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Biomedical subjects

J M Allen

Publications and source records attributed to J M Allen.

At least 253 records · Page 14Linked to original sources
PubMed1981

Cardiac tamponade in medical patients.

We reviewed the cases of 56 medical patients wih cardiac tamponade who were treated at the University of Cincinnati. A paradoxic arterial pulse was critical in the diagnosis because most patients did not have a small quiet heart, and blood pressure was often well maintained. Fifty-two of 55 patients had enlarged cardiac silhouette by chest radiogram; heart sounds were diminished in 19 patients; arterial systolic pressure was greater than or equal to 100 mm Hg in 35, and arterial pulse pressure was greater than or equal to 40 mm Hg in 27. Echocardiograms in 23 patients showed abnormally increased right ventricular dimensions and decreased left ventricular dimensions during inspiration, except in one patient with left ventricular dysfunction. The causes of cardiac tamponade were metastatic tumor in 18 patients, idiopathic pericarditis in eight and uremia in five; five cases of tamponade occurred after heparin administration in acute cardiac infarction. Myxedema and dissecting aneurysm each caused tamponade in two patients. Pericardiocentesis relieved tamponade initially in 40 of 46 patients; however, two suffered fatal complications. Pericardial resection was done in 18, including 12 of these 46.

Adolescent↗
PubMed1980

Cadiovascular complications of homozygous familial hypercholesterolaemia.

Seven patients with homozygous familial hypercholesterolaemia, two female and five male, aged 12 to 25 years, underwent clinical and angiographic assessment to define the associated cardiovascular abnormalities. Four patients had angina, two of whom also had syncope on exertion. All had an ejection systolic murmur but no ejection click and a loud aortic second sound. All but one had a systolic gradient between the left ventricle and aorta, ranging from 20 to 80 mmHg at the time of presentation. Angiography showed a characteristic narrowing of the aortic root in all and five of the seven patients had coronary ostial stenosis. One patient died after an aortocoronary bypass and aortic valvotomy and two others underwent aortocoronary bypass and aortic valve replacement, one of whom also died after operation. The survivor and three other patients are now undergoing regular plasma exchange and remain well. The seventh patient died suddenly before the latter form of treatment could be started. These findings confirm that premature, severe atheroma of the aortic valve and root is a characteristic feature of homozygous familial hypercholesterolaemia and carries a high mortality.

Adolescent↗
PubMed1980

Echocardiographic study of the paradoxical arterial pulse in chronic obstructive lung disease.

In nine subjects with chronic obstructive pulmonary disease (COPD) and pulsus paradoxus, M-mode echocardiograms showed inspiratory augmentation of right ventricular dimensions and inspiratory decrease of left ventricular diastolic dimensions. In five subjects in whom the echocardiographic transistor was in the subxiphoid position, mean right ventricular dimensions increased during inspiration from 1.4 +/- 0.20 to 2.96 +/- 0.38 cm (p < 0.01). With inspiration, mean left ventricular diastolic dimensions decreased from 4.8 +/- 0.61 to 3.7 +/- 0.63 cm (p < 0.01) in these five subjects. Two-dimensional echocardiograms, performed in three subjects, confirmed inspiratory augmentation of right ventricular cross-sectional area. Similar changes were produced in two normal volunteers by artificial obstruction to breathing. Left ventricular ejection time measurements demonstrated an inspiratory decline in left ventricular stroke volume. Inspiratory filling of the right ventricle is not hampered, but rather is exaggerated in patients with COPD and pulsus paradoxus, and left ventricular stroke volume is reduced during inspiration. Exaggerated variations in intrathoracic pressure alone did not explain pulsus paradoxus. Increased right ventricular filling and stroke volume during inspiration probably play a part.

Adult↗
PubMed1980

Diminished polymorphonuclear leukocyte adherence. Function dependent on release of cyclic AMP by endothelial cells after stimulation of beta-receptors by epinephrine.

To investigate the biochemical and cellular basis for the rise in polymorphonuclear leukocyte (PMN) count during epinephrine administration, PMN from subjects receiving epinephrine were studied for their capacity to adhere to nylon wool fibers and endothelial cell monolayers. After administration of epinephrine, the PMN count increased by 80% at 5 min, and isolated PMN adherence to nylon fibers fell from a base line of 44+/-2-18+/-3%. In contrast, when subjects were infused with the beta-antagonist propanolol before receiving epinephrine, the PMN count failed to rise and PMN adherence was normal. Exposure of PMN endothelial cell monolayers to 0.1 muM epinephrine led to diminished PMN adherence that could be blocked by 10 muM propanolol but not by 10 muM phentolamine. Sera obtained from subjects 5 min after receiving epinephrine or from supernates derived from endothelial cell monolayers exposed to 90 nM epinephrine inhibited PMN adherence to nylon fibers. Addition of anticyclic AMP antisera but not anticyclic guanosine monophosphate antisera to the postepinephrine sera or to the postepinephrine supernate derived from the endothelial cell monolayers abolished their inhibitory effect of PMN adherence to nylon fibers. In contrast, direct exposure of PMN to epinephrine failed to affect their adherent properties. Because it has been previously shown that endothelial cells contain beta-receptors and respond to catecholamines by raising their intracellular concentrations of cyclic AMP, and that PMN adherence is attenuated by cyclic AMP, it would appear that diminished PMN adherence after epinephrine administration is mediated through endothelial cell beta-receptor activity, which in turn impairs PMN margination in vivo and could account for the rise in circulating PMN.

