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

The dynamics and regulation of red blood cell flow in the cerebral microcirculation was studied by intravital fluorescence video-microscopy in a closed cranial window preparation in the rat. The studies revealed that capillary perfusion in the brain is essentially continuous but a stationary difference from capillary to capillary within the same microvascular network exists. The main mechanism of an increase in flow in cerebral capillaries is an increase in linear velocity with no or minor role for classical capillary recruitment. While cyclic opening and closing of capillaries is not evident, low frequency oscillations in capillary flow velocity are present when perfusion or oxygen supply to tissue is challenged. In hypoxic hypoxia and moderate hypercapnia, RBC velocity increases in all capillaries while in severe hypercapnia, redistribution of RBC velocity in the capillary network occurs. Both systemic hypotension and severe hypercapnia are accompanied by an increase in the homogeneity of capillary flow; this change involves the redistribution of RBC flow between thoroughfare channels and exchange capillaries. Thoroughfare channels may thus provide a recruitable flow reserve in the cerebral microcirculation. The capillary flow response to hypoxic and anemic hypoxia depends on the activity neuronal nitric oxide synthase. These findings suggest the presence of a physiological regulatory mechanism of cerebral capillary red blood cell flow and oxygen supply which may involve neuronal nitric oxide as a mediator.
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PMID:Regulation of oxygen supply in the cerebral circulation. 950 93

Histological studies have detected nitric oxide (NO) synthase in the central nervous system of all vertebrates examined, from lampreys to mammals. However, there are still very few comparative physiological studies on the function of NO synthase in the brain of non-mammalian vertebrates. So far, we know that acetylcholine can cause an NO-dependent increase in brain blood flow in turtles and some fish species (crucian carp and rainbow trout), whereas some other fishes appear to lack such a mechanism. Hypercapnia can induce NO-dependent cerebral vasodilation in mammals, but such a mechanism appears to be lacking in the ectothermic vertebrates examined. The number of species studied needs to be expanded before we can draw any firm conclusions about the origin of NO-dependent brain blood flow regulation: if it has evolved more than once or if it has been occasionally lost during evolution. We conclude that NO synthase may be present in all vertebrate brains but that its functions can vary, as judged from its role in cerebral blood flow regulation. The diversity of functions that NO has proven to have within the mammalian brain is likely to be paralleled by the same degree of diversity of function between vertebrate groups.
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PMID:Comparative aspects on nitric oxide in brain and its role as a cerebral vasodilator. 950 13

The presence of meconium in the respiratory tract causes atelectasis, hypoxemia, hypercapnia, persistent pulmonary hypertension, inflammatory changes, and surfactant inactivation. Prevention is the most important factor in the management of meconium aspiration syndrome and it includes both prenatal and postnatal care. Prenatal procedures include constant fetal heart rate monitoring during labor, examination of acid-base equilibrium in the capillary blood from the fetal scalp, and eventually amnioinfusion. Amnioinfusion is not a widely accepted care and further studies to confirm its benefits are required. Postnatal procedures include obligatory suction of the oral-pharyngeal cavity and nose before the first breath, and selective endotracheal suction only in depressed neonates or neonates born from thick meconium-stained amniotic fluid. Conventional therapy of meconium aspiration syndrome includes monitoring of vital functions, chest physiotherapy, site drainage, airway suction, oxygen supply, respiratory support, antibiotics, sedation, normal fluid balance and calories intake, and when indicated, agents stabilizing blood pressure and heart rate. New management methods of meconium aspiration syndrome, not recommended as standard procedures at present include high-frequency oscillatory or jet ventilation as a lifesaving therapy, the use of exogenous surfactant, surfactant lavage of the bronchial tree, liquid ventilation, and inhalation of nitric oxide. Extracorporeal membrane oxygenation is of considerable importance in the treatment of the most severe meconium aspiration syndrome, but its role is diminishing with the development of other therapeutic methods.
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PMID:Contemporary treatment options for meconium aspiration syndrome. 957 71

The vascular tone, vascular resistance and blood flow in the brain are regulated by neural and humoral factors in quite a different way from those of peripheral organs and tissues. In contrast to the dominant vasoconstrictor control in the periphery, the intracranial vascular tone is predominantly influenced by vasodilator mediators over vasoconstrictor ones. Recent studies have revealed that nitroxidergic vasodilator nerve and endothelium-derived hyperpolarizing factor (EDHF) or K+ channel opening substance appear to play important roles in the regulation of cerebral arterial and arteriolar tone in primate and subprimate mammals, in addition to the accepted information concerning the crucial contribution of endothelium-derived relaxing factor (EDRF) or nitric oxide (NO), polypeptides, prostanoids, etc. This article summarizes characteristic properties of vasodilator factors in controlling the cerebral arterial and arteriolar tone that undoubtedly contribute to circulatory homeostasis. The content includes vasodilator nerve, endogenous vasodilator substances, and vasodilator interventions such as hypoxia, hypercapnia and hyperosmolarity.
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PMID:Cerebral vasodilators. 962 14

