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PubMed1993

Succinylcholine causes profound hyperkalemia in hemorrhagic, acidotic rabbits.

Two recent clinical reports suggested that succinylcholine (SCh) may cause severe hyperkalemia in hemorrhagic, acidotic humans. To investigate this, we anesthetized rabbits with halothane and N2O, and inserted venous and arterial catheters. Control rabbits (Group C, n = 4) remained anesthetized and undisturbed. Hemorrhage/profound acidosis (HPA) was accomplished by withdrawal of 25-30 mL/kg of blood and waiting until pHa approximately 7.05 (Group HPA, n = 5). Hemorrhage/minimal acidosis (HMA) was accomplished by withdrawal of 25-30 mL/kg of blood, but acidosis was minimized by not waiting for it to occur and by administering NaHCO3 0-1.4 mEq/kg (Group HMA, n = 4). In a metabolic acidosis group (n = 4), HCl was infused until pHa approximately 7.05. Respiratory acidosis (n = 4) was accomplished by partial obstruction of the endotracheal tube until PaCO2 approximately 120 mm Hg and pHa approximately 7.05. Potassium levels were determined before the above interventions (baseline), immediately before (pre-SCh), and 1, 3, 5, 7, 10, and 13 min after SCh 1 mg/kg intravenously. In Group C, potassium gradually increased from 3.5 +/- 0.2 mEq/L to 4.8 +/- 0.2 mEq/L 13 min after SCh. In Group HPA, potassium increased from 3.8 +/- 0.3 to 7.0 +/- 1.8 mEq/L after hemorrhage/acidosis and then to 11.4 +/- 1.7 mEq/L at 13 min after SCh. The metabolic acidosis group was significantly different from Group C at 7, 10, and 13 min after SCh (maximum at 13 min, 6.8 +/- 1.2 mEq/L).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed2004

[Analysis and adjustment of acid-base disturbances according to the Stewart-Fencl principle].

In 1983, P. J. Stewart proposed a new approach for evaluation of acid-base balance of body fluids. He defined three independent variables responsible for hydrogen ion concentration in body fluids: 1. the partial pressure of carbon dioxide (pCO2); 2. strong ion difference, SID, i.e. the difference between the sums of all the strong (fully dissociated, chemically nonreacting) cations and sums of the strong anions; 3. the total concentration of all the non-volatile weak acids (mainly albumin) designated as [Atot]. On the basis of this theory, V. Fencl invented a new classification of clinical acid-base disturbances. Respiratory acidosis and alkalosis result from abnormalities of pCO2. The classifications of the respiratory disturbances of ABR is identical as in the conventional viewing which is based on the dissociation equation of carbonic acid. Metabolic acidoses or alkaloses result from derangements of the SID and/or [Atot]. The change of SID value is a consequence of either dehydration (alkalosis) or hyperhydration (acidosis). Other mechanisms of SID deviation are either changes of serum chloride concentration (an increase causes acidosis, a decrease causes alkalosis) or an increase of concentrations of substances not routinely measured (ketones, lactate, exogenous acids). [Atot] value is determined mainly by the serum albumin concentration (alkalosis in hypoalbuminemia, acidosis in hyperproteinemia). The Stewart-Fencl approach to acid-base balance enables to understand and predict what happens to hydrogen ions in body fluids and to control the pH abnormalities quantitatively.

Acid-Base Equilibrium↗
PubMed1994

Different effects of respiratory and metabolic acidosis on preganglionic sympathetic nerve activity.

