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Biomedical subjects

M D Allen

Publications and source records attributed to M D Allen.

116 records · Page 7Linked to original sources
PubMedDate not supplied

Vascular cell adhesion molecule-1 is induced on endothelium during acute rejection in human cardiac allografts.

An infiltration of mononuclear leukocytes into the myocardium of a cardiac allograft is diagnostic of transplant rejection. The presence of these leukocytes implies their adhesion to, and subsequent migration through, the vascular endothelium. Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 are endothelial proteins that have been shown to be involved in the binding of mononuclear leukocytes to the endothelium in vitro. We investigated the induction of these proteins in a random series from 99 endomyocardial biopsy specimens obtained from 1 week to 4 years after cardiac allograft transplantation. Intercellular adhesion molecule-1 was found to be expressed constitutively by the myocardial microvasculature in the recipient's original heart and in the posttransplantation biopsy specimens. No correlation was found between the presence or absence of intercellular adhesion molecule-1 expression and cellular rejection. In contrast, no endothelial expression of vascular cell adhesion molecule-1 was observed in the recipient heart or in endomyocardial biopsy specimens lacking cellular rejection. The presence of vascular cell adhesion molecule-1 significantly correlated with the presence of mild or moderate rejection. The de novo induction of vascular cell adhesion molecule-1 on the myocardial vasculature during periods of rejection, in addition to the recruitment of mononuclear leukocytes that are known to bind to this protein, suggests that the expression of this endothelial adhesion protein could be of use in diagnosing rejection.

Antigens, CD↗
PubMedDate not supplied

Limited cytomegalovirus-specific immunoglobulin M and immunoglobulin G profiles in heart transplant recipients.

Twenty heart transplant recipients were assayed serially with cytomegalovirus cultures and with Western blot techniques for development of anticytomegalovirus immunoglobulin M (IgM) and immunoglobulin G (IgG). Patients were followed up 3 to 29 months (mean, 15 months) after transplantation. All but three patients received a 5-week perioperative course of passive immunization with immune globulin. Of nine seronegative patients with seropositive grafts, positive cytomegalovirous cultures developed in all, secondary organ involvement (gastrointestinal or pneumonia) developed in four of nine. Four of nine patients produced limited IgM profiles, consisting of only one to three bands; six of the nine patients had atypical, restricted IgG profiles. Three of four patients in whom secondary organ invasion developed had limited IgM profiles, and all four had atypical IgG profiles. Four of five patients with primary infection without symptoms produced full IgM profiles. Delay of IgM production until a time coincident with or after evidence of viral shedding was documented in all patients with primary infection and secondary organ involvement. Among 11 seropositive patients, five received seropositive grafts and six seronegative grafts. Of the five patients with seropositive grafts, positive cultures (reinfection) developed in three; all three responded with full IgM profiles. However, secondary organ involvement developed in two of these three in spite of full IgM profiles. Symptomatic illness did not develop in any patient with a seronegative donor, even in the presence of positive cultures (reactivation). Persistence of IgM for up to 26 months was found in all patients with primary infection or reinfection. In heart transplant recipients, limited IgM and IgG profiles in primary infection may confer increased risk of secondary organ invasion whereas the early development of full IgM profiles may correlate with disease without symptoms. In seropositive patients, production of full IgM profiles may not protect from reinfection with secondary organ involvement if the organ donor is seropositive, a potential source of a new viral strain.

Antibodies, Viral↗
PubMedDate not supplied

Effect of cyclosporine on the uptake of monoclonal antibody to cardiac myosin.

Monoclonal antibody to cardiac myosin labeled with indium-111 diethylenetriamine pentaacetic acid holds promise as a noninvasive marker of cardiac graft rejection. Uptake of antibody has correlated with histologic evidence of rejection in nonimmunosuppressed animals. Whether this correlation will apply with immunosuppression has important clinical implications. Fifty-two heterotopic heart transplantations were performed between isogeneic and nonisogeneic strains of rats. Cyclosporine-treated (15 mg/kg day subcutaneously for 9 days) and untreated control animals were killed on day 9, 48 hours after injection of radiolabeled antibody. Donor and recipient hearts were submitted for scintillation scanning and histologic analysis. In untreated animals, antibody uptake was significantly greater in nonisogeneic than in isogeneic donor hearts, correlating with a significantly higher rejection score and increased myocyte necrosis in the former. Between isogeneic groups, cyclosporine-treated donor hearts had significantly higher antibody uptake and donor/native antibody uptake ratios than did untreated isogeneic hearts. There was, however, no significant difference in the histologic degree of rejection or myocyte necrosis between isogeneic groups. Between cyclosporine-treated and untreated nonisogeneic animals, donor heart antibody uptake and donor-native heart antibody uptake ratios were not significantly different. Nonetheless, the histologic grade of rejection and presence of myocyte necrosis was significantly greater in untreated than in treated nonisogeneic hearts. There were no abnormalities in the native hearts. In this model, cyclosporine treatment correlates with an increased uptake of antimyosin antibody in both isogeneic and nonisogeneic donor hearts, out of proportion to histologic evidence of rejection or myocyte necrosis. This effect may lead to false-positive results in clinical tests utilizing antimyosin antibody uptake as a marker of rejection in the presence of cyclosporine therapy.

Animals↗
PubMedDate not supplied

Diastolic mechanical properties of the left ventricle after global ischemia.

The purpose of this study was to evaluate left ventricular (LV) diastolic mechanical properties after induced global ischemia using reliable new methods. The diastolic function of nonoxygenated crystalloid solution (CC sO2) was compared with those of oxygenated crystalloid (CC cO2) and oxygenated fluorocarbon cardioplegic (FC cO2) solutions. Postischemic ventricular performance was studied in 3 equal (no. 7) groups of dogs subjected to 120 minutes of global ischemia induced at an average myocardial temperature of 18.5 +/- 1.4 degrees C. LV diastolic function (chamber and myocardial stiffness) and relaxation (the exponential fall in LV pressure) were evaluated by sonomicrometry and Millar micrometers before ischemia and at 45 and 60 minutes after ischemia. LV chamber and myocardial stiffness in the CC sO2 group was significantly (p less than 0.05) elevated after ischemia, while the CC cO2 and FC cO2 groups did not show increases in LV chamber and myocardial stiffness after ischemia. LV relaxation before and after ischemia was not changed in any group. The myocardial water content of the CC sO2 group was significantly higher than that of the CC cO2 and FC cO2 groups (p less than 0.05). We conclude that (1) the postischemic increase in LV chamber stiffness in the CC sO2 group was dependent not only on the increase in intrinsic myocardial stiffness but also due to an increase in myocardial edema, and (2) there was no correlation between the LV relaxation rate and the leftward shift of diastolic compliance curves in the CC sO2 group.

Animals↗
PubMedDate not supplied

Toxicity of aerosols of sodium reaction products.

Sodium is used as the heat transfer medium in several new energy technologies such as liquid-metal fast-breeder reactors and solar-thermal collection systems. Because sodium burns in air and reacts violently with water, the potential exists for an airborne release of sodium combustion products and subsequent human exposure. To help evaluate the potential short-term hazard from an accidental sodium fire, male juvenile or adult Wistar rats were exposed to sodium aerosols for 2 hours to determine the dose at which 50 percent of the animals were affected (ED50) for each age group. The estimated ED50 of 510 microgram/l for adults was not significantly different from the estimated ED50 of 489 microgram/l for juveniles. The incidence of acute laryngitis, attributed to exposure, was three times higher for juvenile rats than for adults, and the degree of severity of this lesion was significantly (P less than 0.05) higher for juveniles.

Aerosols↗