1. The role of endogenous nitric oxide (NO) generated by neuronal nitric oxide synthase (NOS-1) in the control of respiration during hypoxia and hypercapnia was assessed using mutant mice deficient in NOS-1. 2. Experiments were performed on awake and anaesthetized mutant and wild-type control mice. Respiratory responses to varying levels of inspired oxygen (100, 21 and 12% O2) and carbon dioxide (3 and 5% CO2 balanced oxygen) were analysed. In awake animals, respiration was monitored by body plethysmograph along with oxygen consumption (VO2), CO2 production (VCO2) and body temperature. In anaesthetized, spontaneously breathing mice, integrated efferent phrenic nerve activity was monitored as an index of neural respiration along with arterial blood pressure and blood gases. Cyclic 3',5'-guanosine monophosphate (cGMP) levels in the brainstem were analysed by radioimmunoassay as an index of nitric oxide generation. 3. Unanaesthetized mutant mice exhibited greater respiratory responses during 21 and 12% O2 than the wild-type controls. Respiratory responses were associated with significant decreases in oxygen consumption in both groups of mice, and the magnitude of change was greater in mutant than wild-type mice. Changes in CO2 production and body temperature, however, were comparable between both groups of mice. 4. Similar augmentation of respiratory responses during hypoxia was also observed in anaesthetized mutant mice. In addition, five of the fourteen mutant mice displayed periodic oscillations in respiration (brief episodes of increases in respiratory rate and tidal phrenic nerve activity) while breathing 21 and 12% O2, but not during 100% O2. The time interval between the episodes decreased by reducing inspired oxygen from 21 to 12% O2. 5. Changes in arterial blood pressure and arterial blood gases were comparable at any given level of inspired oxygen between both groups of mice, indicating that changes in these variables do not account for the differences in the response to hypoxia. 6. Respiratory responses to brief hyperoxia (Dejours test) and to cyanide, a potent chemoreceptor stimulant, were more pronounced in mutant mice, suggesting augmented peripheral chemoreceptor sensitivity. 7. cGMP levels were elevated in the brainstem during 21 and 12% O2 in wild-type but not in mutant mice, indicating decreased formation of nitric oxide in mutant mice. 8. The magnitude of respiratory responses to hypercapnia (3 and 5% CO2 balanced oxygen) was comparable in both groups of mice in the awake and anaesthetized conditions. 9. These observations suggest that the hypoxic responses were selectively augmented in mutant mice deficient in NOS-1. Peripheral as well as central mechanisms contributed to the altered responses to hypoxia. These results support the idea that nitric oxide generated by NOS-1 is an important physiological modulator of respiration during hypoxia.
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PMID:Altered respiratory responses to hypoxia in mutant mice deficient in neuronal nitric oxide synthase. 967 81

Nitric oxide (NO) is a novel neurotransmitter candidate to which a large number of physiological roles has been ascribed. In the present study, immunocytochemistry was used to demonstrate NO synthase (NOS) and to investigate possible co-localization with other neurotransmitters. In the trigeminal ganglion of the cat, a moderate number of NOS immunoreactive nerve cell bodies was seen, of which the major part also expressed calcitonin gene-related peptide (CGRP). The nerve cell bodies expressing NOS in the trigeminal ganglion were predominantly of small to medium size; while numerous cell bodies of varying size contained CGRP. With in situ hybridization using oligonucleotide probes, CGRP mRNA was demonstrated in almost all trigeminal neurons of the cat. Stimulation of the nasociliary nerve resulted in a frequency-dependent increase in ipsilateral local cortical blood flow by 30 +/- 6%. Administration of the NOS inhibitor NG-nitro-L-arginine-methylester (L-NAME) did not significantly alter this response when applied intravenously or on the cortical surface. Local cortical administration of the CGRP blocker h-CGRP (8-37) did not alter the cerebral vasodilator response to hypercapnia or resting flow. However, the nasociliary nerve response was reduced by 50% after h-CGRP (8-37), with a general shift to the right of the frequency-response curve. These data suggest that although NOS is seen in several trigeminal ganglion cells and coexists with CGRP in a subpopulation of the sensory neurons, its role in trigeminally mediated vasodilatation was not significant.
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PMID:Calcitonin gene-related peptide and nitric oxide in the trigeminal ganglion: cerebral vasodilatation from trigeminal nerve stimulation involves mainly calcitonin gene-related peptide. 968 99

Carbon monoxide (CO) is an endogenously produced gas sharing many properties with nitric oxide (NO), notably activating soluble guanylate cyclase and relaxing blood vessels. The brain can generate high quantities of CO from a constitutive enzyme, haem oxygenase (HO-2). To determine whether CO is involved in the regulatory mechanisms of cerebral blood flow (CBF), two conditions associated with a reproducible CBF increase were studied in rats: epileptic seizures induced by kainate, and hypercapnia. The HO inhibitor tin protoporphyrin (Sn-PP) did not modify the basal level of CBF, significantly reduced the increase in CBF during status epilepticus, and did not affect the cerebrovascular response to hypercapnia. It is concluded that CO participates in the regulation of CBF in specific conditions, notably those associated with glutamate release.
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PMID:Carbon monoxide regulates cerebral blood flow in epileptic seizures but not in hypercapnia. 969 25

