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

Fluid percussion models produce brain injury by rapidly injecting fluid volumes into the cranial cavity. The authors have systematically examined the effects of varying magnitudes of fluid percussion injury in the rat on neurological, systemic physiological, and histopathological changes. Acute neurological experiments showed that fluid percussion injury in 53 rats produced either irreversible apnea and death or transient apnea (lasting 54 seconds or less) and reversible suppression of postural and nonpostural function (lasting 60 minutes or less). As the magnitude if injury increased, the mortality rate and the duration of suppression of somatomotor reflexes increased. Unlike other rat models in which concussive brain injury is produced by impact, convulsions were observed in only 13% of survivors. Transient apnea was probably not associated with a significant hypoxic insult to animals that survived. Ten rats that sustained a moderate magnitude of injury (2.9 atm) exhibited chronic locomotor deficits that persisted for 4 to 8 days. Systemic physiological experiments in 20 rats demonstrated that all levels of injury studied produced acute systemic hypertension, bradycardia, and increased plasma glucose levels. Hypertension with subsequent hypotension resulted from higher magnitudes of injury. The durations of hypertension and suppression of amplitude on electroencephalography were related to the magnitudes of injury. While low levels of injury produced no significant histopathological alterations, higher magnitudes produced subarachnoid and intraparenchymal hemorrhage and, with increasing survival, necrotic change and cavitation. These data demonstrate that fluid percussion injury in the rat reproduces many of the features of head injury observed in other models and species. Thus, this animal model could represent a useful experimental approach to studies of pathological changes similar to those seen in human head injury.
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PMID:A fluid percussion model of experimental brain injury in the rat. 359 59

Autonomic dysfunction, including arrhythmias, has been shown to be associated with epileptogenic activity. This study examines the potential role for enkephalins in this process. A long lasting elevation of immunoreactive methionine (met)-enkephalin content in the septum, hypothalamus, amygdala, and hippocampus of rats occurs after pentylenetetrazol-induced convulsions (Brain Research 297: 121-125, 1984). Brennan et al (Life Sciences 27: 1097-1101, 1980) reported a greater percent inhibition of potassium-stimulated GABA release with increasing concentrations of met-enkephalin. Snead and Bearden (Science 210: 1031-1033, 1980) found that leucine-enkephalin in the central nervous system may induce epileptogenic activity. In addition, (d-alanine2) met-enkephalin has been shown to produce a centrally mediated vasopressor response as well as attenuation of the baroreceptor reflex in conscious cats (Hypertension 3: 395-407, 1981), possibly leading to autonomic imbalance. The latter may precipitate arrhythmias and sudden unexplained death in the epileptic patient. Resolution of the question of whether enkephalins elicit epileptogenic activity and autonomic dysfunction via inhibition of GABA release is important since an understanding of this mechanism should eventually allow the design of pharmacologic agents to prevent the epileptogenic activity, autonomic dysfunction and the associated sudden death.
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PMID:The role of enkephalins in the production of epileptogenic activity and autonomic dysfunction: origin of arrhythmia and sudden death in the epileptic patient? 361 1

A diagnosis of eclampsia has been considered inappropriate when the onset of a convulsion is greater than 24 hours after delivery. The observations presented here provide strong support for waiving the 24-hour rule, at least when convulsions from no other apparent cause and accompanied by hypertension and proteinuria occur in a primipara as late as 10 days postpartum. Late postpartum eclampsia seems an appropriate term for this very uncommon condition.
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PMID:Convulsions in hypertensive, proteinuric primiparas more than 24 hours after delivery. Eclampsia or some other cause? 362 13

Twenty-four cases of eclampsia managed in a hospital in Hong Kong over a five-year period were reviewed. Four patients had antepartum eclampsia and one had postpartum eclampsia following elective caesarean section. Four of these five patients had severe pregnancy-induced hypertension (PIH) (greater than 160/100 mmHg). The other 19 patients had eclampsia occurring during labour or within six hours of delivery. This group included 10 patients with labour-onset PIH, none of whom developed severe hypertension before their convulsions. In the remaining nine patients, only five had severe hypertension before convulsion. The results suggest that labour-related eclampsia has become more common than antepartum eclampsia, and severe hypertension before convulsion is an infrequent finding and therefore an unreliable sign in these patients.
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PMID:Labour-related eclampsia. 366 77

