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

Cerebral vascular carbon dioxide (CO2) reactivities were compared in normotensive (NTR) and hypertensive (SHR) rats. Cerebral blood flow (CBF) in cortex and thalamus were evaluated before and during one hour of hyperventilation. After one hour of hyperventilation brain lactate, pyruvate, and ATP concentrations were also determined. Significant and similar reductions of CBF due to hyperventilation induce hypocapnia were found in both NTR and SHR groups. In contrast the percent increase in cerebrovascular resistance (CVR) per unit decrease in paCO2 was significant, indicating that hypocapnia induced vasoconstriction is greater in NTR than in SHR groups. During hyperventilation the average value for lactate in the NTR group was 3.98 mM/kg. In contrast it was 3.15 mM/kg in the SHR group, a significant difference (p less than 0.05). When paCO2 fell below 15 mm Hg the cerebral lactate increased strikingly in the NTR group and cortical CVR was reduced suggesting that an accumulation of the ischemic metabolites caused dilatation of the constricted cerebral vessels. In contrast the SHR group disclosed no such changes. The increase CVR characteristic of SHR appeared to diminish the cerebral vasoconstrictive response to hypocapnia. As a result ischemic metabolites in the brain do not increase in this group to the degree that they do in NTR.
Stroke
PMID:Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats. 681 44

The haemodynamic effects of nitroprusside (SNP) were studied in six patients undergoing surgery for intracranial aneurysm under controlled hypotension in endotracheal anaesthesia with halothane-nitrous oxide during hypocapnia. Mean arterial pressure was reduced with SNP from mean 12.25 kPa to mean 8.29 kPa (32%). There were concomitant statistically significant decreases in systemic vascular resistance (-21%), cardiac index (-17%), stroke index (-23%), pulmonary arterial mean pressure (-27%) and pulmonary capillary wedge pressure (-27%). Heart rate, central venous pressure and pulmonary vascular resistance did not change significantly. After the infusion of SNP was discontinued all parameters, except cardiac index and heart rate, returned to values not significantly different from the control values. The hypotension induced by SNP resulted from reductions in cardiac index and systemic vascular resistance. The reduction in cardiac index did not reach a critical level in any of the patients.
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PMID:Haemodynamic changes during sodium nitroprusside induced hypotension and halothane/nitrous oxide anaesthesia. 683 56

This investigation tests the hypothesis that the normal cerebral image obtained non-invasively during continuous inhalation of C15O2 is related to cerebral blood flow. Trace amounts of CO2 labeled with the positron-emitting radionuclide 15O were administered to 4 normal subjects at normo- and hypocapnia and to 2 of these subjects at hypercapnia. Hypocapnia typically caused a marked decrease in cerebral 15O activity, and hypercapnia a small increase in activity. The relative difference in the change in count rate in response to hypo- and hypercapnia is what one would expect if the activity represented bloow flow, according to a mathematical model which assumes the 15O label enters the brain as water of perfusion. The findings in this study suggest that the normal cerebral image obtained during continuous inhalation of C15O2 is related to cerebral blood flow, but in a non-linear fashion, and that the technique would be more sensitive to ischemic events than to hyperemic phenomena.
Stroke
PMID:Positron imaging of cerebral blood flow during continuous inhalation of C15O2. 696 50

We measured cerebral vasomotor reactivity during normoventilation, hyperventilation (hypocapnia), and breathing of 6% CO2 (hypercapnia) in 20 normal subjects during the hours of 6 to 8 AM, 1 to 3 PM, and 7 to 9 PM. Cerebral vasomotor reactivity was calculated, using transcranial Doppler, as percent change in the mean blood flow velocity of the middle cerebral artery per mm Hg change in end-tidal CO2 during hypocapnia and hypercapnia. Vasomotor reactivity during hypercapnia was lower in the morning (1.72 +/- 0.66 %/mm Hg) than in the afternoon (2.34 +/- 0.74 %/mm Hg, p < 0.01) and evening (2.31 +/- 0.56 %/mm Hg, p < 0.001). Vasomotor reactivity during hypocapnia did not vary significantly during the three periods (2.34 +/- 0.59 %/mm Hg in the morning, 2.43 +/- 0.51 %/mm Hg in the afternoon, and 2.26 +/- 0.52 %/mm Hg in the evening). This reduced morning response to hypercapnia suggests diminished vasodilator reserve during this period, and may be related to the increased stroke risk during the morning hours.
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PMID:Morning reduction of cerebral vasomotor reactivity. 793 45