We studied sympathetic nerve activity (SNA) responses, recorded in multifiber preparations of left third thoracic white ramus, to respiratory or isocapnic metabolic acidosis or to CO2 enhancement at constant pH in chloralose-anesthetized paralyzed artificially ventilated cats. Cardiopulmonary, baro-, and peripheral chemoreceptors were denervated by bilaterally cutting vagus and carotid sinus nerves. Acidosis was induced by either decreasing artificial ventilation or infusing HCl (0.5 M i.v.). Both respiratory and isocapnic metabolic acidosis induced a decrease in local extracellular pH, measured directly with pH-sensitive microelectrodes within medulla region containing sympathoexcitatory bulbospinal neurons. The magnitude of changes in medullary pH was independent of the way systemic acidosis was generated. Despite uniformity of changes in local medullary extracellular pH due to systemic respiratory or isocapnic metabolic acidosis, different responses were observed in preganglionic SNA. Isocapnic metabolic acidosis resulted in a slight increase in SNA, averaging 6.4% per 0.05 systemic pH unit decrease. In contrast, respiratory acidosis induced by decreasing artificial ventilation produced a more pronounced increase of SNA, reaching peak changes of approximately 70% compared with control level with normal blood gases, an average increase of 13% per 0.05 systemic pH unit decrease. We conclude that systemic CO2 and H+ concentrations represent different stimuli to sympathetic nervous system. Despite similar changes of local extracellular pH within rostral ventrolateral medulla during systemic acidosis, different responses of SNA suggest other sites or as yet unknown additional effects of CO2 as being responsible for excitation of sympathetic activity.

Acidosis↗
PubMed1983

Influence of alterations in acid-base conditions on intracellular pH of intact renal cortex.

Intracellular pH (pHI) of intact rat renal cortex was estimated using [14C]-5,5-dimethyl-2,4-oxazolidinedione and 22Na+ under conditions of metabolic acidosis and alkalosis, potassium depletion and carbonic anhydrase inhibition. In metabolic acidosis and alkalosis, pHI and bicarbonate concentration changed in the same direction as occurred in plasma. In potassium depletion, systemic acid-base balance was unaltered but a marked intracellular acidosis developed. Carbonic anhydrase inhibition with acetazolamide was associated with an extracellular respiratory acidosis and a rise in intracellular bicarbonate concentration. Another carbonic anhydrase inhibitor, benzolamide, caused no change in systemic acid-base state but produced a decrease in intracellular bicarbonate concentration. When appropriate corrections were made for predicted change in tubular fluid bicarbonate and for intracellular sodium, modification in the absolute values of the above changes occurred but the directions of the changes in pHI and bicarbonate concentration were unaltered.

Acid-Base Equilibrium↗
PubMed1996

Effect of stepwise normalization of perfusate pH on post-ischemic functional recovery and Ca2+ overload in isolated rat hearts.

The purpose of this study was to examine whether initial acidic reperfusion after ischemia followed by stepwise normalization of perfusate pH could improve functional recovery and to assess whether this is associated with a reduction in Ca2+ overload. Isolated rat hearts were subjected to global ischemia for 25 min, followed by 30 min of reperfusion. In the control group (Group C), the perfusate pH was 7.4 throughout reperfusion. In the acidic groups, the perfusate pH was 6.8 for the first 5 min, 7.1 for the second 5 min, and 7.4 for the remainder of reperfusion. Acidic buffer was produced either by adding HCl (metabolic acidosis, Group MA) or by bubbling with gas containing 12 to 24% CO2 (respiratory acidosis, Group RA). The recovery of ventricular function, Ca2+ uptake, and energy metabolites were analyzed. Thirteen of the 15 hearts in Group C, 14 of the 15 in MA and 8 of the 15 in RA recovered regular cardiac rhythm at the end of reperfusion. In these hearts which exhibited normal rhythm, the percent recovery in developed pressure was higher (MA: 73 +/- 8, RA: 68 +/- 6, C: 51 +/- 5%, p < 0.05) and left ventricular end-diastolic pressure was lower (MA: 5.1 +/- 1.4, RA: 5.9 +/- 1.3, C: 14.2 +/- 2.7 mmHg, p < 0.05) in the acidic groups. The improved recovery was associated with a significant reduction in Ca2+ uptake which persisted with the restoration of normal pH. These results demonstrate that early acidic reperfusion enhances contractile recovery and diminishes Ca2+ overload. Moreover, these salutary effects are maintained after stepwise normalization of the perfusate pH to physiological values.

Animals↗
PubMed1992

[Drug-induced acid-base disorders].

