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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. An intracellular micro-electrode was used to record action potentials from superficial cells of a cat papillary muscle during isometric contractions. The muscle was stimulated regularly and test stimuli were interpolated at various times between regular (control) responses. 2. The duration of test action potentials (measured at 80% repolarization) increases exponentially with time as the interval between the test stimulus and the preceeding stimulus is increased and a curve drawn through the data reaches a plateau at test intervals of 1.0-1.5 s. This curve is considered to reflect the time course with which membrane conductances return to their pre-stimulus values after a control response, and it is known as the 'electrical restitution curve'. 3. At much longer test intervals the action potential duration duration increases again and it approaches the rested state value of about 0.5 s when the interval between stimuli is 200-300 s. 4. Interventions that raise the peak tension developed in isometric contractions, such as an increase in the rate of stimulation or in the bathing calcium concentration, displace the electrical restitution curve downwards (to shorter action potential durations) and to the left (to shorter stimulus intervals). This shift in the curve is accompanied by a reduction in its magnitude (i.e. the difference in duration between the earliest possible action potential and the plateau value), but the interventions differ in their effects on the time course of electrical restitution: an increase in stimulus frequency causes a marked slowing, whereas an increase in bathing calcium concentration produces a slight speeding up of its time course. 5. The reduction in action potential duration produced by an increase in stimulus frequency (rate-dependent shortening) can be separated into two components, one resulting from the downward displacement of the electrical restitution curve and the other depending on the time available between consecutive responses for membrane recovery. The second component becomes increasingly important at stimulus frequencies above 100 min-1. 6. Changes in action potential duration observed during the tension staircases produced by regular stimulation of a rested preparation and by paired pulse stimulation can also be accounted for by interaction of downward displacement of the electrical restitution curve and variations in the degree of recovery of the membrane between consecutive responses. 7. Downward displacement of the electrical restitution curve is thought to result from intracellular accumulation of calcium and/or extracellular accumulation of potassium, and the available evidence is considered to favour the former mechanism.
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PMID:A study of the factors responsible for rate-dependent shortening of the action potential in mammalian ventricular muscle. 74 95

Without treatment, about 60% of atrial arrhythmia patients suffer a relapse within 3 months and 70% within one year. Antiarrhythmic treatment intended to reduce this percentage is therefore justified, on condition that it is well tolerated. Several preliminary questions have to be settled before this medical prophylaxis: 1) Justification of antiarrhythmic treatment (sometimes pointless to deal with very occasional episodes); 2) Treatment of the underlying heart disease (valve disease, cardiothyrotoxicosis, etc.) or promoting factors (potassium depletion etc.); 3) Accurate assessment of any associated conduction abnormalities, which may constitute a contraindication to antiarrhythmic treatment (WPW syndrome in the case of verapamil and the digitalis-like drugs) or require additional treatment (pacemaker); 4) Definition of the mechanism (vagal or sympathotonic) inducing arrhythmia; 5) Evaluation of the hemodynamic parameters of the underlying heart disease (size of the atria, ventricular function, coronary or valvular lesions) which may limit the efficacy of the treatment. Once these parameters have been identified, the primary treatment should be type la or lb antiarrhythmics, which have been shown to be effective, despite the fact that they are not without arrhythmic risks (the Ib antiarrhythmics are less effective and have a poor safety profile). The beta-blockers have preferential indications (hypersympatheticotonia, hyperthyroidism, hypertrophic myocardiopathy, mitral prolapse, angina etc.) and can be replaced by verapamil or bepridil if there are non-cardiac contraindications (ulcers, asthma, diabetes). Amiodarone is extremely effective, but its poor extracardiac safety restricts its long-term use. Complementary treatments (digitalis-like, anticoagulants or anti-PAF and cardiostimulant drugs) should be added if necessary. Recurrences (to be confirmed by ECG or Holter) should lead to rigorous confirmation of therapeutic compliance and observance of simple hygienic and dietary measures (no excessive exertion, elimination of stimulants etc.). With strict clinical and ECG monitoring, it would then be possible either to increase the dose levels (accompanied by plasma determinations if possible) or to switch to a treatment with more effective, but more aggressive drugs (amiodarone, flecainide) or to use drug associations (la and lb, la and II etc.). Repeated failure of such attempts should lead to a non-medical approach to treatment.
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PMID:[Preventive drug therapy of recurrence of atrial fibrillation]. 129 92

Fifteen years after a partial maxillectomy and radiation therapy for left antral carcinoma, a 53-year-old woman presented to the Eye Plastics and Orbit Service of the Massachusetts Eye and Ear Infirmary, Boston, with phthisis and a large, black corneal lesion in the left eye. She had been treated for unilateral glaucoma in the left eye for more than 10 years with topically administered epinephrine borate, timolol maleate, and pilocarpine hydrochloride. Clinically, the lesion was smooth, black, and homogeneous, and was thought to represent uveal prolapse covered by a thin layer of epithelium. An eyelid-sparing anterior exenteration was performed. Histopathologic examination revealed an acellular, homogeneous substance that stained positively with the Fontana Masson stain for melanin and bleached with potassium permanganate, findings consistent with corneal adrenochrome deposition. Since adrenochrome can be easily dissected free from the cornea, this case illustrates that misdiagnosing adrenochrome deposition may lead to unnecessary surgery.
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PMID:'Black cornea' after long-term epinephrine use. 152 Jan 15

