Spiny Sphere Research Articles

Multifunctional hollow silica carriers with spiny structure for enhanced foliar adhesion and triple-responsive pesticide delivery

Intelligent responsive pesticide formulations hold great promise for enhancing foliage retention and effective utilization. Herein, hollow silica (S-HS) nanocarriers with spiny structure were constructed for pesticide delivery. The S-HS nanocarriers presented homogeneous spiny spheres with an average size of 220 nm. This spiny structure can achieve effective retention on foliage by the “hanger-hat” topology effect. For constructing the responsive layer, the S-HS nanocarriers were further functionalized with surface vinyl groups. After loading imidacloprid (IMI), the temperature sensitive poly N-isopropylacrylamide (pNIPAm) and tannic acid–Fe complexes (TA-Fe) were introduced to encapsulate pesticides (IMI@S-HS-pNT). The TA-Fe complex layer served as a wall material and photothermal agent. The S-HS-pNT carriers achieved a loading capacity for IMI (26.6 %), high photothermal conversion effect (η = 36.1 %), and good biocompatibility. Except for excellent photostability and foliar adhesion property, the IMI@S-HS-pNT exhibited pH, temperature and near infrared (NIR) responsive release behavior. Moreover, the S-HS nanocarriers could be effectively transported to various parts of tobacco plants under the root immerse or foliar spray. The IMI@S-HS-pNT showed the high control efficacy against Plutella xylostella. Overall, this work provides insight into improving the efficiency of utilization and prolonging pesticide retention on plant leaves.

Synthesis of cuprous oxide with morphological evolution from truncated octahedral to spherical structures and their size and shape-dependent photocatalytic activities

In this study, a facile room-temperature solution-chemical route has been developed to synthesize Cu2O crystals with various sizes and morphologies. Adjustment of feeding speed of the aqueous mixture of polyvinyl pyrrolidone (PVP) and ascorbic acid (AA) enables the Cu2O crystal morphology and size evolution. It is also interesting to find that, simple alteration of the feeding speed of AA aqueous solution enables the size of Cu2O crystals evolved, while the morphology of Cu2O crystals keep unchanged. These Cu2O crystals samples were used as photocatalysts for the decomposition of methyl orange (MO) under visible light irradiation. The results show that Cu2O spiny spheres with hierarchical structure exhibited superior photocatalytic activity compared with truncated octahedrons and spheres. In addition, the photocatalytic activity of truncated octahedral Cu2O can be greatly improved by decreasing the size of Cu2O particles. The work demonstrated a novel strategy for the shape and size-controlled synthesis of Cu2O crystals with superior photocatalytic activities.

“Imperfections and oddities” in the origin of the nucleus

We outline a plausible evolutionary sequence that led from prokaryotes to the origin of the first nucleated cell. The nucleus is postulated to evolve after the archaebacterium and eubacterium merged to form the symbiotic ancestor of amitochondriate protists. Descendants of these amitochondriate cells (archaeprotists) today thrive in organic-rich anoxic habitats where they are amenable to study. Eukaryosis, the origin of nucleated cells, occurred by the middle Proterozoic Eon prior to the deposition in sediments of well-preserved microfossils such as Vandalosphaeridium and the spiny spheres in the Doushantou cherts of China.

The von Willebrand Factor-Glycoprotein Ib/V/IX Interaction Induces Actin Polymerization and Cytoskeletal Reorganization in Rolling Platelets and Glycoprotein Ib/V/IX-transfected Cells

Platelet adhesion to sites of vascular injury is initiated by the binding of the platelet glycoprotein (GP) Ib-V-IX complex to matrix-bound von Willebrand factor (vWf). This receptor-ligand interaction is characterized by a rapid on-off rate that enables efficient platelet tethering and rolling under conditions of rapid blood flow. We demonstrate here that platelets adhering to immobilized vWf under flow conditions undergo rapid morphological conversion from flat discs to spiny spheres during surface translocation. Studies of Glanzmann thrombasthenic platelets (lacking integrin alpha(IIb)beta(3)) and Chinese hamster ovary (CHO) cells transfected with GPIb/IX (CHO-Ib/IX) confirmed that vWf binding to GPIb/IX was sufficient to induce actin polymerization and cytoskeletal reorganization independent of integrin alpha(IIb)beta(3). vWf-induced cytoskeletal reorganization occurred independently of several well characterized signaling processes linked to platelet activation, including calcium influx, prostaglandin metabolism, protein tyrosine phosphorylation, activation of protein kinase C or phosphatidylinositol 3-kinase but was critically dependent on the mobilization of intracellular calcium. Studies of Oregon Green 488 1, 2-bis(o-amino-5-fluorophenoxy)ethane-N,N,N',N-tetraacetic acid tetraacetoxymethyl ester-loaded platelets and CHO-Ib/IX cells demonstrated that these cells mobilize intracellular calcium in a shear-dependent manner during surface translocation on vWf. Taken together, these studies suggest that the vWf-GPIb interaction stimulates actin polymerization and cytoskeletal reorganization in rolling platelets via a shear-sensitive signaling pathway linked to intracellular calcium mobilization.

