Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PALLOR”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1987

Myocardial bridging of coronary arteries associated with an impending acute myocardial infarction.

A 57-year-old woman developed severe substernal chest pain radiating to the left arm accompanied by pallor and marked diaphoresis. These symptoms appeared at rest, lasted 45 minutes, and terminated spontaneously. The patient had been treated for mild hypertension during the last 6 months. An ECG tracing obtained at the beginning of treatment was unremarkable. However, an ECG tracing recorded shortly after the end of the symptoms showed T-wave inversion in all anterior leads. Coronary arteriography was then performed and showed no fixed obstructive coronary artery disease. Nonetheless, a lengthened and constricted myocardial bridging of both the left anterior descending coronary artery and its major diagonal branch was detected. Also, the left anterior descending coronary artery was observed to be very short, terminating before the cardiac apex. The left ventricle was hypertrophied. The patient was treated with a beta-blocking agent which eliminated all symptoms. An ECG tracing obtained about three months after the onset of the clinical picture was normal. Our findings suggest that marked myocardial ischemia at rest does occur in patients having myocardial bridges under special circumstances, such as lengthened and constricted myocardial bridging of a short coronary artery which supplies a hypertrophied ventricle. This anomaly should be taken into account as a possible cause of a threatened myocardial infarction, which may be successfully treated with a beta-blocking agent.

Coronary Vessel Anomalies↗
PubMed1987

Chronic Chagas' heart disease presenting as an impending myocardial infarction: a case favoring the neurogenic pathogenesis concept.

A 55-year-old Caucasian woman suddenly developed substernal chest pain at rest accompanied by pallor, diaphoresis, nausea, and vomiting. Physical examination was otherwise unremarkable. The resting ECG showed T-wave inversion in all anterior leads which returned to normal 24 h after the onset of the symptoms. The pain was eliminated promptly by sublingual isosorbide dinitrate. "Impending" acute myocardial infarction was diagnosed. Coronary arteriography, however, failed to reveal any change in any major coronary artery but an apical aneurysm of the left ventricle was detected. As the complement-fixation test for Chagas' disease was positive, the diagnosis of chronic Chagas' heart disease was then established. This unusual clinical manifestation of Chagas' disease is thought to be the consequence of a transient imbalance in the cardiac autonomic nervous system, which is considered to play a central role in the pathogenesis of chronic Chagas' heart disease. In addition, the present case may alert clinicians to the thus far neglected atypical chest pain, which is frequently seen in chagasic patients but whose etiology remains obscure.

Chagas Cardiomyopathy↗
PubMed2002

Neuronal organization of the melanin-concentrating hormone system in primitive actinopterygians: evolutionary changes leading to teleosts.

Hypothalamic melanin-concentrating hormone (MCH) neurones occur in all vertebrates and have an apparent neuromodulatory role. In teleost fish, however, MCH is used also as a neurohypophysial hormone, controlling skin color, and as a hypophysiotrophic peptide. This work describes the central location of immunoreactive MCH perikarya and their projections to the pituitary in a range of ancestral fish to determine the phylogenetic stage when the peptide adopted these roles. In all actinopterygians examined, including polypteriformes, chondrosteans, holosteans, and teleosts, immunoreactive fibers were abundant in the median eminence or, in the case of teleosts, within the pars distalis itself, suggesting MCH acquired a hypophysial regulatory role early in vertebrate evolution. MCH fibers appeared to be absent from the posterior neurohypophysis of the polypteriform Calamoichthys but were evident in this region in the chondrostean Acipensor, the holosteans Lepisosteus and Amia, and all teleosts, suggesting its use as a neurohypophysial hormone. The ability of MCH to induce skin pallor seems to have arisen at a later stage, probably in the preholosteans. This hormonal role coincides with the migration of MCH perikarya away from the ventricular surface and their enlargement into magnocellular neurones. In the higher teleosts, magnocellular hypothalamo-neurohypophysial neurones predominate in size and number, whereas smaller periventricular MCH neurones associated with the paraventricular organ, that are prominent in lampreys, early actinopterygians and tetrapods, are reduced in teleosts. The data suggest that, in teleost fish, earlier functions of the peptide may have become subordinate to its novel pigmentary role.