Cell Adhesion↗
PubMed1980

Inhibition of polymorphonuclear leukocyte adherence by prostacyclin.

The adherence of human PMNs to nylon fibers or endothelial cells is inhibited by exposure in vitro of the phagocytic cells to PGl2. The impaired adherence is transient and correlates with a rise in intracellular levels of cyclic AMP. Similarly, stimulation of human endothelial cells with sodium arachidonate, a precursor of PGl2, leads to impaired PMN adherence. On the other hand, PGl2 failed to alter O2- release and the bactericidal capacity of the PMNs. These findings suggest that PGl2 may play a role in regulating PMN adhesiveness to endothelial cells without compromising host defense.

Cell Adhesion↗
PubMed1979

Protection of granulocytes by vitamin E in glutathione synthetase deficiency.

The administration of vitamin E (alpha-tocopherol) was found to improve polymorphonuclear leukocyte function in an infant with congenital deficiency of glutathione synthetase activity. Before therapy with vitamin E the abnormal leukocytes exposed to phagocytic challenge showed oxidant damage. They released 60 per cent more hydrogen peroxide than did normal leukocytes, iodinated only 20 to 25 per cent of the normal number of particles, and were unable to kill bacteria as effectively as normal leukocytes although the rates of phagocytosis were normal. These functional abnormalities disappeared when the patient was placed on 400 IU of alpha-tocopherol daily for three months. Associated with the functional improvement was a normalization of microtubule assembly during phagocytic challenge.

Blood Bactericidal Activity↗
PubMed1979

Oxidative damage to neutrophils in glutathione synthetase deficiency.

Several episodes of neutropenia were observed in a child with glutathione synthetase deficiency (5-oxoprolinuria). Studies of the patient's glutathione-deficient neutrophils were undertaken to examine the responses of the cells to oxidative stress associated with phagocytosis. The patient's neutrophils contained 10--20% of normal glutathione content. Circulating neutrophils in infection-free periods appeared less mature than normal by morphologic criteria, suggesting increased cell turnover. The cells ingested particles, responded to chemotactic stimuli, and oxidized 1-14C glucose normally. However, following ingestion of particles, the cells accumulated excess hydrogen peroxide compared with normal cells, and showed impaired protein iodination and bacterial killing. Electron micrographs revealed damage to microtubules and membranous structures in the patient's neutrophils during phagocytosis. The level of glutathione in the cells appears inadequate to protect against peroxide generated during normal cell function, and the cells are thus damaged and rendered less effective in bacterial killing. The data provide evidence for a protective role of glutathione in normal neutrophil function.

Chemotaxis, Leukocyte↗
PubMed1979

Oxidative metabolic responses of rabbit pulmonary alveolar macrophages.

During phagocytosis of opsonized lipopolysaccharide-coated paraffin oil droplets, rabbit alveolar macrophages reduced nitroblue tetrazolium, which effect was in part inhibitable with the use of superoxide dismutase. Exposure of cytochalasin-B-treated rabbit alveolar macrophages to opsonized zymosan led to the generation of superoxide, as quantitated by ferricytochrome C reduction. It was found that nitroblue tetrazolium in the presence of ferricytochrome C could in turn serve as scavenger of superoxide during stimulation of cytochalasin-B-treated rabbit alveolar macrophages. Following challenge with either opsonized zymosan or the membrane perturbant digitonin, rabbit alveolar macrophages released hydrogen peroxide into the extracellular medium. Employment of the surface membrane stimulant phorbol myristrate acetate led to activation of the hexose monophosphate shunt, which activity could be further enhanced in the presence of superoxide dismutase or attenuated in the presence of catalase. These studies demonstrate that rabbit alveolar macrophages release superoxide and hydrogen peroxide during surface membrane perturbation. In turn, hydrogen peroxide generation can stimulate the hexose monophosphate shunt.

Animals↗
PubMed1978

In vitro functional capabilities of canine polymorphonuclear neutrophils collected simultaneously by continuous-flow centrifugation and continuous-flow filtration leukopheresis.