Drug-induced acid-base disorders may be classified into four categories with respect to the mechanism. 1. Metabolic acidosis is induced by a large acid loads incurred from exogenous sources (e.g. NH4Cl, or toxin ingestion) or endogenous acid production (e.g. generation of ketoacids or lactic acids by alcohol or phenformin) or base loss (e.g. abuse of laxatives). 2. Metabolic alkalosis results from exogenous bicarbonate loads (e.g. milk-alkali syndrome) or effective extracellular fluid contraction, potassium depletion plus hyperaldosteronism (e.g. vomiting, diuretics, or licorice). 3. Renal tubular acidosis is induced by the drugs which mainly impair proximal and/or distal tubules (e.g. vitamin D, NSAID, acetazolamide or amphotericin B). 4. Respiratory acidosis or alkalosis results from drug-induced respiratory center depression or neuromuscular impairment (e.g. anesthetic, sedative overdosage or curare) or hyperventilation (salicylates, paraldehyde, epinephrine, or nicotine).

Acid-Base Imbalance↗
PubMed2000

Respiratory gas transport, metabolic status, and locomotor capacity of the Christmas Island red crab Gecarcoidea natalis assessed in the field with respect to dichotomous seasonal activity levels.

Red crabs, Gecarcoidea natalis, exhibit seasonal activity patterns: low activity during the dry season when they shelter in burrows to avoid dehydration, and high activity during the wet season. Red crabs were examined in situ in the rainforest of Christmas Island to determine if there were underlying seasonal differences in the capacity for exercise and associated metabolism. During both seasons, free-ranging (FR) crabs engaged in their normal activities and, together with crabs induced to exercise for 5 min, were sampled for haemolymph and muscle tissue. Respiratory gases in the haemolymph and key metabolites were measured to assess differences in metabolic status of FR and exercised crabs. Actively foraging FR crabs during the wet season exhibited a relative haemolymph hypoxia (2.9 kPa) and accumulated an extra 3 mmol. litre(-1) of CO(2) compared to the relatively inactive FR crabs during the dry season. Wet-season crabs appeared to be in a state of relative respiratory acidosis compared to dry-season animals. This hypercapnia may arise as a consequence of a relative hypoventilation in animals with a relatively higher metabolic rate during the wet season. Oxygenation of pulmonary and arterial haemolymph was similar and remained high after 5 min of exercise, indicating that the gills and lungs functioned similarly in gas exchange in both FR and exercised crabs. During exercise, venous O(2) reserves decreased and red crabs experienced a mixed respiratory/metabolic acidosis. Similar changes, after 5 min of enforced exercise, in metabolite concentrations, pH and respiratory gas status in the haemolymph during both sampling seasons suggest that the crabs maintain similar capacity to increase exercise during the wet and the dry seasons, despite the differences in underlying physiological status. This is important since after prolonged inactivity during the dry season, with the arrival of moonsoonal rains, red crabs must engage in their annual breeding migration.

Animals↗
PubMed1985

The effect of carbonic anhydrase inhibition on breathing movements and electrocortical activity in fetal sheep.

Fetal breathing movements (FBM) indicated by repetitive negative intrathoracic pressures and biparietal electrocorticograms (ECoG) were recorded from 8 fetal sheep for 3 h before (control) and 3 h after the administration of a carbonic anhydrase inhibitor, acetazolamide. FBM and the low voltage (LV) ECoG state occurred 36 +/- 5% (SEM) and 60 +/- 3% of the control period, respectively. Virtually no FBM occurred during high voltage (HV) ECoG while in 57 +/- 6% of the LV state the fetuses were making FBM. The peak magnitude of the negative intrathoracic (tracheal) pressure deflections was 4 +/- 1 Torr. Following acetazolamide the incidence of FBM rose to 53 +/- 4% (P less than 0.01) but there was no significant change in the incidence of the LV state (58 +/- 3%). Most of the increase in the incidence of FBM remained confined to periods of LV ECoG activity so that an increased proportion of this state (88 +/- 2%, P less than 0.001) was occupied with respiratory efforts. The amplitude of the FBM also increased to 8 +/- 1 Torr (P less than 0.05). The increased incidence and depth of FBM is most likely due to an elevated hydrogen ion concentration and differs from a fetal respiratory acidosis induced by increasing the inspired CO2 fraction to the ewe in that the respiratory stimulation induced by acetazolamide is not associated with an increased incidence of the permissive LV ECoG state.

