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)

It has been suggested that generalized endothelial damage and permeability changes, induced by prolonged activation of the complement system and ensuing release of lysosomal enzymes, prostaglandins and toxic oxygen products, underlie the genesis of the Adult Respiratory Distress Syndrome (ARDS) and Multiple Organ Failure (MOF). The effects in New Zealand white rabbits were investigated of a 4 h infusion of activated complement and its combination with a short hypoxic episode on respiratory function, leukocyte count, platelet count and morphology of the lungs, heart, liver, kidney and spleen. Prolonged activation of the complement system induced hyperventilation with respiratory alkalosis and hypocapnia, depletion of granulocytes (PMN), and a variable accumulation PMN in the capillaries of all organs examined, in combination with interstitial, and, in the liver, cellular oedema. Electron microscopy of the lungs revealed degranulation of PMN, endothelial swelling and widening of the alveolar septa. The combination of hypoxia and systemic complement activation appeared to aggravate this microvascular injury with the occurrence of protein rich alveolar oedema and haemorrhage in the lungs and accumulation of PMN debris containing macrophages in the spleen. The alterations in respiratory function and pulmonary morphology in these rabbits, imitate the clinical and morphological characteristics of the early phase of ARDS. The inflammatory reaction, found in all other organs examined, might represent the early phase of MOF. If so, ARDS and MOF -- clinically closely interconnected syndromes -- might be interpreted as manifestations of the same syndrome and as the clinical expression of an uncontrolled whole body inflammation.
 ...
PMID:Acute generalized microvascular injury by activated complement and hypoxia: the basis of the adult respiratory distress syndrome and multiple organ failure? 309 Oct 57

Alkalosis is prominent among the many physiologic and biochemical effects of sodium lactate infusion. Though this is partially due to the conversion of lactate to bicarbonate, the metabolic component, it may also be secondary to hyperventilation before and during the infusion, the respiratory component. We analyzed pH, carbon dioxide pressure, bicarbonate, and inorganic phosphate from patients with panic disorder and agoraphobia with panic attacks and from normal controls both before and during lactate infusion. Our findings extend earlier work demonstrating that many such patients are chronic hyperventilators. Both metabolic and respiratory alkalosis develop in all subjects during lactate infusion, but only hyperventilation-induced hypocapnia differentiates patients at the point of lactate-induced panic from nonpanicking patients and normal controls. Finally, low inorganic phosphate levels at baseline appear associated with patients who will panic during the subsequent lactate infusion. This last unexpected finding may reflect hyperventilation or an abnormality in intracellular glycolysis.
 ...
PMID:Blood gas changes and hypophosphatemia in lactate-induced panic. 309 75

The objective of this study was to determine whether arterial PCO2 (PaCO2) decreases or remains unchanged from resting levels during mild to moderate steady-state exercise in the dog. To accomplish this, O2 consumption (VO2) arterial blood gases and acid-base status, arterial lactate concentration ([LA-]a), and rectal temperature (Tr) were measured in 27 chronically instrumented dogs at rest, during different levels of submaximal exercise, and during maximal exercise on a motor-driven treadmill. During mild exercise [35% of maximal O2 consumption (VO2 max)], PaCO2 decreased 5.3 +/- 0.4 Torr and resulted in a respiratory alkalosis (delta pHa = +0.029 +/- 0.005). Arterial PO2 (PaO2) increased 5.9 +/- 1.5 Torr and Tr increased 0.5 +/- 0.1 degree C. As the exercise levels progressed from mild to moderate exercise (64% of VO2 max) the magnitude of the hypocapnia and the resultant respiratory alkalosis remained unchanged as PaCO2 remained 5.9 +/- 0.7 Torr below and delta pHa remained 0.029 +/- 0.008 above resting values. When the exercise work rate was increased to elicit VO2 max (96 +/- 2 ml X kg-1 X min-1) the amount of hypocapnia again remained unchanged from submaximal exercise levels and PaCO2 remained 6.0 +/- 0.6 Torr below resting values; however, this response occurred despite continued increases in Tr (delta Tr = 1.7 +/- 0.1 degree C), significant increases in [LA-]a (delta [LA-]a = 2.5 +/- 0.4), and a resultant metabolic acidosis (delta pHa = -0.031 +/- 0.011). The dog, like other nonhuman vertebrates, responded to mild and moderate steady-state exercise with a significant hyperventilation and respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Arterial blood gases and acid-base status of dogs during graded dynamic exercise. 309 50

