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Biomedical subjects

S F Mohammad

Publications and source records attributed to S F Mohammad.

At least 37 records · Page 2Linked to original sources
PubMed1990

Quantification of perivalvular thrombus formation in blood pumps by polar coordinate mapping.

A polar coordinate mapping technique (PCMT) to quantitatively describe perivalvular thrombus formation was applied in the examination of prosthetic valves from paracorporeal assist devices. The method begins by photographing the upstream and downstream views of the freshly retrieved valves using transparency film. The valve images are then projected onto 10 x planforms of the valves, and the boundaries of the observable thrombi are traced. The radial thrombus length is then measured at 5 degrees increments and plotted on Cartesian coordinates as a function of polar coordinate. Mean radial thrombus length and incidence of thrombus are calculated. Statistical analysis can then be used to test for differences in the length, incidence, and pattern of thrombus formation between test groups. The effect of valve selection, anti-coagulant regime, and other factors that influence thrombus formation can be quantitatively compared with the PCMT. Consequently, the PCMT could be a valuable assessment tool for efforts being made to reduce thrombosis in prosthetic blood pumps.

Animals↗
PubMed1990

Detection of microemboli by constant-pressure filtration during in vitro circulation of bovine and human blood.

The constant-pressure filtration (CPF) method has been developed to assess blood microemboli (BME) in terms of their ability to occlude microvascular flow. Previous reports suggest that the method is sensitive to the effects of platelet stimulation and to blood-pumping conditions. BME production and heparin activity were studied in bovine and human blood pumped by a Pellethane ventricle with Pellethane molded valves connected via smooth quick-connects to a Pellethane horseshoe-shaped reservoir. In each experiment, blood was collected into heparin by cardiac puncture from a stunned animal or by venepuncture from a human donor. The blood from each donor was filled into three ventricle-reservoir systems (50 cc ventricle and 1,500 cc reservoir for the bovine blood, and 20 cc ventricle and 150 cc reservoir for the human blood). One of the systems received aspirin (ASA; 25 mg/dl) shortly after the onset of pumping, whereas the other two served as pumping and non-pumping controls. The blood was pumped in a full-fill/full-eject mode for up to 10 h. BME concentration was measured by the CPF method in which the blood was filtered through 20-microns pore filters at 20 mm Hg for 10 s, and the flowrate curves were evaluated from occlusion model. Heparin activity was measured by the activated partial thromboplastin time (APTT) test. In the early period after the onset of pumping, the BME concentration increased, whereas the APTT decreased from an initial value of greater than 250 s, with the relative rate of change for both the BME and the APTT being the following: pumping control greater than pumping ASA blood greater than quiescent control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Prostacyclin production following in vitro mixing of normal with hemolytic-uremic-syndrome serum.

Serum from patients with the hemolytic-uremic syndrome (HUS) usually has a diminished ability to support the production of prostacyclin (prostaglandin [PG] I(2)). An impaired ability to produce this potent antiaggregatory substance could account for the thrombotic microangiopathy that is characteristic of the syndrome. We did in vitro mixing experiments to determine if adding normal serum in various concentrations would improve the ability of HUS serum to support PGI(2) production when incubated with cultured human endothelial cells. Mixing normal with HUS serum in a 1:2, 1:3, and 1:6 ratio generally enhanced the PGI(2)-supporting capacity of the HUS serum. Moreover, adding normal serum yielded a mixture whose supporting capacity was between the normal and the HUS serum's value, and the PGI(2)-supporting capacity could be predicted by calculating the weighted average value of the components of the mixture. There was a strong correlation between the calculated (predicted) and the actual experimental values (r = .95, P<.001).

Child↗
PubMed1986

Characterization of a potent inhibitor of platelet aggregation and release reaction isolated from allium sativum (garlic).

When added to platelet-rich plasma, aqueous extracts of garlic inhibited platelet aggregation and the release reaction. Subsequent experiments designed to characterize the inhibitory component revealed that the inhibitory activity was i) associated with small molecular-weight components, ii) the inhibitory component possessed the typical garlic odor and contained an abundance of sulfur, iii) the inhibitory activity could be extracted with organic solvents, and iv) temperatures above 56 degrees C and alkaline pH above 8.5 quickly destroyed the inhibitory activity. The Rf value of the major inhibitory component after thin-layer chromatographic separation was similar to that of allicin, an unique thiosulfinate in garlic previously shown to possess strong antibiotic and antifungal properties. Allicin was synthesized. On thin-layer chromatographic plates, allicin co-migrated with the inhibitory component in garlic. At 10 microM concentration, allicin inhibited completely platelet aggregation and the release reaction. Comparative studies suggest that the major platelet aggregation and release inhibitor in garlic may be allicin.