Hypercapnia elicits hypothermia in a number of vertebrates, but the mechanisms involved are not well understood. In the present study, we assessed the participation of the nitric oxide (NO) pathway in hypercapnia-induced hypothermia and hyperventilation by means of NO synthase inhibition by using Nomega-nitro-L-arginine (L-NNA). Measurements of ventilation, body temperature, and oxygen consumption were performed in awake unrestrained rats before and after L-NNA injection (intraperitoneally) and L-NNA injection followed by hypercapnia (5% CO2). Control animals received saline injections. L-NNA altered the breathing pattern during the control situation but not during hypercapnia. A significant (P < 0.05) drop in body temperature was measured after both L-NNA (40 mg/kg) and 5% inspired CO2, with a drop in oxygen consumption in the first situation but not in the second. Hypercapnia had no effect on L-NNA-induced hypothermia. The ventilatory response to hypercapnia was not changed by L-NNA, even though L-NNA caused a drop in body temperature. The present data indicate that the two responses elicited by hypercapnia, i.e., hyperventilation and hypothermia, do not share NO as a common mediator. However, the L-arginine-NO pathway participates, although in an unrelated way, in respiratory function and thermoregulation.
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PMID:Effect of nitric oxide synthase inhibition on hypercapnia-induced hypothermia and hyperventilation. 972 71

1. We examined the vasodilatory effect of hypercapnia in the rat isolated mesenteric vascular bed. The preparation was perfused constantly (5 ml min(-1) with oxygenated Krebs-Ringer solution, and the perfusion pressure was measured. In order to keep the extracellular pH (pHe) constant (around 7.35) against a change in CO2, adequate amounts of NaHCO3 were added to Krebs-Ringer solution. 2. In the endothelium intact preparations, an increase in CO2 from 2.5% to 10% in increments of 2.5% decreased the 10 microM phenylephrine (PE)-produced increase in the perfusion pressure in a concentration-dependent manner. Denudation of the endothelium by CHAPS (3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulphonate) (5 mg l(-1), 90 s perfusion) abolished the vasodilatory effect of hypercapnia. 3. An increase in CO2 from 5% to 10% reduced the increases in the perfusion pressure produced by 10 microM PE and 400 nM U-46619 by 48% and 44%, respectively. NG-monomethyl-L-arginine (100 microM) and indomethacin (10 microM) did not affect the vasodilatory effect of hypercapnia, whereas the vasodilatory response of the preparation to hypercapnia disappeared when the preparation was contracted by 60 mM K+ instead of PE or U-46619. 4. The vasodilatory effect of hypercapnia observed in the PE- or U-46619-precontracted preparation was affected by neither tetraethylammonium (1 mM), apamin (500 microM), glibenclamide (10 microM), nor 4-aminopyridine (1.5 mM). On the other hand, pretreatment with Ba2+ at a concentration of 0.3 mM abolished the hypercapnia-produced vasodilation. 5. An increase in the concentration of K+ in Krebs-Ringer solution from 4.5 mM to 12.5 mM in increments of 2 mM reduced the PE-produced increase in the perfusion pressure in a concentration-dependent manner. Pretreatment of the preparations with not only Ba2+ (0.3 mM) but also CHAPS abolished the vasodilatory effect of K+. 6. The results suggest that an increase in CO2 produces vasodilation by an endothelium-dependent mechanism in the rat mesenteric vascular bed. The membrane hyperpolarization of the endothelial cell by an activation of the inward rectifier K+ channel seems to be the mechanism underlying the hypercapnia-produced vasodilation. Neither nitric oxide nor prostaglandins are involved in this response.
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PMID:Involvement of barium-sensitive K+ channels in endothelium-dependent vasodilation produced by hypercapnia in rat mesenteric vascular beds. 977 57

Acute respiratory distress syndrome (ARDS) is a severe condition with a high mortality rate, despite conventional treatment using mechanical ventilation. Better understanding of the pathophysiology and awareness of important iatrogenic lung injury secondary to mechanical ventilation has led to new therapeutic principles. Mechanical ventilation strategy during ARDS is characterized by positive end-expiratory pressure, increase in the inspiratory time, high inspiratory oxygen concentration and, more recently, use of permissive hypercapnia. High frequency ventilation allows optimal lung recruitment under small tidal volume. The effectiveness of extracorporeal oxygenation techniques is demonstrated, but because of their cost and morbidity these therapies are rational only in patients who seem likely to die. Partial liquid ventilation and inhaled nitric oxide have great potential but require further studies. Intratracheal exogenous surfactant might be beneficial but controlled trials are needed to confirm the usefulness of this expensive therapy. Finally, a number of adjuncts to mechanical ventilation are currently available to minimize iatrogenic lung injury and improve the outcome. The role of these new treatments must be defined with randomized and controlled clinical trials using homogenous inclusion criteria.
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PMID:[Recent developments in the treatment of pediatric acute respiratory distress syndrome]. 980 55


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