The effects of hypoxic hypoxia on physiological variables, cerebral circulation, cerebral metabolism, and blood-brain barrier were investigated in conscious, spontaneously breathing rats by exposing them to an atmosphere containing 7% O2. Hypoxia affected a marked hypotension, hypocapnia, and alkalosis. Cortical tissue high-energy phosphates and glucose content were not affected by hypoxia, glucose 6-phosphate, lactate, and pyruvate levels were significantly increased. Blood-brain barrier permeability, regional brain glucose content and lumped constant were not changed by hypoxia. Local cerebral glucose utilization (LCGU) rose by 40-70% of control values in gray matter and by 80-90% in white matter. Under hypoxia, columns of increased and decreased LCGU were detectable in cortical gray matter. Local cerebral blood flow (LCBF) increased by 50-90% in gray matter and by up to 180% in white matter. Coupling between LCGU and LCBF in hypoxia remained unchanged. The data suggest a stimulation of glycolysis, increased glucose transport into the cell, and increased hexokinase activity. The physiological response of gray and white matter to hypoxia obviously differs. Uncoupling of the relation between LCGU and LCBF does not occur.
 ...
PMID:Cerebral circulation, metabolism, and blood-brain barrier of rats in hypocapnic hypoxia. 310 71

In prior studies at high altitude, we have found that pregnancy increases maternal hypoxic ventilatory response (HVR) but the factors responsible are unknown. Changes in metabolic rate and hormones that occur during pregnancy have previously been shown to influence HVR. We therefore sought to determine the contribution of metabolic rate and hormonal changes to the pregnancy-associated rise in HVR. Pregnancy increased HVR in each of 20 normal, low-altitude (1,600 m) residents. As measured by the shape parameter A, HVR at week 36 was 237 +/- 26 (SE) or twofold higher than the 124 +/- 13 value measured 3 mo postpartum (P less than 0.01) despite the presence of the potentially depressant effects of hypocapnia [change in alveolar partial pressure of CO2 (delta PACO2) = -4 +/- 1 mmHg] and alkalosis [change in arterial pH (delta pHa) = 0.02 +/- 0.01 U] during pregnancy. Sixty percent of the increase in HVR values had occurred by week 20 of gestation at which time O2 consumption (VO2) and CO2 production (VCO2) were unchanged relative to values measured postpartum. The remaining 40% rise in HVR paralleled increases in VO2 and VCO2, and further elevation in VO2 and VCO2 with moderate exercise produced an additional increase in HVR. Serum estradiol and progesterone levels increased with pregnancy, but levels did not correlate with HVR. The women reporting the greatest symptoms of dyspnea had higher HVR A values at week 36 than the least dyspneic women (285 +/- 28 vs. 178 +/- 34, respectively, P less than 0.05). We concluded that factors intrinsic to pregnancy in combination with increased metabolic rate raised HVR twofold with pregnancy and may have contributed to the often-reported symptoms of dyspnea in pregnant women.
 ...
PMID:Increased HVR in pregnancy: relationship to hormonal and metabolic changes. 310 85

The results of the investigation of the acid-base state of the arterial and venous blood have proved that during the emotional stress compensated metabolic acidosis develops. Respiratory alkalosis which is a compensatory shift results in the pronounced hypocapnia. The given state of the acid-base equilibrium is found under conditions of simultaneous transport violation and oxygen use by tissues.
 ...
PMID:[Acid-base equilibrium of the blood and oxygen metabolism during stress]. 311 Oct 50

Hyperventilation can undermine cardiovascular homeostasis by generating autonomic imbalance, sympathetic dominance, hypokalaemia, and intracellular alkalosis with calcium ion shifts. The role of hyperventilation in episodic disorders such as arrhythmia and coronary vasospasm can be difficult to identify if the patient does not present in an attack and so a provocation challenge is required. Today, the standard challenge is the forced hyperventilation provocation test (FHPT). A capnograph enables the resting end-tidal PCO2 to be compared with the level 3 min after the period of overbreathing. We report the use of a patient-specific challenge. After the FHPT, the subject is invited to close his eyes and think about the circumstances of an attack, feelings and sensations experienced (breathing is not mentioned) or topics that were seen to disturb the rhythm of breathing when the medical history was taken. A fall of end-tidal PCO2 of 10 mmHg or more lasting at least one minute was taken as a positive response. Out of 57 patients with cardiovascular symptoms suggesting a hypocapnic influence, resting hypocapnia (end-tidal PCO2 = 30 mmHg) was present in 3 (5%). Of the remaining 54, the FHPT was positive in 16 (30%) and the 'think test' in 33 (61%). This suggests that patient-specific stimulation has advantages over an unspecific challenge in testing for episodic hypocapnia.
 ...
PMID:The 'think test': a further technique to elicit hyperventilation. 313 76

