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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

100% oxygen breathing during submaximal exercise in patients with diffuse interstitial lung disease diminishes cardiac output and pulmonary artery hypertension. The pressure drop in the pulmonary artery is most marked in patients with concomitant bronchial obstruction. At rest hyperoxia produced only minimal cardiopulmonary changes. The ventilatory and hemodynamic responses are discussed to find out if differences in these variables during oxygen breathing could be a reliable index for functional classification.
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PMID:Oxygen breathing during exercise in patients with diffuse interstitial fibrosis. 88 Apr

In anaesthetized rats, ventilatory stimulation induced by phentolamine, an alpha sympatholytic agent, emphasizes the role of some adrenergic mechanisms in the control of the respiratory centres activity. Phentolamine (5 and 10 mg.kg-1, iv) stimulates ventilation after a 4 s latency, tidal volume and respiratory rate being both increased. A same response can also be provoked 10 min later, by a second identical iv administration, systemic blood pressure remaining then stable at its previous low level. Hyperventilation is also observed when phentolamine is injected in totally denervated rats, without any remaining baro- or chemosensitivity. Stimulation is thus due to a central activity in relation with the release of inhibitory influences. Phentolamine also causes hyperventilation after prazosin pretreatment indicating that the alpha 1 adrenergic blockade is not involved in the post-phentolamine stimulation. This is an alpha 2 adrenergic transmission dependent mechanism. Variation of the systemic blood pressure is not the main mechanism involved in the hyperventilation induced by phentolamine. Meanwhile, baroreceptor activity modulates the central response to the drug, as shown by the negative influence of the post-vasopressin arterial hypertension. Hyperoxia is also a modulating factor acting by two ways: an inhibition of the peripheral chemoreceptors activity is added to an arterial hypertension. On the other side, activation of these chemoreceptors by almitrine bismesilate increases the respiratory responses to phentolamine. As already shown by one of us (Lagneuax, 1986), phentolamine pretreated rats are more responsive to hypoxia and to almitrine. Moreover, these phentolamine pretreated rats are protected against cardiovascular collapses and against apnea, frequently observed during hypoxia without CO2 compensation.
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PMID:[Alpha 2 adrenergic control of ventilation in the rat]. 170 84

15 patients with obstructive sleep apnea syndrome and arterial hypertension (H-OSAS), 25 normotensive patients with sleep apnea syndrome (N-OSAS) and 20 healthy age-matched controls (C) were included in this study. Ventilatory responses to activation (hypoxia) and inactivation (hyperoxia) of carotid chemoreceptors were studied in all subjects. Relationship between hypoxic ventilatory reactivity and nocturnal bradycardia during apnea-phases was analysed in both groups of patients. Results and conclusions. 1. We found an impairment of ventilatory response to hypoxia in H-OSAS and N-OSAS patients. However, the increase in ventilation in response to hypoxia was significantly greater in H-OSAS as compared to N-OSAS patients. 2. An augmented ventilatory response to inactivation of carotid chemoreceptors (the decrease in ventilation), observed in H-OSAS patients, indicates an increase in resting peripheral chemoreceptors drive in this group of patients. 3. The relationship between ventilatory response to hypoxia and nocturnal bradycaria in obstructive sleep apnea patients suggests, that hypoxic reactivity of arterial chemoreceptors might be involved in the origin of bradycardia during apnea events.
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PMID:Peripheral chemoreceptor reflex in obstructive sleep apnea patients; a relationship between ventilatory response to hypoxia and nocturnal bradycardia during apnea events. 186 15

Neutrophilic granulocytes were exposed to an atmosphere of nearly 100% oxygen (hyperoxia) for one hour. The nitroblue tetrazolium (NBT) reduction, reflecting oxygen radical release, was decreased both in resting and stimulated cells, but lysozyme release was unchanged. Short time exposure of patients to oxygen hypertension might therefore be beneficial as therapy, in conditions where reduced production of oxygen radicals is required. The NBT reduction of resting and stimulated neutrophils in an atmosphere of purified argon (hypoxia) was also considerably decreased, and the lysozyme release unchanged. This reflects the anaerobic conditions in abscesses, where the contribution of neutrophil oxygen metabolites to the killing of microorganism might be reduced.
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PMID:Significance of oxygen availability for release of oxygen free radicals and lysozyme by neutrophils. 196 35