Nasal intermittent positive-pressure ventilation (nIPPV) is used for the treatment of respiratory failure in patients with neuromuscular disease. The aim of the present study was to demonstrate that nIPPV may activate nose receptors, the consequence of which being reflex changes in lung resistance. The changes in interrupter resistances (Rint) in response to nIPPV were tested before and after local anaesthesia of the nasal mucosa in normal subjects. They were compared to the Rint changes induced by oral intermittent positive-pressure ventilation (oIPPV) in the same individuals. Rint was measured during 10-min periods of nIPPV or oIPPV at a constant rate (15 L x min(-1)), but at two different stroke volumes (0.8 and 1.2 L). Inspired temperature and relative humidity were held constant. nIPPV with 1.2 L (17 mL x kg(-1)) significantly increased the Rint value (+22%). This effect disappeared after nose anaesthesia or after inhalation of a cholinergic antagonist. oIPPV never changed Rint, even though the associated hypocapnia was present and more accentuated than during nIPPV. Adding CO2 to the inspired gas during nIPPV and oIPPV trials suppressed the Rint changes. The present study suggests the existence of a nasopulmonary bronchoconstrictor reflex elicited through the stimulation of nasal mechanoreceptors, their activity being markedly influenced by the changes in expired CO2 concentration.
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PMID:Changes in airway resistance induced by nasal or oral intermittent positive pressure ventilation in normal individuals. 1036 55

This study investigates the effect of stroke on the corticodiaphragmatic pathway and attempts to clarify the relationship between neurophysiological data and degree of motor disability, site of infarction in computerized tomography (CT) scan, diaphragmatic excursion, blood gases and pulmonary function in stroke patients. Using magnetic stimulation of the scalp sites and cervical roots, an assessment of corticodiaphragmatic pathway was made. The study included 34 sequentially selected patients from a total of 250 patients with acute ischemic stroke. Twenty-five (age- and sex-matched) volunteers served as controls. Sixteen patients had cortical infarction, 13 had subcortical infarction and five had both cortical and subcortical infarction. The mean according to the Scandinavian Stroke Scale was 32.2. Decreased diaphragmatic excursion was observed in 41% of the patients. Twenty-four patients (70.5%) had abnormal magnetic evoked potentials (MEPs) in the affected hemisphere. In five patients MEPs could not be elicited from the affected hemisphere; the remaining 19 patients had abnormal values of both cortical latency and central conduction time (CCT). Cortical latency, CCT, amplitude of compound muscle action potentials (CMAPs) and excitability threshold of the affected hemisphere were significantly altered compared with both the unaffected hemisphere and the control group. Those patients with hemiplegia had a greater degree of hypoxia, hypocapnia and decreased serum bicarbonate level compared with the control group. Also, hemiplegic patients had different degree of respiratory dysfunction. A statistically significant association was found between neurophysiological data and disability score, diaphragmatic excursion, site of infarction in CT scan and degree of respiratory dysfunction. Central diaphragmatic impairment may occur in acute stroke and could contribute to the occurrence of hypoxia in those patients.
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PMID:Assessment of corticodiaphragmatic pathway and pulmonary function in acute ischemic stroke patients. 1088 17

Pulmonary embolism alters the distribution of ventilation/perfusion relationships, and increases pulmonary vascular resistance. These changes lead to hypoxemia and hypocapnia, and eventually, to right heart failure. The thin-walled and compliant right ventricle adapts to any increase in afterload by dilatation and decreased stroke volume, but this is largely prevented or delayed by the pulmonary circulation being a low resistance, recruitable and distensible circuit. Pulmonary embolism cannot be associated with a mean pulmonary artery pressure higher than 40 mmHg. More severe pulmonary hypertension indicates the presence of a hypertrophied right ventricle in the context of preexistent cardiac or pulmonary disease. Gas exchange is initially affected because of increased ventilation/perfusion ratios in embolized lung areas, and decreased ventilation/perfusion ratios in remaining non embolized lung areas. Both physiologic shunt and physiologic dead space increase accordingly, resulting in hypoxemia and hypocapnia. However, these changes are rapidly affected by an increase in ventilation, and by a "pneumoconstriction" which decreases physiologic dead space in embolized areas. In addition, a series of secondary alterations contribute to increase perfusion to lung units with low ventilation/perfusion ratios, thereby aggravating hypoxemia, while hypocapnia persists.
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PMID:[Physiopathology of pulmonary arterial hypertension and gas exchange in acute pulmonary embolism]. 1090 37