Pufferfish inflation: Functional morphology of postcranial structures in Diodon holocanthus (Tetraodontiformes).

For the purpose of defending itself against predators, the balloonfish (Diodon holocanthus) can triple its body volume by pumping water into its stomach. Diodon holocanthus exhibits striking structural and functional specializations for inflation. The stomach of the balloonfish is highly extensible and has lost its digestive function, it is repeatedly folded upon itself and is lined with transitional epithelium. The peritoneal cavity of the balloonfish is also large and extensible. During inflation, the stomach expands into an existing peritoneal space surrounding the axial musculature and presses the folded peritoneum out into potential peritoneal spaces ventral to the head and surrounding the dorsal fin, anal fin, and caudal peduncle; only the dorsal and lateral surfaces of the head are unaffected. Balloonfish skin is also specialized for inflation. Because the collagen fibers in the dermis of unstretched skin are wavy, little force is required to extend the skin up to 40% of its rest length. At high strains, the collagen fibers are stressed directly and the skin suddenly becomes stiff. Stiff skin surrounding a ball of incompressible water provides a rigid framework for the support of the erectile spines, and the balloonfish becomes a formidable, spiny sphere. However, not all of the structural and functional features that contribute to the ability of balloonfish to inflate are evolutionary adaptations specifically for inflation. Absence of pleural ribs, absence of a pelvis, and the orthogonal arrangement of dermal collagen sheets in the skin were all present in the ancestor of pufferfishes, and thus, must be considered exaptations. Sagittal plane flexibility of the vertebral column may be an epiphenomenon of the lengthening of the body cavity for more spherical inflation. Together these structural and functional features-whether adaptations, exaptations, or epiphenomena-combine to produce a highly effective mechanical defense. © 1994 Wiley-Liss, Inc.

Relevance of platelet serotonergic mechanisms in pregnancy induced hypertension

Platelet functions are becoming the useful tool for delineating the etiology of pregnancy induced hypertension. Electronmicroscopic studies, efflux and content of 5-HT in platelets and platelet aggregation reponses towards various aggregating agents have been measured in 25 normotensive pregnant subjects and 31 PIH subjects. Marked decrease changes have been noted in aggregation parameters with transformation from discoid to “spiny sphere” of platelets with long pseudopods alongwith prolonged time for spontaneous aggregation by platelets in PIH. Serotonin release from platelets was decreased and reserpine-induced release-reaction showed enhanced kinetics in PIH. Platelet serotonin content was raised and inversely related to platelet count with severity of syndrome. Hence, a check and balance for platelet activation and aggregation in PIH might be crucial in the development of PIH.

Thrombin enhanced adhesion of platelets to von willebrand factor substrates

When exposed to thrombin, the adhesion of platelets to a von Willebrand factor (vWf) substrate, relative to a control substrate, is selectively increased. Adhesion to a vWf substrate is dependent upon the concentration of vWf, the duration of the adhesion assay, the concentration of thrombin, and the presence of divalent cations. The enhanced adhesion results from an action of thrombin on the platelets; no effect on the vWf substrate is involved. Once adherent to the substrate, the platelets undergo a profound change in morphology from the spiny sphere phenotype characteristic of activated platelets to a flattened and highly spread state. The adhesion of activated platelets to solid phase vWf is not inhibited by physiological concentrations of fibrinogen.

Stochastic response of human blood platelets to stimulation of shape changes and secretion.