Health-promotion efforts often employ HRA as a device for providing an individual with quantitative information about the consequences of personal health-related behaviors and as an attempt to motivate the client to adopt recommendations directed at establishing a healthier lifestyle. From a behavioral science perspective, the HRA approach and process contain elements that (at least in retrospective analysis) appear to be founded in relevant bodies of theory. First, HRA seems to be a reasonably efficient mechanism for transmitting information relative to associations between personal health behaviors and mortality risks. Moreover, while general knowledge and advice about the untoward consequences of risk factors (such as smoking, obesity, high blood pressure, etc.) are currently widespread, HRA provides new and specific information: the client's own relative risks. Some individuals who voluntarily participate in HRA bring to the experience an already high level of readiness to take action; for them, the technique may constitute the final necessary stimulus or "cue to action" [12]. Referring to a "borrowing from the future" phenomenon, Green points out that "some educational efforts are really only triggers to behavior that would have changed eventually anyway" [44, p. 159]. Thus, where motivation is sufficiently high, receipt of HRA feedback information may by itself be capable of inducing behavior change. Second, the focus on awareness and personalization of mortality risk fits well with most theoretical formulations concerning attitudes and beliefs involved in health-related decision making. Although the emphasis on mortality and often distant negative outcomes is problematic, increasing the client's perception of personal vulnerability is a psychologically defensible approach, and fear arousal can generate attitude change (although questions of appropriate level, duration of effects obtained, acceptability, etc. still need to be resolved). Third, HRA might be expected to enhance the client's perception of the benefits associated with lifestyle modifications and may even increase personal belief in his or her ability to undertake such changes in behavior. However, in light of the fact that the behaviors to be altered are complex, usually well-established and repetitive, and require different skills to extinguish, the provision of typical HRA feedback should not (on a theoretical basis) ordinarily be expected to accomplish much beyond information transmission, belief or attitude change, and the induction of some level of motivation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Behavioral science perspectives on health hazard/health risk appraisal. 367 42

The differential leukocyte count was studied within the first 24 hours of life in 115 infants of diabetic mothers (IDMs) appropriate for gestational age (AGA), 16 IDMs large for gestational age (LGA), 104 infants of non-diabetic mothers (INM's) AGA, and 22 INMs-LGA. A significant "shift to the left" was found in IDM's-LGA only. The usual cause of "shift to the left" such as maternal hypertension or fever, respiratory distress syndrome, meconium aspiration, neonatal asphyxia, sepsis, convulsions, or hypoglycemia could not explain this finding. It is hypothesized that increased glucocorticoid secretion may possibly play a role.
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PMID:Differential leukocyte count in infants of diabetic mothers. Increased band count associated with macrosomia. 373 70

Some pharmacological effects of a potent tremorgenic mycotoxin, fumitremorgin A (FTA), on the rabbit were studied. FTA (10-200 micrograms/kg, i.v.) caused clonic and tonic convulsion accompanied by nystagmus and miosis in conscious rabbits, after a latent period. Even in decorticated or decerebrated rabbits, FTA (100-200 micrograms/kg, i.v.) could induce violent motor effects similar to those observed in conscious rabbits. Under light anesthesia with urethane and chloralose, a higher dosage (more than 100 micrograms/kg) was needed to cause clonic and tonic convulsion. FTA facilitated phrenic nerve discharges as well as efferent discharges of the vagal nerve and the cervical sympathetic nerve. Hypertension induced by FTA was inhibited by phentolamine, while bradycardia and arrhythmia caused by this toxin was abolished by atropine or bilateral vagotomy. The electroencephalogram showed persistent strong arousal response after intravenous injection of FTA. A seizure pattern was never observed. It was suggested that the main site of action of FTA was in the brain stem.
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PMID:Pharmacological effects of the tremorgenic mycotoxin fumitremorgin A. 373 99