Acetazolamide↗
PubMed1985

In vitro effects of hypoxia and (or) hypercapnic acidosis on the myocardial uptake of digoxin.

A recent study has shown in the conscious dog that hypoxia associated with respiratory acidosis could increase the in vivo distribution of digoxin in the myocardium. The aim of the present study was to evaluate in vitro the effects of hypoxia and (or) hypercapnic acidosis on the digoxin uptake. For this purpose, rat myocardium was incubated for 180 min with radiolabelled [3H]digoxin. The uptake of digoxin which was expressed in nanograms of digoxin bound per 100 mg of myocardium was decreased by hypoxia and increased by hypercapnic acidosis. The association of hypoxia and hypercapnic acidosis had no effect on the digoxin uptake, suggesting that in vitro hypoxia acts in an opposite way to hypercapnia.

Acidosis↗
PubMed2003

Direct suppressive effect of acute metabolic and respiratory alkalosis on parathyroid hormone secretion in the dog.

UNLABELLED: Acute alkalosis may directly affect PTH secretion. The effect of acute metabolic and respiratory alkalosis was studied in 20 dogs. PTH values were lower in the metabolic (5.6 +/- 0.8 pg/ml) and respiratory (1.8 +/- 0.6 pg/ml) alkalosis groups than in the control group (27 +/- 5 pg/ml). Acute alkalosis is an independent factor that decreases PTH values during normocalcemia and delays the PTH response to hypocalcemia. INTRODUCTION: We recently showed that acute metabolic and respiratory acidosis stimulated PTH secretion. This study was designed to evaluate whether acute metabolic and respiratory alkalosis suppressed parathyroid hormone (PTH) secretion. MATERIALS AND METHODS: Three groups of 10 dogs were studied: control, acute metabolic alkalosis, and acute respiratory alkalosis. Metabolic alkalosis was induced with an infusion of sodium bicarbonate and respiratory alkalosis by hyperventilation. Calcium chloride was infused to prevent alkalosis-induced hypocalcemia during the first 60 minutes. During the next 30 minutes, disodium EDTA was infused to induce hypocalcemia and to evaluate the PTH response to hypocalcemia. Because the infusion of sodium bicarbonate resulted in hypernatremia, the effect of hypernatremia was studied in an additional group that received hypertonic saline. RESULTS: After 60 minutes of a normocalcemic clamp, PTH values were less (p < 0.05) in the metabolic (5.6 +/- 0.8 pg/ml) and respiratory (1.8 +/- 0.6 pg/ml) alkalosis groups than in the control group (27 +/- 5 pg/ml); the respective blood pH values were 7.61 +/- 0.01, 7.59 +/- 0.02, and 7.39 +/- 0.02. The maximal PTH response to hypocalcemia was similar among the three groups. However, the maximal PTH response was observed after a decrease in ionized calcium of 0.20 mM in the control group but not until a decrease of 0.40 mM in the metabolic and respiratory alkalosis groups. In contrast to the metabolic alkalosis group, hypernatremia (157 +/- 2 mEq/liter) in the hypertonic saline group was associated with an increased PTH value (46 +/- 4 pg/ml). Finally, the half-life of intact PTH was not different among the control and two alkalosis groups. CONCLUSIONS: Acute metabolic and respiratory alkalosis markedly decreased PTH values during normocalcemia and delayed the PTH response to hypocalcemia. Whether acute metabolic and respiratory alkalosis affect PTH and calcium metabolism in such settings as the postprandial alkaline tide (metabolic alkalosis) and acute sepsis (respiratory alkalosis) deserves to be evaluated in future studies.

Acute Disease↗
PubMed1975

[The role of neuromediators in changes in the character of respiration and in its correction following cranio-cerebral trauma].

Experimental studies on dogs and clinical examinations of patients with brain injuries permitted to state that the activity of the sympathicoadrenal system in the posttraumatic period is increased. The cholinergic processes in such conditions are inhibited, the concentration of blood serotonin is decreased. Depending upon the character of changed neurohumoral blood factors the parameters of external respiration (hypotachypnoe with respiratory acidosis) are also changed. In such condition hydrocortison fulfills the normalizing effect on the respiratory function only in a stimulation of the inhibited cholinergic system by cholinomimetics.