1. Synchronization of spontaneous sympathetic discharge during the respiratory cycle was studied in the cervical and renal nerves of vagotomized, normotensive Wistar-Kyoto rats (WKYs) and age-matched spontaneously hypertensive rats (SHRs). Phrenic nerve discharge was used as an index of central inspiratory activity. 2. In normotensive Wistar-Kyoto rats depression of sympathetic activity appeared at the onset of inspiration reaching a minimum at mid-inspiration. Peak maximal sympathetic discharge corresponded to postinspiratory phase; a second increase sometimes appeared in late expiration. Variations of respiratory frequency over wide range of experimental conditions by hypoxia, hyperoxia, hyper- or hypocapnia and transection of carotid sinus nerves did not affect this pattern. 3. In SHRs the respiratory-phase-related timing of sympathetic discharge was variable. In normoxia, the maximal sympathetic activity occurred in late inspiration, preceded by short depression at early inspiration and followed by postinspiratory depression. A second increase in sympathetic activity was observed in mid-expiration. 4. The pattern of respiratory phase modulated sympathetic activity in SHRs was altered by hypoxic stimulation of the peripheral chemoreceptors. The early inspiratory depression of sympathetic activity was substantially prolonged and the maximal sympathetic discharge was shifted from inspiration to early expiration. This effect was abolished after carotid sinus nerves had been cut. 5. Hypercapnic stimulation of central chemoreceptors in SHRs with carotid sinus nerves cut did not influence the timing of the sympathetic activity in relation to the respiratory phase, though the magnitude of rhythmical sympathetic discharges was increased. 6. We discuss the possibility that altered synchronization between central respiratory drive and sympathetic neuronal system may contribute to the neurogenic mechanisms of arterial hypertension in SHRs.
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PMID:Respiratory-related discharge pattern of sympathetic nerve activity in the spontaneously hypertensive rat. 223 3

The effects of oxygen inhalation (FiO2 = 0.4-0.5) and/or induced hypertension (delta MBP = around 20%) on the cortical oxygen tension (CoPO2) and the cortical oxidative metabolism (NADH/NAD redox state) in acute focal ischaemia were studied in 44 rabbits. CoPO2 was recorded by a polarographical method and NADH/NAD redox state was measured with a compensated fluorometer/reflectometer. The acute focal ischaemia was induced by the occlusion of the middle cerebral artery. With oxygen inhalation, CoPO2 improved 24.8 +/- 23.2% (mean +/- SD) in ischaemic areas where CoPO2 decreased to less than 40% of control. The oxygen inhalation also partially improved NADH levels in ischaemia by 1.5 +/- 1.6% in 8 rabbits, where NADH elevated 17.6 +/- 12.1% from the normal stage. CoPO2 and NADH redox level in ischaemia were also improved by induced hypertension. delta CoPO2/delta MBP were 1.29 +/- 1.53%/mmHg in the severely ischaemic area (less than 20% of control), 1.52 +/- 0.93 in the moderately ischaemic area (20-40% of control), and 1.03 +/- 0.62 in the mildly ischaemic area (greater than 40% of control), respectively. delta NADH/delta MBP were statistically greater in the ischaemic area than in the normal cortex (p less than 0.005). It is concluded that mild hyperoxia and induced hypertension both of which are easily employed not only can improve cortical oxygen tension but also partially restore the oxidative metabolism in acute focal ischaemia.
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PMID:The effects of mild hyperoxia and/or hypertension on oxygen availability and oxidative metabolism in acute focal ischaemia. 257 48