Polymorphonuclear neutrophils were simultaneously collected from dogs by continuous-flow centrifugation and continuous-flow filtration leukapheresis. In vitro studies were performed on cells obtained by the two methods as well as on control cells. Studies consisted of assessment of phagocytic capacity, degranulation, chemotaxis, hexose monophosphate (HMP) shunt activity, and bacterial killing. The cells obtained from the filter were metabolically more active than those harvested by centrifugation, as evidenced by increase in resting HMP shunt activity and dimunition in total available lysozyme-secreting activity compared to centrifuged cells. Despite their impaired phagocytic capacities, the filtered cells were able to kill Staphylococcus aureus as efficiently as the centrifuged cells. Both cell populations responded to chemotactic gradients equally.

Animals↗
PubMed1978

Improvement of polymorphonuclear leucocyte oxidative and bactericidal functions in chronic granulomatous disease with 4-amino-4'-hydroxylaminodiphenyl sulphone.

In an effort to restore oxidant-dependent capabilities to chronic granulomatous disease (CGD) polymorphonuclear leucocytes (PMN), we studied a dapsone derivative, 4-amino-4'-hydroxylaminodiphenyl sulphone (DDS-NOH), known to generate H2O2. After incubation of CGD PMN with 0.2 and 1.0 mM DDS-NOH for 30 min, the rate of glucose-1-14C oxidation via hexose monophosphate (HMP) shunt increased 2--4-fold and that of iodination of ingested zymosan particles 1.5--2.7-fold. Both effects could be further enhanced by superoxide dismutase (SOD) but inhibited by catalase. In three patients, 0.2 mM DDS-NOH improved in vitro killing of Staph. aureus. DDS-NOH 0.02 mM induced capping of Concanavalin A (Con A) receptor complexes suggesting interference by the drug with microtubule-associated function. Thus, optimal concentrations of DDS-NOH may be employed as an oxidant to improve metabolic and bactericidal functions of PMN from patients with CGD.

Aminobiphenyl Compounds↗
PubMed1978

Role of microtubules in granulocyte adherence.

The adherence of human polymorphonuclear leukocytes (PMN) to nylon fibers is inhibited in a dose-dependent fashion by exposure in vitro of these cells to either colchicine or VM-26, both of which agents prevent microtubule assembly. Mean adherence of human PMN was 48% +/- 2%, following treatment with 10(-5) M colchicine or 10(-4) M VM-26 it was reduced to 31% +/- 2% and 7%, respectively. Peritoneal PMN obtained from mice and mink with Chediak-Higashi syndrome (CHS) thought to have a microtubule-membrane disorder affecting the PMN had a mean adherence of 29% +/- 3% and 40% +/- 8% compared to control values of 46% +/- 5% and 73% +/- 8%, respectively, from the mice and mink. Both ascorbic acid and bethanechol, shown previously to enhance microtubule assembly in humans with CHS, normalized granulocyte adherence in PMN obtained from mice with CHS. Cyclic nucleotide levels were not altered by treatment of human PMN with colchicine, nor did they differ between normal and CHS animals. Thus it appears that the state of microtubule assembly may directly affect the properties of the PMN plasma membrane without requiring alterations of cyclic nucleotides as an intermediary.

Animals↗
PubMed1978

Potentiation of polymorphonuclear leukocyte motile functions by 2,3-dihydroxybenzoic acid.

DHB potentiates PMN phagocytosis of opsonized lipopolysaccharide-coated PO droplets by 53% to 45% and chemotaxis by 36% to 10% at 10-3M and 10-4M concentrations, respectively. The effect is reversible in vitro. In the presence of DHB, PMNs released significantly less superoxide and H2O2 to the extracellular media but were able to oxidize 1-14C-glucose normally during phagocytosis. Although iodination of opsonized particles was decreased in the presence of DHB, the PMNs were able to kill Staphylococcus aureus 502A normally. These results support the hypothesis that directed cell movement and phagocytosis can be enhanced by protecting the PMN membrane against auto-oxidative damage from scavenging superoxide and H2O2 by means of DHB.

Cell Movement↗
PubMed1977

Improvement of Chediak-Higashi leukocyte function by cyclic guanosine monophosphate.

The addition of cholinergic agents and cyclic 3'5'-guanosine monophosphate (cGMP) to polymorphonuclear leukocytes in vitro from a patient with Chediak-Higashi syndrome corrected the impaired release of the lysosomal enzyme, beta-glucuronidase, to normal. Coinciding with the improvement in degranulation, the bactericidal capacity was enhanced to normal. Similar concentrations of cholinergic agents potentiated chemotaxis to control values. On the other hand, the phagocytic rate of lipopolysaccharide-coated paraffin-oil droplets was not altered by the cholinergic agents. The improvement in Chediak-Higashi syndrome polymorphonuclear leukocyte function by the addition of cholinergic agents and dibutyryl cGMP suggested disturbed intracellular cyclic nucleotide levels.

Blood Bactericidal Activity↗