Stopped-flow turbidimetric data indicate that platelets stimulated with low levels of thrombin undergo a shape transformation from disc to "sphere" to smaller spiny sphere that is indistinguishable from the shape change induced by ADP through different membrane receptor sites and a dissimilar receptor trigger mechanism. Under conditions where neither secretion nor aggregation occur, the extinction coefficients for total scattering by each of the three platelet forms are independent of the stimulus applied, and both reaction mechanisms can be described as stochastic (Poisson) processes in which the rate constant for the formation of the transient species is equal to the rate constant for its disappearance. This observation is independent of the shape assignment, and as the concentration of thrombin is increased and various storage organelles secrete increasing amounts of their contents into the external medium, the stochastic pattern persists. Progressively larger decreases in the extinction coefficients of the intermediate and final platelet forms, over and above those that reflect shape alterations alone, accompany or parallel the reaction induced by the higher thrombin concentrations. The excess turbidity decrease observed when full secretion occurs can be wholly accounted for by a decrease in platelet volume equal in magnitude to the fraction of the total platelet volume occupied by alpha granules. Platelet activation, as reported by the whole body light scattering of either shape changes alone or shape changes plus parallel (but not necessarily also stochastic) alpha granule secretion, thus manifests itself as a random series of transient events conceivably with its origins in the superposition of a set of more elementary stochastic processes that could include microtubule depolymerization, actin polymerization, and possibly diffusion. Although the real nature of the control mechanism remains obscure, certain properties of pooled stochastic processes suggest that a reciprocal connection between microtubule fragmentation and the assembly of actin-containing pseudopodal structures and contractile elements--processes that may exhibit reciprocal requirements for calcium--might provide a hypothetical basis for a rate-limiting step.

Optimal efficiency of human platelet shape changes.

The light scattering extinction coefficients and kinetic rate constant(s) for the disc to sphere and the sphere to (smaller) 'spiny sphere' shape changes induced in platelets by saturating amounts of ADP are compared at 31, 37 and 41 degrees C. Platelets exhibit optimum efficiency at 37 degrees C, as judged by not only the rates of the shape changes but also by alterations in the overall sizes and shapes of the three platelet forms. Unstimulated (discoid) platelets appear to be flatter at 37 degrees C, the disc to sphere reaction appears to be impaired at other than 37 degrees C, and the pseudopodia which characterize the final spiny sphere may be more prominent at 41 degrees C.

Transient kinetics of the rapid shape change of unstirred human blood platelets stimulated with ADP.

Unstirred (isotropic) suspensions of human blood platelets stimulated with ADP in a stopped-flow laser turbidimeter exhibit a distinct extinction maximum during the course of the classical rapid conversion of initially smooth flat discoid cells to smaller-body spiny spheres. This implies the existence of a transient intermediate having a larger average light scattering cross section (extinction coefficient) than either the disc or the spiny sphere. Monophasic extinction increases reaching the same final value were observed when either discoid or spiny sphere platelets were converted to smooth spheres by treatment with chlorpromazine, and sphering of discoid cells was accompanied by a larger total extinction change than the retraction of pseudopods by already spherical cells. These and other results suggest that the ADP-induced transient state represents platelets that are approximately as "spherical" as the irregular spiny sphere but lack the characteristic long pseudopods and as a consequence are larger bodied. Fitting the ADP progress curves to the series reaction A leads to B leads to C by means of the light scattering equivalent of the Beer-Lambert law yielded scattering cross sections that are consistent with this explanation. The rate constants for the two reaction steps were identical, indicating that ADP activation corresponds to a continuous random (Poisson) process with successive apparent states "disc," "sphere," and "spiny sphere," whose individual probabilities are determined by a single rate-limiting step.

Adenosine diphosphate induces binding of von Willebrand factor to human platelets.

Blood platelets seal off leaks in the vessel wall to prevent haemorrhage by a mechanism involving their activation, adhesion to the zone of vessel injury and aggregation1. This physiologically important haemostatic process requires Factor VIII/von Willebrand factor (vWF), a plasma glycoprotein missing in the genetic, haemorrhagic disorder called von Willebrand disease, in which platelets cannot adhere to the subendothelial layer of the vessel wall2. Thus vWF is necessary for anchoring platelets to the vessel wall, and it mediates platelet–platelet interaction. This interaction requires an appropriate receptor on the platelet surface. Until recently, the antibiotic ristocetin was used to induce in vitro receptor-mediated binding of vWF to platelets and to cause their aggregation or agglutination3–7. But although a useful laboratory tool8, ristocetin is clearly non-physiological, so we turned our attention to thrombin, which appears in venous blood within 45 s of venipuncture and is a very potent physiological inducer of platelet aggregation. Thrombin causes platelets to change shape from discoid to spiny spheres, and alters the platelet membrane resulting in release of ADP, serotonin and other constituents of platelet storage granules9. We recently showed that low concentrations (0.1–0.5 nM) of thrombin, attainable in blood, induce binding of vWF to a specific platelet receptor10. We now report that the binding of vWF to platelet receptors is also induced by ADP on its addition to platelets. Moreover, ADP released from platelet storage granules by thrombin is, at least in part, responsible for subsequent binding of 125I-labelled vWF.

