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

In normal humans, both hypoxia and hypercapnia result in sympathetic nerve activation, and when combined, i.e. hypoxic hypercapnia, synergistically increase sympathetic activity. Apnea during the hypoxic and hypercapnic stress results in further increases in sympathetic activity. Borderline hypertensive humans have exaggerated sympathetic nerve responses to hypoxia. Hypertensives are also prone to sleep apnea. We suggest that sleep apnea may result in very high levels of sympathetic activity which may contribute to daytime hypertension and/or precipitate cardiovascular catastrophe in hypertensive people during sleep.
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PMID:Sympathetic activation by hypoxia and hypercapnia--implications for sleep apnea. 307 27

Regional cerebral blood flow (rCBF) during hypertension and hypercapnia was studied in 33 patients with putaminal hemorrhage, using a single photon emission CT by means of Xenon 133 inhalation method. The results obtained were as follows: 1) A significant relationship was obtained between the impairment of autoregulation, CO2 reactivity and the degree of cerebral ischemia, i. e., in most cases, these vascular responses were impaired in cases of ischemia showing the rCBF decrease over 30 to 40% of normal values. However, there were particular cases with cerebral ischemia of over 30 to 40% in which autoregulation seemed to be preserved in the acute stage, which was considered to be the similar phenomenon as so called "false autoregulation". 2) The cerebrovascular responses such as autoregulation and CO2 reactivity were preserved in cases of less than 50 ml of hematoma volume. In cases with 50 to 74 ml of hematoma volume however, autoregulation and CO2 reactivity were mostly impaired, especially in the affected hemisphere rather than the non-affected, in the period of 1 to 2 months from the onset. Furthermore, the impairment was also involved in both hemispheres if the hematoma was over 75 ml in volume. 3) The cerebrovascular responses were markedly impaired in the region of basal ganglia of the affected hemisphere which corresponded well to the hematoma site. 4) There was a close correlation between the cerebrovascular responses and the activity of daily life (ADL), i. e, the prognosis might be poor in cases with global impairment, but which seemed to be rather good in cases with local impairment. It might be concluded, from the results mentioned above, that the study of autoregulation and CO2 reactivity is probably significant in estimating the pathogenesis and the treatment of cerebral ischemia following hypertensive putaminal hemorrhage.
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PMID:[A study of cerebrovascular autoregulation and CO2 reactivity in putaminal hemorrhage]. 310 23

The objectives of the present study were to determine whether an intracisternal injection of fibrinogen-sodium citrate, a model of neurogenic pulmonary edema (NPE), produces protein-rich or protein-poor pulmonary edema, and to determine whether the edema is associated with pulmonary vascular hypertension and pulmonary congestion. Fibrinogen (6-10 mg/ml) dissolved in 0.055 M sodium citrate was injected into the cisterna magna of six New Zealand White rabbits. Six additional rabbits were injected with saline to control for the effects of intracranial hypertension and pulmonary vascular hypertension. The fibrinogen-sodium citrate solution or sodium citrate alone, as opposed to saline, produced systemic and pulmonary vascular hypertension, pulmonary edema, hypoxemia, hypercapnia, and acidosis. The lungs from fibrinogen-injected rabbits were edematous, congested, and liverlike in appearance. Tracheal froth that was blood tinged and protein rich was present in five of the six rabbits. Microscopic examination of lung biopsies revealed erythrocytes and plasma in the alveoli and focal injury to the pulmonary microvascular endothelium. Fibrinogen-sodium citrate increased (P less than 0.05) the extravascular lung water (EVLW) (10.3 +/- 2.0 vs. 5.5 +/- 0.6 g, means +/- SE), lung blood weight (9.7 +/- 1.3 vs. 3.8 +/- 0.6 g), total dry lung weight (3.2 +/- 0.4 vs. 2.0 +/- 0.1 g), and the EVLW-to-blood-free dry lung weight ratio (7.0 +/- 0.8 vs. 4.0 +/- 0.3 g) from saline-control values. There was no difference in the blood-fre dry lung weight (1.4 +/- 0.1 vs. 1.3 +/- 0.1 g) between the two groups. These findings demonstrate that pulmonary congestion, pulmonary vascular hypertension, and focal endothelial injury contribute to the development of NPE.
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PMID:Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits. 311 22