Acetylcholine↗
PubMed1990

Suicidal ingestion of formalin with fatal complications.

After ingestion of an unknown amount of formalin with suicidal intent, a 55-year-old female and a 34-year-old male were admitted to the hospital with extensive gastrointestinal corrosive damage, circulatory shock, metabolic acidosis, respiratory insufficiency and impairment of renal function, which rapidly progressed to acute renal failure. Metabolic acidosis was in part due to high plasma levels of formic acid, the main metabolite of formaldehyde, and hyperlactatemia. Both patients underwent hemodialysis and hemofiltration treatment. In the male patient, a gastrectomy had to be performed. The further clinical course in the patients was characterized by sepsis and protracted pulmonary complications. Both patients died after developing adult respiratory distress syndrome and global cardiac insufficiency. In vitro experiments on formaldehyde reactivity to proteins yielded evidence for almost complete but reversible binding to plasma and blood. Formaldehyde probably exerts systemic toxicity in the form of its labile Schiff's base with proteins, but not as free formaldehyde.

Adult↗
PubMed2003

Cross-talk between two organs: how the kidney responds to disruption of acid-base balance by the lung.

Hypoventilation increases PaCO(2) (hypercapnia) and initiates the acid-base disorder known as respiratory acidosis. Hyperventilation decreases PaCO(2) (hypocapnia) and initiates the acid-base disorder known as respiratory alkalosis. The impact on acidity of these primary changes in PaCO(2) is ameliorated by secondary, directional changes in plasma bicarbonate concentration that occur in two stages. Acutely, modest changes in plasma bicarbonate originate from titration of the body's nonbicarbonate buffers. In chronic hypercapnia and hypocapnia, larger changes in plasma bicarbonate occur that reflect adjustments in renal acidification mechanisms. As a result, the amelioration of systemic acidity is more pronounced in the chronic forms of the respiratory acid-base disorders.

Acid-Base Imbalance↗
PubMed1984

Mechanical controlled hypoventilation in status asthmaticus.

This study reports the results obtained with mechanical ventilation in severe respiratory failure secondary to status asthmaticus. Of the 159 patients with status asthmaticus admitted to the Intensive Respiratory Unit over a 5-yr period, 26 required mechanical ventilation for a total of 34 episodes of acute respiratory acidosis. At the time of intubation, 10 patients were in coma and 5 were in respiratory arrest. Controlled mechanical ventilation was maintained for a mean of 2.5 days. Complications were few and reversible. All patients survived. These favorable results are attributed to a new strategy: mechanical ventilation is used to obtain a correction of hypoxemia with hyperoxic mixtures without attempting to restore an adequate alveolar ventilation. The respirator is adjusted to avoid high airway pressures, which appear to be more dangerous than persistent hypercapnia itself. Correction of hypercapnia is obtained later when bronchial obstruction relief provides better conditions of ventilation-perfusion distribution. So the risks of barotrauma and cardiocirculatory failure, which are frequently reported as fatal complications, appear to be significantly decreased.

Acid-Base Equilibrium↗
PubMed1998

pHo, pHi, and PCO2 in stimulation of IP3 and [Ca2+]c in piglet cerebrovascular smooth muscle.

Hypocapnia produces cerebral vasoconstriction. The mechanisms involved in hypocapnia-induced elevation of vascular smooth muscle tone remain unclear. We addressed the hypothesis that, in cerebrovascular smooth muscle, increases in extracellular pH (pHo) cause increases in Ins(1,4,5)P3 and cytosolic calcium ([Ca2+]c). Superfused primary cultures of piglet cerebral microvascular smooth muscle cells were exposed to artificial CSF (aCSF) of control (pHo 7. 4, PCO2 36 mm Hg), metabolic alkalosis (pHo 7.7, PCO2 36 mm Hg), or respiratory alkalosis (pHo 7.7, PCO2 19 mm Hg). Intracellular pH (pHi) and [Ca2+]c were measured, using BCECF and fura-2, respectively, with dual wavelength spectroscopy. Ins(1,4,5)P3 was determined by a protein binding assay. Both metabolic and respiratory acidosis treatments increased pHi from the control value of about 7.2 to 7.35. Metabolic and respiratory alkalosis increased Ins(1,4,5)P3, as we showed previously. Metabolic and respiratory alkalosis increased [Ca2+]c about 80% and 110%, respectively. Neither Ins(1,4,5)P3 nor [Ca2+]c increased in cells treated with aCSF that produced control pHo with increased pHi (7.3). In contrast, when pHo increased (7.7), but pHi was maintained at control (7.2), Ins(1,4,5)P3 increased from 123 pmol/well to 307 pmol/well and [Ca2+]c increased 46%. However, the increase of [Ca2+]c was less than with either respiratory or metabolic alkalosis. Thus, hypocapnia-induced cerebral vasoconstriction could involve production of Ins(1,4,5)P3 with resultant elevation in [Ca2+]c. While the Ins(1,4,5)P3 signal appears to be dependent on an increase in extracellular pH, a role for intracellular pH cannot be completely excluded.