Animals↗
PubMed1977

Acute hormonal response to cigarette smoking.

Preliminary smoking studies using non-smokers were unsatisfactory because the subjects became obviously "ill" with nausea, pallor, sweating, etc. The rise in adrenocorticotropic hormone and growth hormone in these individuals could not be attributed to a cigarette effect as opposed to a nonspecific stress. A small number of female smokers seemed less consistent in their responses than did male subjects. The final study employing male, habitual smokers showed the following results: (1) A sharp rise in circulating cortisol occurred after two cigarettes which was maintained through the 2nd hour and fell slowly after the smoking period. (2) Circulating growth hormones also began to rise after two cigarettes, peaked at 1 hour, and then fell back to control levels while smoking continued. (3) Urinary catecholamines tended to be higher on smoking days than on nonsmoking days, but results were variable and of questionable significance. (4) Luteinizing hormone, follicle stimulating hormone, testosterone, and thyroid-stimulating hormone did not show any significant variations with smoking as compared to non-smoking.

Catecholamines↗
PubMed1995

Histopathologic study following administration of liposome-encapsulated hemoglobin in the normovolemic rat.

Liposome encapsulated hemoglobin is being developed as an artificial resuscitative fluid for in vivo oxygen delivery. In the present report, we examine the effect of accumulation of liposome encapsulated hemoglobin on the structure of reticuloendothelial organs following administration of liposome encapsulated bovine hemoglobin in the normovolemic rat. We have also examined the administration of the liposome vehicle, tetrameric bovine hemoglobin, and liposome encapsulated bovine hemoglobin that had been lyophilized with 300 mM trehalose and rehydrated just before injection. Following injection into the tail vein, rats were sacrificed and liver, spleen, kidney, and lung harvested at 2 h, 24 h, 1 week, and 2 weeks for analysis. Gross pathologic findings of animals injected with liposome encapsulated hemoglobin showed statistically significant splenomegaly with a waxy parenchymal pallor at early time points. Microscopic findings indicate that the liver and spleen are principally involved with liposome encapsulated hemoglobin removal over the course of 24 h with transient cytoplasmic vacuolization in tissue resident phagocytes as evidenced by both light and electron microscopic examination. Presence of liposome encapsulated hemoglobin in these vacuoles was confirmed by oil red O and prussian blue stains. Splenic weight was observed to decline after 24 h but still remained significant above sham-treated controls at 2 weeks and could be correlated with increased hematopoietic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

The use of N,N-diethyl-m-toluamide to enhance dermal and transdermal delivery of drugs.

A dermal penetration enhancer has been found which improves the dermal delivery of a wide variety of drugs and at the same time has a history of low toxicity for human dermal application. N,N-Diethyl-m-toluamide (I) has been shown to improve the delivery of many drugs through hairless mouse skin in an in vitro diffusion cell model. A topically applied steroid, hydrocortisone, has been used to demonstrate the in vivo effectiveness of I on human skin. The degree of pallor produced on human skin by the corticosteroids was used as a measure of the relative delivery of hydrocortisone from formulations with and without I.

Animals↗
PubMed1994

Toxicity of photodynamic therapy with photofrin in the normal rat brain.

