Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unanaesthetized rats whose arterial chemoreceptors were stimulated by an one hour acute exposition to hypoxic gaseous mixtures with various carbon dioxide concentrations, presented depletion of the catecholamines content of their adrenal glands only when hypocapnia or increased pH was present (non compensated hypoxia). Moreover, exposition to simultaneous hypoxia and hypercapnia increased the epinephrine stock of the adrenal glands. No changes were found in the myocardium amine content in the same conditions. When anaesthetized rats were treated by iv injection of almitrine bismesylate, a peripheral chemoreceptors stimulating drug, adrenal catecholamines content was insignificantly reduced. In the myocardium, the amines remained at control levels. The most powerful factor related to catecholamines depletion in the adrenals seems to be the hypocapnia or the alkalosis induced by the hyperventilation provoked by glomic stimulation. No indication has been found in favor of an effective adrenergic stimulation caused directly by chemoreceptors stimulation.
 ...
PMID:[Chemostimulation and catecholamine content of the rat adrenal medulla]. 171 97

The effect of hypocapnic alkalosis (HA) on nicardipine-induced cerebral vasodilatation was studied in 2 groups of patients undergoing stereotaxic brain biopsy under general anaesthesia. Arterial diameter (AD) was measured in 16 different locations on a carotid arteriogram (lateral view), and intracranial pressure (ICP) was recorded with an intraventricular catheter. At time T0, in normocapnia an arteriogram was performed in both groups. The first group (GI) was then studied in hypocapnia (T1) and following an injection of nicardipine (T2), while the second group (GII) was studied first after injection of nicardipine (T1) and then in hypocapnia (T2). Groups GI (n = 6; 44 y) and GII (n = 6; 46 y) were similar with regard to age, blood pressure, heart rate and PaO2 at all three phases of the study. HA caused a 9.5% decrease in AD (GI.T1) compared to baseline values, and a 15.2% decrease when preceded by injection of nicardipine (GII.T2). In the latter case the decrease was 3% in comparison with baseline. Nicardipine increased AD by 14.7% (GII.T1) and by 18.5% when preceded by HA (GI.T2), but the rise (7.3%) was not significant in comparison with the baselines value. The changes variations were similar whether the entire arterial trunk or only the supraclinoid region were studied. HA decreased ICP by 44% (GI.T1) and by 50% after nicardipine (GII.T2). Nicardipine did not cause an increase in ICP. Nicardipine and HA antagonise each others vasomotor effects, as previously shown in the baboon using nimodipine.
 ...
PMID:Combined effects of nicardipine and hypocapnic alkalosis on cerebral vasomotor activity and intracranial pressure in man. 174 37

Sufentanil, a synthetic opioid that is 5-10 times as potent as fentanyl, has been suggested for use during neurosurgical procedures because it maintains cardiovascular stability and produces hypnosis without the use of additional anesthetic agents. Doses as low as 2.5 micrograms.kg-1 are reported to create deep levels of anesthesia as demonstrated by EEG changes to high-amplitude delta-waves. However, there are no reports concerning the effects of sufentanil on blood flow and metabolism in the human brain. The present study was designed to investigate the influence of high-dose sufentanil-O2 anesthesia on the cerebral circulation, metabolism, and the cerebrovascular response to CO2 in man. METHODS. Nine male and 2 female patients between 41 and 60 years of age who were scheduled for coronary artery bypass surgery were studied. Premedication consisted of flunitrazepam 2 mg orally and piritramide 15 mg and promethazine 50 mg i.m. 1 h before arrival in the induction room. Measurements were performed with the patients awake (I), after sufentanil 10 micrograms.kg-1 as an induction dose followed by 0.15 micrograms.kg-1.min-1 as an infusion with normocapnia (pa CO2 42.1 +/- 2 mmHg) (II), during hypercapnia (pa CO2 53.7 +/- 3.5 mmHg) (III), and during hypocapnia (pa CO2 31.7 +/- 2 mmHg) (IV). Cerebral blood flow (CBF) was measured using the argon wash-in technique. Cerebral venous blood was obtained from a catheter in the superior bulb of the right internal jugular vein. Cerebral metabolic rates of oxygen (CMRO2) glucose (Mgluc) lactate (CMlac) were calculated by multiplying the arterial-cerebral venous oxygen and substrate differences by CBF. The Anaerobic Index was calculated from the equation avD lactate x 100/2 x avD glucose = ANI (%) Cerebral electrical activity was recorded by aperiodic analysis of the EEG (Lifescan). RESULTS AND DISCUSSION. In the EEG sufentanil anesthesia was characterized by a decrease in the number of high-frequency waves and an increase in the number and amplitude of delta-waves, a pattern that did not change throughout the study period. Concomitantly, under normocapnic conditions high-dose sufentanil led to the significant decrease in CBF by 29% accompanied by an 18% increase in cerebral vascular resistance (CVR). CMRO2 decreased by 22% while CMRgluc and CMRlac changed only insignificantly such that the ANI, which represents the percentage of anaerobically metabolized glucose, essentially remained unchanged. Mean perfusion pressure declined by 18% but stayed within the range of autoregulation. Hypoventilation (III) was followed by an 82% increase in CBF as a result of a 55% reduction in CVR, whereas cerebral metabolic parameters did not show important changes when compared to measurement II. Hyperventilation (IV), on the other hand, produced a distinct fall in CBF by 56% to a value that was 21% below the one obtained under normocapnia. This was due to an increase in CVR of the same magnitude. There was a 31% rise in CMRO2, resulting in a decrease in cerebral venous oxygen tension, but in no case did it fall below the critical value of 20 mmHg at which tissue hypoxia becomes severe. Although CMRlac increased and CMRgluc did not significantly change, the ANI remained essentially unchanged, which suggests a predominantly aerobic metabolism. The increase in metabolic activity with sufentanil during hypocapnia might be caused by an alkalosis-induced stimulation of glycolysis. It might also be related to a reduction in the depth of anesthesia, although neither the EEG nor the hemodynamic parameters indicated this. This study shows that the coupling between CBF and metabolism is well maintained and that the cerebrovascular response to CO2 is unimpaired during high-dose sufentanil anesthesia.
 ...
PMID:[The effect of sufentanil on cerebral blood flow, cerebral metabolism and the CO2 reactivity of the cerebral vessels in man]. 182 62