Evoked responses of various modalities are being used for sensory and neurological clinical assessment. An additional application is their use in studying the functional activity of several sensory pathways and many brain regions during induced deviations from homeostasis in the intact animal. The auditory nerve-brain-stem evoked response (ABR) has been studied during hypoxia, hypercapnia, acidosis, hypoglycemia, systemic hypotension, intracranial hypertension and decreased cerebral perfusion pressure. In many such experiments the following were also recorded: EEG, cortical evoked potential (EP), somatosensory EP (including peripheral nerve, brain-stem and cortical components), visual and vestibular EP. Even though the EEG was already isoelectric, the ABR and many of the other EPs were not affected by relatively severe deviations in homeostasis, several of which have been shown to induce brain lesions and severe perturbations of energy metabolism. The ability of these brain pathways to produce electrical activity in such conditions may be due to the generation of such EP by oligosynaptic pathways and to compensatory mechanisms such as increased local cerebral blood flow. Clinically, these findings point out the usefulness of ABR recordings in the diagnosis of brain death and to the possibility that when ABR is continuously monitored in the intensive care patient, alterations in the ABR may indicate the need for immediate intervention.
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PMID:Auditory evoked potentials during deviations from homeostasis: theoretical and clinical implications. 330 16

Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.
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PMID:[Dangerous snoring. Sleep-apnea syndrome]. 331 92

Doppler estimation of the blood flow in the descending aorta of the fetus and waveform analysis of the maximum aortic velocity provide valuable information on fetal circulation. When estimating fetal aortic flow, it is important to consider possible sources of error; even when recording the maximum aortic velocity for waveform analysis, to obtain reproducible results it is important to use a low high-pass filter, a well-defined angle of insonation, and a standardized site of measurement and to avoid periods of fetal breathing and activity. In normal pregnancy the time-averaged mean velocity in the descending aorta is stable throughout the third trimester. The weight-related flow is stable until 37 weeks, after which it falls slightly. The placental proportion of the flow in the thoracic descending aorta decreases toward term. In the aorta of normal fetuses there is positive flow throughout the whole heart cycle, which is due to the low vascular resistance in the placental circulation. The waveform of the aortic velocity can be characterized by the PI, which is stable during the last trimester of gestation. Caution is required when interpreting changes in the aortic PI, as it is not only affected by the peripheral resistance but also by the heart performance. Furthermore, PI is related to fetal heart rate. Near term different values of PI are found in different fetal behavioral states. In fetuses with retarded growth and in fetuses at distress, characteristic changes of the aortic velocity waveform have been reported by several researchers: the end-diastolic velocity diminishes and disappears, and in extreme cases a brief reversal of flow in diastole was observed. Consequently, the PI increases in such cases. The absence of the end-diastolic aortic velocity can easily be determined and is the best indicator of fetal status: in fetuses with absent end-diastolic velocity the incidence of perinatal mortality and morbidity is significantly higher than in fetuses with positive flow throughout the cycle. In pregnancies with hypertension or diabetes mellitus, normal aortic flow has been reported, as long as the fetuses were not growth retarded. In cases of severe Rh-isoimmunization, the mean aortic velocity correlates with fetal hematocrit. In hypoxic fetuses the mean velocity was reported to correlate with the degree of hypoxia, hypercarbia, and acidosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Blood flow in the fetal descending aorta. 332 52