A 23-year-old male student (height 180 cm, weight 63 kg) without any cardiac symptoms underwent a cardiological examination and consultation before a marathon run. A holosystolic mitral valve prolapse was discovered. After the marathon run he developed anorexia nervosa, interrupted by brief bulimic periods, to a minimal weight of 48 kg. After psychosomatic in-patient treatment and a weight gain to 60 kg an anorexic period recurred and he lost weight. In this phase he had an iron deficiency anaemia (Hb 11.9 g/dl), leucopenia (2,900/microliters) and (compared with the status at the first examination) mild decrease in heart size, while the valve prolapse was unchanged. Ergometric capacity was still above normal, at 300 W. After taking iron, magnesium and potassium salts in-patient psychosomatic treatment was renewed.
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PMID:[Anorexia/bulimia nervosa and mitral valve prolapse in a marathon runner]. 193 72

A sensitive and selective high-performance liquid chromatographic (HPLC) method for the determination of bupivacaine and its two metabolites, desbutyl- and 4'-hydroxybupivacaine, in human serum and urine is described. Bupivacaine, both metabolites and the internal standard, etidocaine, are extracted with diethyl ether and then back-extracted into an acidic aqueous phase. After subsequent extraction into diethyl ether, evaporation and reconstitution in the mobile phase, bupivacaine and the metabolites are determined by HPLC using a reversed-phase C8 column with tetrahydrofuran-potassium phosphate buffer (8:92, v/v, pH 2.4) as the mobile phase. The sensitivity of the method is 10 micrograms/l for bupivacaine and both metabolites and the extraction efficiencies are 95, 54 and 92% for bupivacaine and desbutyl- and 4'-hydroxybupivacaine, respectively. The reproducibility of the method is good, the coefficients of variation varying between 1.8 and 7.4% in the concentration range 0.10-2.00 mg/l. The procedure was applied to human serum and urine samples from two elderly women who had been operated on under epidural analgesia (plain bupivacaine, 1.5 mg/kg) because of uterine prolapse.
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PMID:Simultaneous determination of bupivacaine and its two metabolites, desbutyl- and 4'-hydroxybupivacaine, in human serum and urine. 355 65

This review summarizes those neurological diseases which are accompanied by a drooping of the upper lid, due to weakness of the m. levator palpebrae or m. tarsalis respectively. After connatal ptosis with or without involvement of other bulbar muscles the different types of muscular dystrophies are mentioned. Myositis, disturbances of potassium regulation and myasthenia gravis are other causes of ptosis. Diseases involving the oculomotor nerve (aneurysm, upper herniation, cavernous sinus thrombosis, orbital cavity processes, superior orbital fissure syndrome) may lead to associated ptosis. Metabolic disturbances, such as diabetes mellitus, Wernicke's encephalopathy and botulism may be accompanied by ptosis. Infectious diseases such as polyneuritis, meningitis or encephalitis can lead to ptosis. Sympatholytic ptosis is due to diseases of the central or peripheral course of the sympathetic nerve from the diencephalon via the cervical medulla, the neck, internal carotid artery to the superior orbital fissure. This type of ptosis is usually accompanied by miosis and often by sweating loss on the same side.
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PMID:[Ptosis in the differential diagnosis of neurologic diseases]. 640 79

Horses with hyperkalaemic periodic paralysis were challenged with an oral dose of potassium chloride, and the prophylactic efficacy of phenytoin, acetazolamide and hydrochlorothiazide was evaluated, with at least three weeks separating the trials of each drug. After the administration of potassium chloride without prophylactic medication the horses' clinical signs ranged from generalised fine muscle fasciculations to gross tremors, and weakness with occassional prolapse of the nictitating membrane; plasma potassium concentration increased significantly (P < 0.01) from 4.0 +/- 0.2 to 6.0 +/- 1.01 mmol litre-1. After treatment with acetazolamide the administration of potassium chloride resulted in a significant (P < 0.02) increase in plasma potassium from 3.7 +/- 0.3 to 4.5 +/- 0.4 mmol litre-1 and two of five horses showed clinical signs unless the dosage was increased from 2.2 to 4.4 mg kg-1 twice daily. Three of the four horses treated with hydrochlorothiazide showed clinical signs but their plasma potassium did not rise significantly (3.6 +/- 0.3 to 4.6 +/- 1.0 mmol litre-1). None of the five horses treated with phenytoin showed clinical signs despite a significant increase in plasma potassium from 3.8 +/- 0.6 to 5.3 +/- 1.1 mmol litre-1 (P < 0.05). In general the clinical signs were not correlated consistently with the plasma levels of potassium, and phenytoin appeared to prevent the clinical signs in spite of the hyperkalaemia.
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PMID:Prophylactic efficacy of phenytoin, acetazolamide and hydrochlorothiazide in horses with hyperkalaemic periodic paralysis. 852 15