The authors examined in 60 patients with acute pulmonary embolism values of blood gases and acid-base equilibrium, incl. 30 from arterialized capillary blood, in another 30 subjects from arterial blood. On analysis of capillary blood hypoxaemia was present in all subjects, on analysis of arterial blood only in 63%. Respiratory alkalosis was found on capillary examination in 37%, on arterial examination in 23% of the patients. Hypoxaemia and hypocapnia thus are not specific phenomena in acute pulmonary embolism, in particular when accurate blood collection for analysis is respected, and normal values of paO2 and paCO2 do not rule out the presence of pulmonary embolism. In the development of hypoxaemia in patients with pulmonary embolism participates above all an incomplete right-to-left pulmonary shunt, as revealed during calculation of the magnitude of the shunt by means of the so-called oxygen method in 30 patients with embolism, as compared with a group of 10 healthy subjects.
 ...
PMID:[The importance of blood gas analysis and acid-base equilibrium in pulmonary embolism]. 190 44

1. Blood pressure and pulse rate responses to intravenously (i.v.) administered nifedipine were studied in chloralose-anaesthetized rats subjected to hypoxaemia, hyperoxaemia, alkalosis, acidosis, hypocarbia with alkalosis, or hypercarbia with acidosis. 2. Ventilation with a gas mixture of 17% O2, 28% O2, or 23% O2 with 5% CO2 at a fixed stroke volume (10 mL/kg) and rate (80 strokes/min) induced hypoxaemia, hyperoxaemia or hypercarbia, respectively. Hypocarbia was induced by ventilation with 17% O2 at 160 strokes/min. Acidosis or alkalosis was produced by intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3, respectively, in animals ventilated with room air. 3. There were significant decreases in blood pressure and pulse rate during acidosis, and increases in pulse rate during alkalosis and hypercarbia. No marked changes in these parameters were observed under the other experimental conditions. 4. The control animals showed a dose-dependent decrease in blood pressure without marked changes in pulse rate in response to nifedipine injection. 5. Significant reductions in the hypotensive effect of nifedipine were observed in rats subjected to alkalosis, acidosis, or hypercarbia. A similar tendency was also found during hypocarbia while the responses to nifedipine during hypoxaemia and hyperoxaemia were statistically the same as those in the controls. 6. It is concluded that alterations of blood pH reduce the hypotensive effect of nifedipine, and we suggest that blood pH changes probably play a more important role than PO2 or PCO2 abnormalities in altering the cardiovascular responses to nifedipine in hypoventilated or hyperventilated rats.
 ...
PMID:Cardiovascular responses to nifedipine in anaesthetized rats with abnormal blood gas/pH levels. 190 87