The widespread acceptance of photodynamic therapy (PDT), a potential adjuvant brain tumor therapy under clinical evaluation since 1980, has been partially restrained by its potential toxicity toward normal brain tissue. This study examined PDT-produced injury of normal rat brain as a function of photosensitizer dose. Brain injury was characterized by correlating measurements of the area of cerebral edema using T2-weighted magnetic resonance images, measurement of brain water content at the lesion site, microscopic examination of histological sections through the PDT lesion, and by evaluation of the area of blood brain barrier (BBB) disruption using computerized morphometric analysis of the region of Evans blue (EB) dye-labelled albumin extravasation. Monochromatic red light (630 nm) was delivered intracerebrally using a 5-mm-long cylindrical, diffusion-tip optical fiber at a constant energy dose of 15 joules. A Photofrin dose of 2 mg/kg of body weight produced a transient breakdown in the blood brain barrier around the site of the implanted optical fiber demonstrated by magnetic resonance imaging (MRI), extravasation of EB dye and pallor on hematoxylin and eosin-stained microscopic tissue sections. A much larger area of BBB disruption was seen at a dose of 4 mg/kg of Photofrin, and this drug dose resulted in significant permanent brain injury. In this model, a Photofrin dose of 4 mg/kg body weight is not tolerated by the normal brain.

Animals↗
PubMed2004

Clinicopathological investigation of vascular parkinsonism, including clinical criteria for diagnosis.

Vascular parkinsonism (VP) is difficult to diagnose with any degree of clinical certainty. We investigated the importance of macroscopic cerebral infarcts and pathological findings associated with microscopic "small vessel disease" (SVD) in the aetiology of VP. The severity of microscopic SVD pathology (perivascular pallor, gliosis, hyaline thickening, and enlargement of perivascular spaces) and the presence of macroscopically visible infarcts were assessed in 17 patients with parkinsonism and no pathological evidence of either Parkinson's disease or any histopathological condition known to be associated with a parkinsonian syndrome, and compared with age-matched controls. Microscopic SVD pathology was significantly more severe in the parkinsonian brains. Most patients presented with bilateral bradykinesia and rigidity together with a gait disorder characterised predominantly by a shuffling gait. Four patients presented acutely with hemiparesis and then progressed to develop a parkinsonian syndrome. They could be distinguished from the remaining VP patients by the presence at autopsy of macroscopically visible lacunar infarcts in regions where contralateral thalamocortical drive might be reduced. The clinical features at presentation varied according to the speed of onset and the underlying vascular pathological state. New clinical criteria for a diagnosis of VP are proposed based on the clinicopathological findings of this study.

Aged↗
PubMed1997

Multiple system atrophy: a review of 203 pathologically proven cases.

We report the clinicopathological features of 203 cases of pathologically proven multiple system atrophy (MSA) from 108 publications up to February 1995. The majority of patients showed symptoms in their early fifties, and men were more commonly affected than women (ratio of 1.3:1). Most patients suffered from some degree of autonomic failure (74%). Parkinsonism was the most common motor disorder (87%), followed by cerebellar ataxia (54%) and pyramidal signs (49%). The response to levodopa was poor in most patients, but there was a subgroup with a good response, who also often developed axial levodopa-induced dyskinesias. Other characteristic features included severe dysarthria, stridor, and, in a few patients, contractures and dystonia (antecollis). Mild or moderate intellectual impairment occurred in some cases, but severe dementing illness was most unusual. The main pathological change comprised cell loss and gliosis in the putamen, caudate nucleus, external pallidum, substantia nigra, locus ceruleus, inferior olives, pontine nuclei, cerebellar Purkinje cells, and intermediolateral cell columns of the spinal cord. However, other neuronal populations were also involved to varying degrees, such as the thalamus, vestibular nucleus, dorsal vagal nucleus, corticospinal tracts, and anterior horn cells. Characteristic glial and/or neuronal cytoplasmic inclusions were identified in all cases in which they were sought, irrespective of clinical presentation. Akinesia correlated with the degree of nigral and putaminal cell loss, whereas rigidity was related only to the later. Tremor was unrelated to cell loss at any site. Ataxia correlated with the degree of olivopontocerebellar atrophy. Pyramidal signs were associated with pyramidal tract pallor. Our analysis also confirmed an association of postural hypotension with intermediolateral cell column degeneration.