In three consecutive patients suffering from life-threatening asthma in a comatose state (mean age: 37 +/- 4 yr; Glasgow coma score: 3; bilateral mydriasis), intracranial pressure was monitored with an extradural transducer set-up a mean of 2 h after the onset of the coma. The aims were to detect intracranial hypertension and to improve its therapy. Basal therapy associated: 1) mechanical ventilation; 2) theophylline 1.5 g X 24 h-1, salbutamol 30 mg X 24 h-1, hydrocortisone 2 g X 24 h-1, pancuronium 0.5 mg X kg-1 X 24 h-1; 3) pentobarbitone 35 mg X kg-1 X 24 h-1, normal hydration, normothermia and 30 degrees head-up tilt. If the intracranial pressure rose above 15 mmHg, an i.v. bolus of pentobarbitone (5 mg X kg-1) was given if the barbiturate blood level was equal or below 100 micrograms X l-1. In case of failure, a dose of mannitol (20 mg) completed the therapy if blood therapy was equal or below 320 mosm X l-1. All patients developed intracranial hypertension (21, 53 and 23 mmHg, respectively). The intracranial hypertension followed the bronchospasm and disappeared with it. Hypoxaemia, hypercapnia and high peak airway pressures could explain the intracranial hypertension. All patients recovered without sequelae. This data should make us use with great care all treatments likely to increase the intracranial pressure during life-threatening asthma.
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PMID:[Intracranial hypertension during status asthmaticus]. 357 44

An 87-year-old female, with a history of hypertension controlled with hydrochlorothiazide, was scheduled for excision of a cystic mass of the left lobe of the thyroid. In the course of the anaesthetic, she developed partial airway obstruction that resulted in respiratory acidosis (PaCO2 108 mmHg, pH 7.06), developed premature ventricular contractions and experienced a reduction in plasma potassium concentration from 3.9 to 2.9 mmole X L-1. We interpret this hypokalaemia as a consequence of the epinephrine discharge due to hypercapnia. The case is reported to emphasize the importance of minimizing the sympathetic response to induction of anaesthesia, intubation and surgery in patients with marginal potassium stores.
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PMID:Hypokalaemia and respiratory acidosis following partial obstruction of the airway. 360 55

The purpose of this study was to examine effects of hypercapnia on susceptibility of the blood-brain barrier to disruption during acute hypertension. Two methods were used to test the hypothesis that cerebral vasodilatation during hypercapnia increases disruption of the blood-brain barrier. First, permeability of the blood-brain barrier was measured in anesthetized cats with 125I-labeled serum albumin. Severe hypertension markedly increased permeability of the blood-brain barrier during normocapnia, but not during hypercapnia. The protective effect of hypercapnia was not dependent on sympathetic nerves. Second, in anesthetized rats, permeability of the barrier was quantitated by clearance of fluorescent dextran. Disruption of the blood-brain barrier during hypertension was decreased by hypercapnia. Because disruption of the blood-brain barrier occurred primarily in pial venules, we also measured pial venular diameter and pressure (with a servo-null method). Acute hypertension increased pial venular pressure and diameter in normocapnic rats. Hypercapnia alone increased pial venular pressure and pial venular diameter, and acute hypertension during hypercapnia further increased venular pressure. The magnitude of increase in pial venular pressure during acute hypertension was significantly less in hypercapnic than in normocapnic rats. We conclude that hypercapnia protects the blood-brain barrier. Possible mechanisms of this effect include attenuation of the incremental increase in pial venular pressure by hypercapnia or a direct effect on the blood-brain barrier not related to venous pressure.
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PMID:Protection of the blood-brain barrier by hypercapnia during acute hypertension. 374 Feb 84

A 52-year-old woman presented with increasing pain, weakness, and paraesthesiae of four months' duration in the lower limbs. She suffered from chronic obstructive airways disease and hypertension. Neurological examination revealed wasting of the quadriceps muscles, weakness of the lower limbs, and absent ankle jerks. The sensory examination was normal. Full blood count, ESR, biochemical, immunological, and viral studies, urinary heavy metal assays, and cerebrospinal fluid examination were normal. Nerve conduction studies were consistent with a sensorimotor neuropathy, and electromyographic sampling was consistent with acute denervation. A sural nerve biopsy showed axonal degeneration and segmental demyelination. One month after admission, she developed carbon dioxide retention. Her weakness spread to affect the upper limbs, and she could not be resuscitated after a cardiac arrest three months after admission. General autopsy examination revealed bronchopneumonia. Neuropathological examination showed a lymphocytic infiltrate in the nerve roots of the cauda equina, the lumbosacral plexus, and the sural and vagal nerves. Increased cellularity and collagen were evident in these nerves. A diagnosis of chronic inflammatory polyneuropathy was made. The neuropathology of this entity is discussed.
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PMID:Neuropathological findings in a case of chronic inflammatory polyneuropathy. 384 15


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