Adult↗
PubMed1986

Effect of heparin on platelet aggregation inhibited by PGI2, trifluoperazine and verapamil.

The enhancement of platelet aggregation by heparin in the presence of certain inhibitors of aggregation was investigated in an attempt to discern the mechanism through which heparin alters platelet function in plasma. These studies were performed by adding prostaglandin I2 (PGI2), verapamil, or trifluoperazine to platelet-rich plasma (PRP) in the presence or absence of heparin. Adenosine diphosphate (ADP), collagen, or arachidonic acid were used for induction of platelet aggregation. The inhibitory agents reduced platelet aggregation to 5 to 20% of control in the absence of heparin. When present in the reaction mixture along with the inhibitor, heparin restored aggregation to approximately 57 to 92% of control depending on the inhibitor and aggregating agent. This proaggregatory action of heparin was observed when heparin and PGI2 were preincubated together or separately for 20 min prior to the addition of PRP and ADP. Results were similar regardless of the sequence in which PGI2 and heparin were added to PRP, and irrespective of the time of incubation of platelets with PGI2. No suppression of platelet cyclic AMP concentration was observed with heparin alone. Heparin also failed to reduce the magnitude of platelet cyclic AMP accumulation promoted by PGI2, forskolin, or a mixture of PGI2 and forskolin. These observations suggest that heparin promoted platelet aggregation and partially overcame the effect of certain inhibitory agents by mechanism(s) that did not involve a reduction of platelet cyclic AMP.

Blood Platelets↗
PubMed1986

In vitro prostacyclin production in the hemolytic-uremic syndrome.

Reports from Europe suggest that the hemolytic-uremic syndrome is associated with an impaired ability to produce prostacyclin (prostaglandin [PG] I(2)), a potent inhibitor of platelet aggregation and thrombus formation. In comparing the production of PGI(2) by cultured endothelial cells using serum obtained from 22 children with the hemolytic-uremic syndrome with values obtained using serum from 22 normal children, we found that cultured endothelial cells produced less PGF(1alpha) (the stable metabolite of PGI(2)) when incubated with affected serum. The relationship of this observation to the pathogenesis of the hemolytic-uremic syndrome is unclear.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Disulfide linking of albumin to the hinge region of immunoglobulin G in normal human serum.

A protein-protein complex from human serum was isolated and characterized as a two-component system, containing albumin and IgG in a 1:1 mole ratio. The observations reported here suggest that the albumin-IgG complex may have formed through intermolecular disulfide bonds between albumin and IgG. Immunoelectrophoretic analysis of papain-digested fragments of albumin-IgG complex revealed that the combining sites for albumin may be located in the hinge region between the Fab and the Fc fragments of IgG.

Adult↗
PubMed1983

Ketanserin prevents platelet aggregation and endotoxin-induced pulmonary vasoconstriction.

Pulmonary hypertension secondary to sepsis is due, in part, to release of serotonin from platelets. This study examines the effects of ketanserin, a new, highly specific serotonin antagonist, on platelet aggregation and the cardiovascular changes associated with bacterial endotoxemia in dogs. Ketanserin markedly inhibits in vitro platelet aggregation induced by mixing serotonin and epinephrine. When ketanserin is administered to animals before endotoxin infusion, cardiac output is greater and mean pulmonary artery pressure (MPAP), pulmonary and systemic vascular resistance (PVR and SVR) and arteriovenous oxygen content difference [C(a-v)O2] are less than in animals not receiving ketanserin. Similar results for PVR, SVR, and C(a-v)O2 are obtained when ketanserin is administered after endotoxin infusion. The data indicate that ketanserin inhibits serotonin-induced platelet aggregation and modifies many cardiovascular changes associated with bacterial endotoxemia.

Animals↗
PubMed1983

Adsorption and reactivity of human fibrinogen and immunoglobulin G on two types of hemodialysis membranes.