Aged↗
PubMed2002

Symptomatic hypoglycemia in children receiving oral purine analogues for treatment of childhood acute lymphoblastic leukemia.

BACKGROUND: Antimetabolite-based continuation therapy is commonly used for childhood acute lymphoblastic leukemia (ALL) and hypoglycemia after prolonged fasting has been recently reported. We have found that spontaneous, symptomatic hypoglycemia (SH) may also occur in such patients. PROCEDURE: Between 1995 and 1999, patients treated according to the AIEOP-ALL-95 study received BFM-type intensive chemotherapy; mercaptopurine (6-MP) was given (60 mg/m(2)/days, orally for 14 days) during the second part of induction and during consolidation therapy (25 mg/m(2)/day, orally for 8 weeks); thioguanine (6-TG) was given during reinduction therapy with protocol II (60 mg/m(2)/day, orally for 14 days); continuation therapy consisted of a combination of 6-MP (50 mg/m(2)/day orally) and methotrexate (MTX, 20 mg/m(2)/weekly, i.m.). We reviewed the charts of all patients treated for childhood ALL at our two centers. This was done to assess the incidence and the characteristics of all episodes of SH: sweating, pallor, nausea, abdominal pain with or without transient alterations of alertness, in the presence of blood glucose level of under 60 mg/dl. RESULTS: Six of 86 patients (6.9%) developed 18 episodes of SH. Five were male, none was older than 5 years, and four were only 3 years old. SH episodes occurred during consolidation (n = 2), reinduction (n = 7), and continuation (n = 9) phases. CONCLUSIONS: SH is a rare complication associated with administration of the purine analogues, mercaptopurine and thioguanine to children with reduced fat storage and young age.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2008

Ceftriaxone induced hemolysis complicated by acute renal failure.

Over the last decade, second and third generation cephalosporins have been the most common drugs causing hemolytic anemia (HA). Of these cases, 20% have been attributed to ceftriaxone. The clinical presentation of ceftriaxone-induced HA is usually abrupt with sudden onset of pallor, tachypnea, cardio-respiratory arrest and shock. Acute renal failure (ARF) has been reported in 41% of such cases with a high fatality rate. We report a pediatric patient with ARF complicating ceftriaxone-induced HA who survived. Ceftriaxone is a commonly used drug, and early recognition of HA and institution of supportive care, including dialysis is likely to improve the outcome.

Acute Kidney Injury↗
PubMed1995

HIV-1 envelope glycoprotein gp120 does not bind to galactosylceramide-expressing rat oligodendrocytes.

It may be postulated that the encephalopathy induced by the human immunodeficiency virus HIV-1, in particular, the characteristic "myelin pallor," may result from binding of the envelope glycoprotein gp120 to galactosylceramide and/or its metabolite sulfatide in the plasma membrane of oligodendrocytes, the myelin forming cells in the central nervous system. (1) gp120 has been reported to have a high affinity for these molecules in vitro. (2) The binding of antibodies to these molecules increases intracellular free calcium levels, which may be cytotoxic. (3) The binding of gp120 to the CD4 receptor in the immune system has the same effect. We have investigated the binding of gp120 to rat oligodendrocytes in vitro by indirect immunofluorescence and have monitored changes in intracellular free calcium with the calcium-sensitive dye INDO-1, in individual oligodendrocytes exposed to the glycoprotein. Antibodies against galatosylceramide and sulfatide bound to the cell membrane, but gp120 did not. The antibodies also increased intracellular free calcium levels in the oligodendrocytes, whereas gp120 did not. It, therefore, seems highly improbable that the demyelination observed during HIV encephalopathy is a direct cytotoxic effect of gp120 on oligodendrocytes.

Animals↗
PubMed1996

HIV-1 infection of cultured human adult oligodendrocytes.