36 patients with essential hypertension and 15 of their adult descendants were investigated and compared with age-matched control groups of 33 and 15 healthy subjects, respectively. The ventilatory response to oxygen breathing and to progressive normo- und isocapnic hypoxia were studied. The reduction of ventilation during hyperoxia was significantly greater in all hypertensive patients. An augmented ventilatory response to hypoxia was found in 20- to 40-year-old patients whereas the older patients (41-60 years) were not different from the age-matched control subjects. Our results indicate that the augmented hypoxic sensitivity in early hypertension, as found also in the young adult descendants with family background of hypertension, is attenuated with age, similar to the normotensive subjects.
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PMID:Attenuation of augmented ventilatory response to hypoxia in essential hypertension in the course of aging. 263 44

Experimental study in 156 white rats with renovascular hypertension, posthemorrhagic hypotension and with normal blood pressure revealed that high--ressure oxygen (303.9 kPa--50 min) could activate angiotensin--converting enzyme, the latter taking part in inactivation of endogenous opioid peptides. Involvement of peptide--like links in hemodynamic responses to hyperoxia seems to be an important component of the mechanism of oxygen action upon the cardiovascular system.
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PMID:[Participation of peptide mechanisms in physiological reactions of the cardiovascular system to hyperoxia]. 298 73

Marked damage to the endothelium is associated with the pulmonary hypertension that develops during in vivo exposure to hyperoxia at normobaric pressures. We hypothesized that endothelial cell damage may contribute to initial increases in vascular tone during the development of hypertension by altering the metabolism of vasoactive compounds and/or modulating vessel responses to those agents that require an intact endothelium for their actions. This study reports the effects of in vivo hyperoxic damage to the lung on the pharmacologic properties of isolated pulmonary vessels. Proximal pulmonary arteries isolated from adult and weanling rats that breathed 85% O2 for 7 days were studied using myograph techniques. Isometric tension development was recorded in response to the cumulative addition of prostaglandin F2 alpha (PGF2 alpha) and the ability of acetylcholine (ACh) to relax precontracted vessels was subsequently assessed. Sensitivities to PGF2 alpha were increased in both adult and weanling hyperoxic vessels relative to control. Conversely, relaxation to acetylcholine was reduced following hyperoxic injury. Control vessels relaxed completely to acetylcholine addition, while only a 30% relaxation was recorded in adult hyperoxic arteries and a 50% relaxation was measured in weanling hyperoxic tissues. This effect on vasodilation was specific for the endothelium-dependent dilator ACh. By contrast, relaxation responses to sodium nitroprusside and papaverine, endothelium-independent agonists, were unaffected following hyperoxic injury. These results demonstrate that in vivo exposure to high O2 concentrations increases the sensitivity of isolated pulmonary arteries to the vasoconstrictor PGF2 alpha and markedly diminishes the ability of ACh to relax precontracted pulmonary vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacologic properties of isolated proximal pulmonary arteries after seven-day exposure to in vivo hyperoxia. 320 69

To examine the interrelationship between the duration of apnea and changes in oxygen saturation, blood pressure, electroencephalogram (EEG), and heart rate, reflex apnea of 10, 20, 40, and 60 s duration was induced by stimulating the superior laryngeal nerves. Piglets (n = 11, age 5-14 days) were chronically instrumented for continuous monitoring of SaO2 and blood pressure and for sampling arterial blood. Ventilation was recorded using whole body plethysmography and EEG and electrocardiogram were measured by acutely placed subcutaneous electrodes. Central apnea produced an immediate rise in blood pressure and a decrease in SaO2 by 20 s. By 30 s into the apnea, EEG amplitude had already decreased. Major cardiac slowing did not occur until 80 s after the start of apnea. Hyperoxia delayed the start of desaturation, hypertension, and EEG attenuation. These data suggest that during superior laryngeal nerve-induced apnea in young piglets: 1) desaturation can reach profound levels rapidly, 2) EEG amplitude decreases substantially and becomes nearly isoelectric within 1 min, and 3) bradycardia is a late manifestation when compared to changes in oxygen saturation, blood pressure, and EEG.
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PMID:Cardiovascular and neurophysiologic changes during graded duration of apnea in piglets. 337 94


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