Historical, clinical and experimental data were collected from 9 horses homozygous for HYPP (H/H). All showed episodes of respiratory stertor, described as a rattling or honking sound, usually within the first week post partum. Five horses had one or more episodes of dysphagia, in 3 horses this was accompanied by drooling and in 3 by weight loss. In comparison, only one of 35 contemporaneous half siblings (of which approximately half would be expected to be of the H/N genotype and half N/N) was observed to have respiratory stertor prior to weaning and none had problems with dysphagia. One mature homozygous stallion was infertile secondary to urospermia. Six homozygous horses died or were subjected to euthanasia; 4 age less than a year, one age 20 months and one age 5 years. The remaining 3 cases were still alive at the end of the study. A comparison of homozygous and heterozygous horses using standardised potassium chloride challenge testing indicated that during attacks homozygotes showed significantly more frequent signs of drooling, prolapse of the third eyelid, respiratory stridor and weakness than heterozygous horses. Homozygotes also had significantly more total abnormalities (including myotonic discharges, high frequency repetitive discharges, and spontaneous activity) on electromyographic examination than heterozygotes. These data imply that HYPP is inherited as a codominant genetic defect, because the homozygotes showed more severe clinical signs of disease than heterozygotes. Homozygous foals would be expected to be produced in 25% of matings in which both parents are heterozygous. Owners and veterinarians should be aware of the risks of this mating.
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PMID:Hyperkalaemic periodic paralysis in homozygous and heterozygous horses: a co-dominant genetic condition. 1021 28

Stroke mortality represents the third leading cause of death worldwide, after coronary artery disease and cancer. It has been demonstrated that in Mongolian gerbils, a unilateral hemispheric cerebral infarction can be produced following unilateral occlusion of the carotid artery because of the absence of connecting arteries between the basilar and carotid systems in these animals. The objective of this study was to comprehensively characterize the model of cerebral infarction in gerbil, clinically, biochemically and especially morphologically for prospective use in testing new therapeutic agents. Cerebral infarction was produced by ligation of the left common carotid artery in experimental gerbils. The control animals were sham-operated. One hour after surgery, 0.5 ml of 1% trypan blue was administered intraperitoneally to all animals. Initial clinical evaluations were made 8 h after surgery and every day thereafter for 30 days. On each of days 10 and 30, 4 animals were sacrificed. The degree of cerebral infarction was evaluated on the basis of clinical response, electrolyte and enzyme changes, vascular permeability of blood-brain barrier and morphological alterations. The total post-infarction mortality rate was 50%. The clinical symptoms presented as ipsilateral hemiparesis, ptosis of the eyelid, circling behavior, decreased breathing rate, decreased blood pressure and increased heart rate. Such symptoms developed within 8 h of ligation and persisted to sacrifice at day 30. Creatine kinase increased significantly on the 10th day and remained high to day 30. Increased potassium from the damaged cells and breakdown of the blood-brain barrier were first detected 72 h post-infarction. The morphological data showed evidence of brain cell necrosis, autolysis and phagocytosis 10 and 30 days post-ligation in left hemispheres. Minor intercellular edema and some cell shrinkage was evident in the right brain. Areas of focal necrosis in the vicinity of blood vessels, especially in the left brain suggested a reperfusion injury as a consequence of minimal collateral reflow from the right brain into the left brain microvasculature. Experimental infarction in gerbil recreates the ischemic conditions causing stroke in humans. The animal model may be used for evaluating the efficacy of therapeutic agents that may ameliorate the condition in man.
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PMID:Mongolian gerbil (Meriones unguiculatus) as a model of cerebral infarction for testing new therapeutic agents. 1093 31

A 17-yr-old Division I-AA collegiate offensive lineman developed unilateral ptosis shortly after minor head trauma during a scrimmage. The subsequent temporal profile of the ptosis, a history of a similar event lasting a short period of time 2 yr earlier, and the results of his clinical and electrophysiologic examinations established a diagnosis of very mild, generalized, antibody-negative myasthenia gravis (MG). His desire to continue playing football posed several additional management problems for which there was no published guidance. We started him on alternate-day, high-dose prednisone therapy with potassium and calcium supplementation, and allowed him to partake in conditioning but no contact. Except for residual decreased exercise tolerance, he improved symptomatically and experienced no serious adverse effects from the illness or the treatment during his first season, despite imperfect drug compliance. His MG eventually came under excellent symptomatic control, allowing initiation of a slow taper of the prednisone before his second season. Shortly thereafter, he abruptly stopped the prednisone without seeking medical advice. He continued to experience mild left ptosis and a mild decrease in intense exercise tolerance. He decided to forego his senior season of collegiate football after a bout of severe mechanical low-back pain incurred during spring football practice and limited his athletic activity thereafter to recreational sports.
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PMID:Myasthenia gravis in a collegiate football player. 1112 38


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