Phase contrast microscopic examination of Cuprophane and polyacrylonitrile. After clinical ex vivo use by uremic patients revealed extensive cellular deposition of erythrocytes, platelets, and leukocytes on Cuprophane but not on polyacrylonitrile. In vitro studies with 125I-labeled human fibrinogen or immunoglobulin G (IgG) showed that the adsorption of fibrinogen or IgG was greater on polyacrylonitrile than on Cuprophane. Further studies on the reactivity of fibrinogen adsorbed on polyacrylonitrile surface indicated that the absorbed fibrinogen: (a) was not desorbed readily from the surface, (b) was not appreciably displaced by other plasma proteins such as albumin, IgG, and fibrinogen, (c) was not readily accessible for reaction with 125I-antifibrinogen-IgG, and (d) did not promote the adhesion of 51Cr-labeled platelets. IgG adsorbed on the surface produced essentially no effect on platelet adhesion to polyacrylonitrile and promoted only slightly on the adhesion of granulocytes to the same material. On the other hand, fibrinogen and IgG augmented greatly the platelet adhesion to Cuprophane and IgG enhanced the granulocyte adhesion moderately. These data indicate that fibrinogen and IgG, though at high concentration on polyacrylonitrile, may adsorb in a biologically inactive form. Our observations suggest that the thrombogenicity of an artificial surface may not be assessed entirely by the types and amount of the various protein species adsorbed but is likely determined by the reactivity of the specific protein species adsorbed on the material.

Absorption↗
PubMed1981

Albumin-IgG complexes in human serum and plasma that inhibit blood platelet adhesion.

Macromolecular albumin-IgG complexes have been isolated from human serum and characterized immunologically. These complexes are shown to be present in plasma also and appear to be normal constituents of blood. The complexes can be demonstrated in normal serum and plasma by immunoelectrophoresis and rocket immunoelectrophoresis, as well as by use of a two-step radioimmunologic binding test. The albumin-IgG complexes inhibit adhesion of human platelets to glass and account for 12-16% of the total protein in serum.

Adult↗
PubMed1981

A human model for study of blood-vascular wall interactions. Effects of enzymatic treatment of intima.

A human umbilical cord vein model was used to study the interaction of human blood with vein intima after treatment with certain enzymes. Treatment of the intima with neuraminidase produced little in the way of morphologic change, and studies showed no increase in the retention of platelets labeled with chromium 51. Treatment of vein intima with collagenase produced severe morphologic changes, with exposure of coarse and fine subendothelial fibers, but with the retention of platelets little enhanced, as determined morphologically or radiometrically. On the other hand, treatment of vein intima with trypsin resulted in loss of endothelium in some areas, with exposure of coarse subendothelial fibers that produced a marked increase in platelet retention, as determined both morphologically and radiometrically. Exposure of the vein intima to thrombin produced apparent contraction of endothelial cells, with focal exposure of subendothelium and platelet adhesion.

Blood Cells↗
PubMed1981

Effects of heparin on platelet aggregation and release and thromboxane A2 production.

Heparin, when added to citrated platelet-rich plasma (PRP), caused potentiation of platelet aggregation and the release reaction induced by the aggregating agents adenosine diphosphate (ADP), arachidonic acid, collagen, and epinephrine. At low concentrations (4.7 x 10(-5) M) arachidonic acid failed to cause aggregation of platelets in citrated PRP. However, in the presence of heparin, the same concentration of arachidonic acid caused aggregation. Examination of PRP for the presence of thromboxane A2 (TxA2) by use of a bioassay revealed that heparin also stimulated release of TxA2. This finding indicated that platelets released more TxA2 when they were challenged by low concentrations of arachidonic acid in the presence of heparin than in its absence. Platelets were labeled with 3H-arachidonic acid and 14C-serotonin, and attempts were made to determine whether heparin stimulated the platelet release reaction first with subsequent increased production of TxA2, or alternatively, whether heparin stimulated TxA2 production first with subsequent enhancement of the release reaction. In view of the demonstrated simultaneous release of 14C-serotonin and 3H-arachidonic acid metabolites, it appeared that either release of 14C and 3H occurs concurrently or, even if one of these events is dependent on the other, both events take place in rapid succession. Timed sequential studies revealed that in the presence of arachidonic acid, the addition of heparin hastened the apparently simultaneous release of both 14C and 3H.

Adenosine Diphosphate↗
PubMed1980

A human model for study of blood-vascular wall interactions. I. Description and demonstration of use of the model.

We fashioned a model for the study of interactions of human blood cells with human vascular wall components. It consists of a segment of human umbilical cord vein formed into a closed loop. The lumen of the vein is filled with anticoagulated platelet-rich plasma propelled through the loop by a peristaltic pump. The results of the present study demonstrated that various degrees of mechanical injury to umbilical vein intimal components result in adhesion and aggregation of platelets. Platelet adhesion can be measured by use of radioisotope-labeled platelets in the model. Other injuries to vascular wall components, such as those produced by occlusive hemostats or punctures of the vascular wall by stylets or needles, demonstrated a striking retention of platelets at the sites of injury as measured by gamma-ray counting and as viewed by scanning electron microscopy.

Adolescent↗