The mechanism through which HIV-1 causes HIV dementia (HIVD) is not well understood. Myelin pallor is a common pathological finding in HIVD and could be explained by a direct infection of oligodendrocytes or interaction with HIV-1 gp 120. To determine if oligodendrocytes could be infected by HIV-1, we purified oligodendrocytes from adult human brain tissues obtained from temporal lobe resections. These cells were exposed to HIV-1 and infectivity was assayed by detection of p24gag antigen, PCR amplification, and cocultivation with CD4+ cells. These results indicate that HIV-1(IIIB and BaL) and one of four primary isolates tested can infect oligodendrocytes, resulting in the production of infectious virus. Furthermore, in an experiment that mimics a potential in vivo scenario, infected microglia were able to transmit virus to oligodendrocytes in a trans-well culture system. These experiments indicate that oligodendrocyte infection should be considered in studying the pathophysiology of HIVD.

Adult↗
PubMed1981

Pallido-luyso-nigral atrophy and amyotrophic lateral sclerosis.

Clinical and neuropathological studies of a case of pallido-luyso-nigral atrophy and amyotrophic lateral sclerosis (ALS) in a young woman with a strong likelihood of a similar familial past medical history have been presented. Microscopic examination revealed neuronal loss and gliosis of globus pallidus, corpus luysii and substantia nigra. Pallor of the pyramidal tracts and neuronal loss in hypoglossal nuclei and anterior horns with gliosis were present. The rarity of the association of a pallido-luyso-nigral atrophy and an ALS, the occurrence of an ALS at such a young age and the fact that her grandmother died of Parkinson disease at age 30 suggest that this association may represent more than a coincidental occurrence.

Adult↗
PubMed1996

Vestibular nucleus projections to the parabrachial nucleus in rabbits: implications for vestibular influences on the autonomic nervous system.

Acute vestibular dysfunction and motion sickness are characterized by autonomic effects such as pallor, nausea, and vomiting. Previous anatomic and physiologic studies suggest that one potential mediator of these effects may be light, direct vestibular nuclear projections to the nucleus tractus solitarius and the dorsal motor nucleus of the vagus nerve. This study presents evidence for relatively dense, direct projections from the vestibular nuclei to the parabrachial nucleus. Male albino rabbits received injections of Phaseolus vulgaris leucoagglutinin into the vestibular nuclei. The tracer was visualized immunocytochemically with standard techniques. Anterogradely labeled axons were traced bilaterally from the vestibular nuclei to the parabrachial nuclear complex, where they terminated around somata in the Kölliker-Fuse nucleus, external medial parabrachial nucleus, medial parabrachial nucleus, and lateral parabrachial nucleus. Less dense terminations were observed in the ventrolateral aspect of the medullary reticular formation, the subtrigeminal nucleus, lateral tegmental field, and nucleus ambiguus. These findings have several important implications. First, they suggest that vestibular input converges directly at brain stem levels with visceral sensory input in both nucleus of the solitary tract and the parabrachial complex. Second, they suggest that vestibular input influences brain stem autonomic outflow via two parallel pathways: (1) direct, light projections to the nucleus of the solitary tract, dorsal motor nucleus of the vagus nerve, and ventrolateral medullary reticular formation; and (2) denser projection to regions of the parabrachial nucleus that project to these brain stem regions. Finally, since the parabrachial nucleus regions that receive vestibular input also project to the hypothalamus and the insular and infralimbic prefrontal cortex, the parabrachial nucleus may serve as an important relay and integrative structure for the cognitive impairment and vegetative symptoms associated with motion sickness, vestibular dysfunction, and responses to altered gravitational environments.

Afferent Pathways↗
PubMed1992

Intraventricular infusion of N-methyl-D-aspartate. 2. Acute neuronal consequences.