Alkalosis, Respiratory↗
PubMedDate not supplied

Bicarbonate transport along the loop of Henle: molecular mechanisms and regulation.

The loop of Henle (LOH) is an important site of renal tubule acidification. A combination of several techniques, including in vivo microperfusion, perfusion in vitro of the S3 segment of the proximal tubule and of the thick ascending limb (TAL) of Henle's loop, as well as quantitative PCR performed on isolated TAL, has permitted the definition of key transporters and their role in modulating bicarbonate reabsorption in physiological and pathophysiological conditions. Na(+)-H+ exchange is the most important transport mechanism responsible for bicarbonate reabsorption, although a small but significant contribution of H(+)-ATPase-mediated bicarbonate reabsorption can also be identified. NHE3 is the main of several NHE isoforms expressed in the TAL and in the S3 segment of the proximal tubule. Special properties of the Na(+)-H+ exchanger in the TAL are its relative insensitivity to changes in cell pH (pHi) and the tight coupling between apical and basolateral Na(+)-H+ exchange. Several hormones, including anti-diuretic hormone (ADH), angiotensin II (AII), and gluco- and mineralocorticoids regulate Na(+)-H+ exchange. Loop diuretics such as furosemide stimulate bicarbonate transport along the LOH. Systemic acid-base disturbances also modulate bicarbonate transport: acidosis increases bicarbonate reabsorption, while metabolic alkalosis has the opposite effect. Neither hypokalemic alkalosis nor respiratory alkalosis or respiratory acidosis alter bicarbonate transport along the LOH. A significant role of HCO3 backflux, most likely through the paracellular pathway of the TAL, can also be observed. Changes in extracellular osmolality also affect bicarbonate reabsorption: hypertonicity inhibits, whereas hypotonicity stimulates transport. Transport activation is also observed as an adaptive response to glomerular hyperfiltration.

Absorption↗
PubMed1986

Role of glial cation and anion transport mechanisms in etiology and arrest of seizures.

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)

Animals↗
PubMed1991

Intermittent short-term negative pressure ventilation and increased oxygenation in COPD patients with severe hypercapnic respiratory failure.

With the aim of testing a method that allows increasing concentrations of oxygen to be administered to patients with severe hypoxemia and hypercapnia while avoiding the risk of increasing respiratory acidosis, we studied 17 male patients with advanced chronic obstructive pulmonary disease (COPD) and severe hypercapnic respiratory failure. During 6 h and on one day only, all patients were given intermittent negative pressure ventilation (INPV) together with oxygenation starting at a concentration of 24 percent and increasing to 30 percent. Using this procedure, it was possible to raise arterial PaO2 to safe levels (from 47.2 +/- 3 mm Hg to 61.5 +/- 6 mm Hg, p less than 0.001) without increasing hypercapnia, and a significant drop in PaCO2 levels (from 74.4 +/- 9 mm Hg to 65.6 +/- 12 mm Hg, p less than 0.005) was even observed. One hour after INPV ended, the mean values of PaO2, PaCO2, oxygen saturation, and pH were also significantly better than prestudy values. We conclude that INPV and oxygen therapy with increasing oxygen flow could constitute an alternative option to intubation and mechanical ventilation in cases of severe hypercapnic respiratory failure due to advanced COPD.

Aged↗