Deviations of the alveolar ventilation rate from normality induce respiratory acid-base disturbances. Alveolar hyperventilation leads to hypocapnia and thus respiratory alkalosis whereas alveolar hypoventilation induces hypercapnia leading to respiratory acidosis. The changes in CO2 induce compensatory alterations of renal bicarbonate transport: Hypercapnia stimulates renal reabsorption of bicarbonate whereas hypocapnia enhances urinary bicarbonates. The plasma bicarbonate concentration rises in response to hypercapnia and falls following hypocapnia. Renal regulation of plasma bicarbonate results in a characteristic dependence on systemic PCO2 permitting the formation of diagnostic criteria for respiratory imbalance of acid-base homeostasis. In chronic respiratory acidosis plasma bicarbonate should rise by 0.35 mmol/l per mmHg increase in PCO2. In chronic respiratory alkalosis, on the other hand, plasma bicarbonate should fall by 0.4 mmol/l for every mmHg decrease in PCO2. If the measured bicarbonate values do not fall into this expected range, acute respiratory or mixed (respiratory and metabolic) acid-base disturbances should be suspected. The clinical significance and application of these diagnostic criteria are illustrated by examples.
 ...
PMID:[Hypo- and hyperventilation: consequences for acid-base balance]. 192 34

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.
 ...
PMID:Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis. 199 47

Rats maintained in a hypoxic environment during the first week after birth (NH rats) show a decrease in body growth and oxygen consumption and an increase in ventilation. At the same time the lungs undergo changes in structure which suggests protection of the gas exchange area. In this study, the extent to which these adaptive changes would persist after return to normoxia was investigated. Control rats (C) were given 10% O2 during the first week of life, then returned to normoxic breathing (NH), and rats exposed to the same level and duration of hypoxia after weaning (AH). Body weight increased very little during the week of hypoxia, but after return to normoxia body growth was more than in control rats, and eventually body weight reached the control value at 2 month of age. Both oxygen consumption and minute ventilation were above control levels in the first week after hypoxia, probably reflecting the higher O2 demands of the rapidly growing animals. However, minute ventilation remained elevated even at 7-8 week of age at a time when both body weight and oxygen consumption were the same as in controls. Measurements of blood gases at this age indicated that the persistent hyperventilation was not due to hypoxemia, and was accompanied by hypocapnia and alkalosis. Hematocrit and total heart weight, elevated in hypoxia, returned to control values within 1 week, whereas dry lung weight and right side heart weight remained above the control values as much as during the hypoxic exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Long-term respiratory effects of neonatal hypoxia in rats]. 204 Dec 52

We studied the relationship between contractile function and intracellular pH (pHi) in the isolated rat diaphragm when superfusate PCO2 was changed during hyperoxia or hypoxia. Superfused diaphragm strips were field stimulated at 0.5 Herz, and twitch tension (TT) was recorded. The pHi was calculated from the volume distribution of a weak acid, dimethyl-oxazolidinedione. In hyperoxia, hypercapnic acidosis (pH 7.06-6.63) depressed diaphragm pHi and TT, whereas hypocapnic alkalosis (pH 7.82-8.15) increased pHi but did not significantly affect TT. TT was maximum at physiological pHi (7.06), but in hyperoxic hypercapnic muscles substantial force was still generated at pHi values as low as 6.44. Hypoxia (PO2 30-38 mm Hg) markedly reduced TT; this effect was slightly exacerbated by hypercapnia and attenuated by hypocapnia. Hypoxia lowered pHi by about 0.2 units, which was insufficient to account for the hypoxic contractile failure. Knowledge of the hyperoxic muscle TT/pHi relationship suggests that, in other contexts, caution should be exercised in attributing severe muscle fatigue or force loss to modest falls in pHi.
 ...
PMID:The effect of pH and hypoxia on function and intracellular pH of the rat diaphragm. 210 18

The major objective was to determine in ponies whether factors in addition to changes in blood PCO2 contribute to changes in plasma [H+] during submaximal exercise. Measurements were made to establish in vivo plasma [H+] at rest and during submaximal exercise, and CO2 titration of blood was completed for both in vitro and acute in vivo conditions. In 19 ponies arterial plasma [H+] was decreased from rest 4.5 neq/l (P less than 0.05) during the 7th min of treadmill running at 6 mph, 5% grade (P less than 0.5). A 5.6-Torr exercise hypocapnia accounted for approximately 2.9 neq/l of this reduced [H+]. The non-PCO2 component of this alkalosis was approximately neq/l, and it was due presumably to a 1.7-meq/l increase from rest in the plasma strong ion difference (SID). Despite the arterial hypocapnia, mixed venous PCO2 was 2.7 Torr above rest during steady-state exercise. Nevertheless, mixed venous plasma [H+] was 1.2 neq/l above rest during exercise, which was presumably due to the increase in SID. Also studied was the effect of submaximal exercise on whole blood CO2 content (CCO2). In vitro, at a given PCO2 there was minimal difference in CCO2 between rest and exercise blood, but plasma [HCO3-] was greater for exercise blood than for rest blood. In vivo, during steady-state exercise, arterial plasma blood. In vivo, during steady-state exercise, arterial plasma [HCO3-] was unchanged or slightly elevated from rest, but CaCO2 was 4 vol% below rest.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Plasma [H+] regulation and whole blood [CO2] in exercising ponies. 210 65


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>