Hypoproteinemia by itself produces a metabolic alkalosis. It is not clear whether a respiratory compensation (hypercapnia) develops with this alkalosis; patients with liver cirrhosis, most of them with hypoproteinemia, are known to hyperventilate. We studied 23 clinically stable patients with hypoproteinemia, with very low albumin-to-globulin ratios (range 0.4 to 1.1), who had either liver cirrhosis (n = 12) or other medical conditions (n = 11). In both groups, there was marked hypocapnia, accompanied by alkalemia (PaCO2 values (mean +/- SD) 31 +/- 2 and 32 +/- 3 torr; pH (mean +/- SD) 7.45 +/- 0.03 and 7.47 +/- 0.03, for the patients with cirrhosis and those without, respectively). Hypoxemia was not the stimulus provoking hyperventilation. The lowering of PaCO2 was proportional to the reduction of serum albumin and total protein concentrations; no detectable difference was seen between the patients with cirrhosis and those without cirrhosis in this apparent dependence of PaCO2 on the concentration of serum proteins. Many of these clinically stable patients with hypoproteinemia, with or without liver cirrhosis, had appreciable concentrations of unidentified anions in plasma (inappropriately high anion gap). Whatever the nonrespiratory acid-base status of the patients with hypoproteinemia, their pulmonary ventilation (hypocapnia) appeared excessive when compared with subjects (presumably) without proteinemia who had similar nonrespiratory acid-base states. The mechanism responsible for the hyperventilation in hypoproteinemia and the nature of the unidentified anions in this condition are obscure.
 ...
PMID:Hyperventilation with hypoproteinemia. 318 88

We determined regional cerebral blood flow (rCBF) using [125I]HIPDm [N,N,N'-trimethyl-N'-(2-hydroxy-3-methyl-5-iodobenzyl)-1,3-propanediamin e] and [125I]iodoantipyrine autoradiography under control and pathologic conditions (hypercapnia [acidosis], hypocapnia [alkalosis], and disrupted blood-brain barrier) conditions in 35 rats. In control rats, HIPDm rCBF (indicator fractionation method, n = 5) was lower than the corresponding IAP rCBF (diffusible indicator method, n = 4), most notably in the infratentorial regions and subcortical nuclei. In hypercapnia, rCBF increased by 100% and 37% in the HIPDm (n = 5) and IAP (n = 5) groups, respectively. In hypocapnia, IAP rCBF (n = 4) decreased 34% but HIPDm rCBF (n = 4) did not change. Following disruption of the blood-brain barrier by intracarotid infusion of mannitol in eight rats, both radiotracers (HIPDm n = 4, IAP n = 4) showed decreased rCBF to regions of disruption as defined by trypan blue extravasation. Our work indicates that modeling HIPDm uptake to quantify rCBF using the indicator fractionation method will underestimate blood flow and that HIPDm kinetics are influenced by compartmental pH dynamics that will limit the accuracy of this method in quantifying rCBF in pathologic conditions.
 ...
PMID:Comparison of [125I]HIPDm and [125I]iodoantipyrine in quantifying regional cerebral blood flow in rats. 318 25

In humans alveolar ventilation (VA) is adjusted almost perfectly to the metabolic demands of mild and moderate exercise. For example, in exercise transitions and in the steady state, PaCO2 rarely deviates by more than 1 to 3 mmHg from the value at rest. This near-homeostasis contrasts to most other mammalian species; equines for example, demonstrate a progressive hypocapnia and alkalosis as exercise intensity is increased to moderate levels. In equines, the control systems seem programmed for a specific hyperventilation that contributes to maintenance of PaO2 homeostasis. Generally, during heavy exercise all species hyperventilate creating hypocapnia, increased PAO2, widened A-a O2 gradient, and PaO2 homeostasis. The origin of the metabolic ventilatory stimulus remains controversial. Evidence exists for: a) "neural" mediation, either central command or peripheral afferent in nature; and b) "humoral" mediation with an intra-thoracic metabolite receptor being a possibility. The mechanism of the species differences in hyperventilation during exercise does not appear to be due to species variation in chemoreceptor "fine tuning". Contrary to traditional thinking, recent findings suggest that the hyperventilation during heavy exercise might not be mediated by lactacidosis stimulation of chemoreceptors. The increase in VA during exercise is achieved efficiently in that airway diameter is modulated and the pattern of breathing and the recruitment of respiratory muscles are set to minimize the O2 cost of breathing. It has been postulated that mechanoreceptors in airways, lung parenchyma and the chest wall are important to efficient breathing. Their role and contribution to the exercise hyperpnea has been shown by reductions in respiratory neural output within breath when respiratory impedance is reduced via helium breathing. Hilar nerve afferents do not appear to be critical to this response. However, carotid chemoreceptors appear essential for "fine tuning" of VA when respiratory impedance is reduced. In most healthy exercising mammals, the efficiency component of the exercise stimulus does not compromise VA. There are two known major exceptions. One is the extremely fit human athlete during very high workloads when atypically there is minimal or no hyperventilation resulting in arterial hypoxemia. That indeed the high O2 cost of breathing compromises VA is indicated by hyperventilation and alleviation of hypoxemia with resistance unloading through helium breathing. A second example of a compromise of VA is that of a galloping racehorse at very high workloads.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Breathing during exercise: demands, regulation, limitations. 328 19


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