The aims of this study were to investigate the effect of stroke on the corticodiaphragmatic pathway and to clarify the relationships between neurophysiological data and degree of motor disability, site of infarction in CT scan, diaphragmatic excursion, blood gases and pulmonary function in stroke patients. The corticodiaphragmatic pathway was assessed using magnetic stimulation of the scalp sites and cervical roots. The study included 34 sequentially selected patients out of 250 patients with acute ischemic stroke. Twenty-five (age and sex matched) volunteers served as controls. Sixteen patients had cortical infarction, thirteen had subcortical infarction and five had both cortical and subcortical infarction. The mean Scandinavian Stroke Scale was 32.2. Decreased diaphragmatic excursion was observed in 41% of the patients. Twenty-four patients (70.5%) had abnormal magnetic evoked potentials (MEPs) of the affected hemisphere. In five patients MEPs were unelicitable from the affected hemisphere. The remaining nineteen patients had abnormal values of both cortical latency and central conduction time (CCT). Cortical latency, CCT, amplitude of compound muscle action potentials (CMAPs) and excitability threshold of the affected hemisphere were significantly altered compared to both the unaffected hemisphere and the control group. The patients with hemiplegia had a greater degree of hypoxia, hypocapnia and decreased serum bicarbonate level compared to the control group. Additionally, hemiplegic patients had a different degree of respiratory dysfunction. A statistically significant association was found between neurophysiological data and disability score, diaphragmatic excursion, site of infarction in CT scan and degree of respiratory dysfunction. Central diaphragmatic impairment may occur in acute stroke and could contribute to the occurrence of hypoxia in those patients.
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PMID:Assessment of corticodiaphragmatic pathway and pulmonary function in acute ischemic stroke patients. 1105 35

Sleep disordered breathing is common in patients with cerebrovascular disease, and could exacerbate the cerebral damage in acute stroke. Data about the effects of continuous positive airway pressure (CPAP) upon cerebral perfusion are conflicting. We investigated whether increasing levels of CPAP may affect cerebral haemodynamics, assessed by transcranial Doppler (TCD) in normal humans. A group of 25 healthy young volunteers were evaluated before (CPAP0-pre), during (CPAP5, CPAP10 and CPAP15, denoting CPAP at 5, 10 and 15 cmH(2)O respectively) and after (CPAP0-post) application of incremental levels of CPAP delivered through a mouthpiece. The mean cerebral blood flow velocity (CBFV) and the pulsatility index (PI; an indirect measure of cerebrovascular resistance) in the middle cerebral artery were measured with TCD. Respiratory rate, heart rate, end-tidal carbon dioxide pressure (PETCO(2)), transcutaneous haemoglobin oxygen saturation (SpO(2)), mean arterial blood pressure and anxiety score were also recorded. Compared with CPAP0-pre, CBFV was significantly decreased as higher levels of CPAP were applied (P <0.0001). CPAP15 increased PI (P <0.05), ETCO(2) was reduced by CPAP10 and CPAP15 (P <0.0001), and anxiety score and SpO(2) increased at all levels of CPAP (P <0.05). Heart rate, respiratory rate and mean arterial pressure did not change. The decrease in CBFV was correlated with the fall in P ETCO(2) (CPAP15) and the increase in PI (CPAP10, CPAP15) (P <0.05). In conclusion, even low levels of CPAP delivered through a mouthpiece in awake, young volunteers led to a decrease in CBFV, measured by TCD. This fall in CBFV was associated with hypocapnia and with an increase in both cerebrovascular resistance and anxiety due to breathing against positive pressure. As the negative consequences of a fall in CBFV may outweigh the therapeutic effects of CPAP in the post-stroke setting, further studies of the cerebrovascular effects of CPAP with different interfaces in elderly patients with and without stroke are needed before intervention trials can be performed safely.
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PMID:Effects of incremental levels of continuous positive airway pressure on cerebral blood flow velocity in healthy adult humans. 1258 Jul 65

In man assuming the upright position, end-tidal P(CO(2)) (P(ETCO(2))) decreases. With the rising interest in cerebral autoregulation during posture change, which is known to be affected by P(ETCO(2)), we sought to determine the factors leading to hypocapnia during standing up from the supine position. To study the contribution of an increase in tidal volume (V(T)) and breathing frequency, a decrease in stroke volume (SV), a ventilation-perfusion (V/Q) gradient and an increase in functional residual capacity (FRC) to hypocapnia in the standing position, we developed a mathematical model of the lung to follow breath-to-breath variations in P(ETCO(2)). A gravity-induced apical-to-basal V/Q gradient in the lung was modelled using nine lung segments. We tested the model using an eight-subject data set with measurements of V(T), pulmonary O(2) uptake and breath-to-breath lumped SV. On average, the P(ETCO(2)) decreased from 40 mmHg to 36 mmHg after 150 s standing. Results show that the model is able to track breath-to-breath P(ETCO(2)) variations (r(2)= 0.74, P P 0.05). Model parameter sensitivity analysis demonstrates that the decrease in P(ETCO(2)) during standing is due primarily to increased V(T), and transiently to decreased SV and increased FRC; a slight gravity-induced V/Q mismatch also contributes to the hypocapnia. The influence of cardiac output on hypocapnia in the standing position was verified in experiments on human subjects, where first breathing alone, and then breathing, FRC and V/Q were controlled.
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PMID:Tidal volume, cardiac output and functional residual capacity determine end-tidal CO2 transient during standing up in humans. 1460 2


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