivity of various methods of characterizing diabetic patients and to use this information when staging patients for clinical therapeutic trials. CRR responses were age dependent in both populations. Either delta R6 or VR was abnormal in 74% of diabetic patients, delta R6 being more sensitive. CRRs correlated well with the presence of symptoms of autonomic dysfunction, abnormalities on the neurological examination, results of nerve conduction studies, and sweating activity in the feet of the same patients. However, both CRRs and sweating were abnormal in a high proportion of patients without any clinical manifestations of neuropathy. The ventilatory reflex response to moderate hypercapnia/hypoxia was also measured. It was normal in most of the diabetic patients tested, including many with severe reduction of CRRs. We conclude from the combined results of CRR, ventilatory response, and other studies that the causative factors for abnormal CRR may not be confined to the vagus nerves, and that in most instances, the depressed CRR may be due to a decrease in the efficacy of sensorimotor nerve conduction around the reflex arc.
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PMID:Physiological and clinical correlates of cardiorespiratory reflexes in diabetes mellitus. 273 59

Cerebral blood flow was measured both under conditions of normocapnia and hypercapnia in 22 diabetic patients and 20 normal control subjects, using either the intravenous 133Xe method or the closely comparable 133Xe inhalation method. While 19 out of 20 control subjects responded appropriately to hypercapnia with an increase in flow, eight of the diabetic patients failed to respond normally, this difference being significant (p = 0.03). Those manifesting an abnormal response included young, insulin-dependent patients with a short duration of diabetes and no clinical evidence of complications.
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PMID:Abnormal cerebrovascular carbon dioxide reactivity in people with diabetes. 295 22

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

The development of important respiratory disorders and significant hypertension in association with increasing body weight is not widely recognized. Altered respiratory function results from a combination of mechanical impedance to breathing exerted by thoracic and abdominal fat and a ventilation-perfusion mismatch. Sleep-disordered breathing with periods of hypoventilation, with or without apnoeic episodes, may commonly occur in patients with extreme obesity. Nocturnal hypercapnia and hypoxia in such patients may lead to a decrease in ventilatory drive, abnormal central respiratory control and possibly, in time, the development of the obese-hypoventilation syndrome. Respiratory abnormalities should be suspected in obese patients with a history of restlessness at night, loud snoring and daytime somnolence. Treatment is substantial weight reduction, but short-term measures include the use of compressed air via nasal cannulae for obstructive apnoea, and drugs which alter sleep pattern or stimulate respiration. The alterations in endocrine function, which accompany weight gain, may contribute to an increase in blood pressure and there appears to be a relationship between plasma insulin and catecholamine concentrations, fat cell size and the development of hypertension. The confirmation of a raised blood pressure requires that readings be taken with an adequately sized arm-cuff. In many instances endocrine function becomes normal with weight loss, and there is a corresponding decrease in blood pressure. The ideal management for an obese hypertensive patient is the combination of a suitable calorie-restricted diet with a programme of physical exercise.
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PMID:Clinical complications of obesity. 639 58

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
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PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74


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