This study documents the ultrastructural features of acute neuronal injury following N-methyl-D-aspartate (NMDA) receptor activation. NMDA (100 nmol/microliters) or vehicle was infused over a 15-min period into the lateral ventricle of adult rats. After perfusion fixation, specimens demonstrating normal and abnormal patterns of vascular permeability to horseradish peroxidase were sampled for ultrastructural analysis. In NMDA-infused rats, brain regions exhibiting protein extravasation contained swollen dendritic profiles and abnormal neuronal perikarya. Although periventricular regions were most severely affected, parenchymal abnormalities were also detected in the cerebral cortex, septum, striatum, thalamus, hypothalamus and cerebellum. Mildly affected dendrites contained dark compact mitochondria, while in severely swollen dendrites mitochondria were enlarged with ruptured cristae. Focal sites of plasma membrane disruption were also detected within swollen dendrites. Swollen neurons commonly displayed peripheral pallor and increased numbers of cytoplasmic vacuoles. Other neurons appeared dark and shrunken, some containing disrupted mitochondria and pyknotic nuclei. Pretreatment with the NMDA antagonist MK-801 (2 mg/kg) attenuated the neuronal and dendritic alterations. In conditions where cerebrospinal fluid levels of glutamate are abnormally elevated, excessive NMDA receptor activation may lead to early vascular and neuronal complications which could work in concert to promote brain injury.

Animals↗
PubMed1986

The pathology and pathogenesis of tuberculous encephalopathy and myeloradiculopathy: a comparison with allergic encephalomyelitis.

The pathology and pathogenesis of tuberculous encephalopathy are reviewed. They confirm the findings in a smaller series previously published. The main features were: diffuse brain edema and myelin pallor in the majority of specimens; microvascular distension or necrosis with perivascular macrophage reaction and greater demyelination; focal glial nodules in the white matter; less frequently, hemorrhagic lesions in the presence of mild-to-moderate tuberculous meningitis (TM), but in the virtual absence of the commoner brain-damaging mechanisms. Focal demyelinating lesions in the nerve roots are now added to the above pathology in the brain in some of the cases of spinal tuberculous meningitis. In addition, a picture similar to that in human postinfectious allergic or experimental allergic encephalomyelitis (EAE) has emerged. The spinal cords from one case of the former condition and from four animals with EAE are described to illustrate this similarity. The pathogenesis of tuberculous encephalopathy and myeloradiculopathy is believed, as before, to be due to delayed hypersensitivity, i.e., cell-mediated immunity (CMI) to tuberculoprotein. Experimental confirmation of this demyelination as a nonspecific consequence of CMI to various forms of tubercle bacillus proteins has recently been published. In a proportion of our cases, where two episodes of TM had occurred, the possibility of a hypersensitivity reaction to the brain's own myelin protein is also considered.

Adolescent↗
PubMed1976

Administration of obidoxime tablets to man. Plasma levels and side reactions.

Twenty-four male volunteers were given obidoxime tablets in quantities ranging from 1.84-3.58 g in a single dose, or 7.36 g divided into 4 equal doses. With the lowest dose, average peak plasma level of the drug was 1.9 mug/ml and after the highest single dose it was 5.6 mug/ml, both attained 1.5 h after administration. In the multiple-dosed individuals, plasma levels of the oxime increased gradually following each additional dose, reaching a peak of 3.5 mug/ml after the last dose. Thirteen individuals complained of one or more of the following side effects: pallor, nausea, pyrosis, headache, generalized weakness, sore throat, and paresthesia of the face muscles. Activities of blood cholinesterase, glutamic oxalacetic transaminase, glutamic pyruvic transaminase, as well as hematocrit values, heart rate, and blood pressure were not affected. It is postulated that due to the undesirable side effects, the general use of obidoxime tablets should not be recommended. However, prophylactic oral treatment with obidoxime could be considered for persons at high risk of organophosphate poisoning or when parenteral administration might not be feasible.

Administration, Oral↗