Among 480,969 births in Sweden during the period 1976 to 1980, 74 parturients with eclampsia were identified. The clinical characteristics of women developing eclampsia before 37 completed weeks of gestation differed markedly from those with eclampsia at term. In the pre-term group, subjective symptoms nearly always preceded the eclamptic attack, the newborns were generally small-for-gestational-age, the perinatal mortality was high, and the mothers more frequently had complications related to eclampsia. The only maternal death occurred in this group. In the term group the first convulsion often came unexpectedly without typical premonitory signs. The infants were with few exceptions within the average for gestational age. The general outcome for mothers and their babies was favorable and the length of hospital stay was on average 3 days longer than that of the overall obstetric population. Eclampsia cases in Sweden represent a small subfraction of parturients with hypertensive disorders of pregnancy. The incidence (29/100,000) in our material is, to our knowledge, the lowest yet reported. Despite the very regular attendance at the antenatal clinic, weekly from 36 weeks onwards, fewer than half of the patients had hypertension diagnosed 4 days or more prior to the eclamptic convulsion. A shortening of the intervals between the antenatal visits therefore does not seem warranted.
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PMID:Eclampsia in Sweden, 1976-1980. 373 42

By defining a model for control of potassium homoeostasis, patients with unexplained hypokalaemia may then be described as fitting or not fitting the model. Fitting the model implies an abnormality of known control mechanisms (e.g. aldosterone); by contrast, not fitting the model suggests other unknown factors responsible for the hypokalaemia and, possibly, hypertension. In the presence of normal acid-base status, potassium excretion (UK+V) is regulated by plasma potassium (PK+), delivery of sodium to the distal tubule and aldosterone secretion. A linear relationship (correlation coefficient of 0.72) was defined by: UK + V/PK+ = 5.1 X log(UAldoV) X log(UNa+ V) + 1.4 based on a 24 h urine collection and plasma sample, in 16 normal subjects, 50 hypertensive normokalaemic subjects and 11 patients with hyperaldosteronism. The relationship was robust and held true for variations in dietary sodium and potassium intake (5-300 and 20-100 mmol/day respectively) and variations in aldosterone excretion produced by enalapril. Patients with abnormal renal potassium wasting due to known extraneous factors (n = 11) all fell outside the 95% confidence limits. Twelve patients with hypertension and hypokalaemia and renal potassium wasting all fitted within the confidence limits, being no different from 22 controls selected on the basis of age and urinary potassium excretion (30-50 mmol/day). This suggests that in these 12 patients the hypokalaemia (but not necessarily the hypertension) was not due to 'unknown' steroids but rather lack of regulation of the controlling variable, aldosterone.
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PMID:A simple method for definition of incomplete suppression of aldosterone and its association with hypertension and hypokalaemia in man. 375 36

Four boys and four girls with brain tumors who were admitted to our department in the last 8 years are herein described. They presented with epileptic fits, which began before the age of 14 years, with neither intracranial hypertension nor localizing signs during the first 6 months of the illness. The length of time between the first fit and the diagnosis of a tumor ranged from 2 months to 11 years (median of 3 years), during which period all patients but one received anticonvulsant therapy. The nontreated patient was under psychiatric treatment for 1 year. The electroencephalographic evolution was disconcerting, showing asymmetry of the recording with association of slow polymorphic waves and acute irregular waves, suggesting encephalitis. The neuroradiological diagnosis was made by cerebral arteriography in one patient and in the others by angiography and CT scans (which revealed hypodense cerebral areas in five cases and hyperdense areas in the other two). The histology of the tumor was that of a grade I astrocytoma in six cases; a grade III oligondendroglioma in one case, and a meningioma in the other. All patients underwent surgical treatment. Four also received radiation therapy, two for a partially excised astrocytoma and one each for an oligodendroglioma and a meningioma. Postoperatively, all patients were put on anticonvulsant drug therapy. There were no mortalities. To date, only one astrocytoma has recurred. The sequellae observed were hemiparesis in one case and marked psychomotor deficit in another. These two patients also still have epileptic fits. The others are all psychologically and neurologically normal, and two are now off antiepileptic drugs.
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PMID:Epilepsy and brain tumors in infancy and adolescence. 377 77


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