Fibrinogen Receptor Exposure and Aggregation of Human Blood Platelets Produced by ADP and Chilling

AbstractADP-induced platelet aggregation is associated with the specific binding of fibrinogen to receptors. Since fibrinogen is also a cofactor for the spontaneous aggregation of chilled human platelets during rewarming, we examined the ability of these platelets to bind purified 126l-labeled fibrinogen. Specific binding similar to ADP-induced binding at room temperature was observed after the platelets had been chilled for 20 min at 0–2°C. Aggregation, however, occurred only when the ambient temperature was increased and was followed within 15–30 sec by loss of most of the bound fibrinogen and disaggregation. ADP- and cold-induced fibrinogen binding and aggregation were inhibited by 0.3 µM PGE“ 1 mM dibutyryl cyclic AMP, and 2.5 mM EDTA, unaffected by 208 µM colchicine, and absent from thrombasthenic platelets. Platelets change shape from discs to spiny spheres when they are exposed to ADP or cold. PGE1 and dibutyryl cyclic AMP prevented the shape change induced by ADP but not by chilling. Shape change, fibrinogen binding, and aggregation induced by ADP. but not by chilling, were inhibited by incubating platelets with 7.3 µM antimycin A and 4.9 mM 2-deoxy-D-glucose. Fixed platelets bound fibrinogen only if they were exposed to ADP before fixation but they failed to aggregate. Studies with fixed platelets showed that EDTA and a low pH prevent the interaction of fibrinogen with exposed receptors, whereas platelets stimulated with ADP in the absence of divalent cations or at low pH prior to fixation bound fibrinogen at physiologic pH, and this binding was inhibited by EDTA. The present studies provide the following clues about the requirements for fibrinogen receptor exposure and platelet aggregation. (1) ADP and chilling activate platelets by exposing fibrinogen receptors via a common pathway that is blocked by elevating cyclic AMP. (2) Chilling can bypass the seemingly ATP-dependent step for ADP-induced fibrinogen receptor exposure. (3) Receptor exposure by both ADP and chilling is independent of platelet shape. (4) Increased cyclic AMP inhibits the shape change induced by ADP but not that caused by chilling. (5) EDTA and low pH prevent aggregation by interfering with the binding of fibrinogen to exposed receptors. (6) Receptor mobility may be as important as fibrinogen binding in supporting platelet aggregation.

Fibrinogen receptor exposure and aggregation of human blood platelets produced by ADP and chilling

Abstract ADP-induced platelet aggregation is associated with the specific binding of fibrinogen to receptors. Since fibrinogen is also a cofactor for the spontaneous aggregation of chilled human platelets during rewarming, we examined the ability of these platelets to bind purified 126l-labeled fibrinogen. Specific binding similar to ADP-induced binding at room temperature was observed after the platelets had been chilled for 20 min at 0–2°C. Aggregation, however, occurred only when the ambient temperature was increased and was followed within 15–30 sec by loss of most of the bound fibrinogen and disaggregation. ADP- and cold-induced fibrinogen binding and aggregation were inhibited by 0.3 µM PGE“ 1 mM dibutyryl cyclic AMP, and 2.5 mM EDTA, unaffected by 208 µM colchicine, and absent from thrombasthenic platelets. Platelets change shape from discs to spiny spheres when they are exposed to ADP or cold. PGE1 and dibutyryl cyclic AMP prevented the shape change induced by ADP but not by chilling. Shape change, fibrinogen binding, and aggregation induced by ADP. but not by chilling, were inhibited by incubating platelets with 7.3 µM antimycin A and 4.9 mM 2-deoxy-D-glucose. Fixed platelets bound fibrinogen only if they were exposed to ADP before fixation but they failed to aggregate. Studies with fixed platelets showed that EDTA and a low pH prevent the interaction of fibrinogen with exposed receptors, whereas platelets stimulated with ADP in the absence of divalent cations or at low pH prior to fixation bound fibrinogen at physiologic pH, and this binding was inhibited by EDTA. The present studies provide the following clues about the requirements for fibrinogen receptor exposure and platelet aggregation. (1) ADP and chilling activate platelets by exposing fibrinogen receptors via a common pathway that is blocked by elevating cyclic AMP. (2) Chilling can bypass the seemingly ATP-dependent step for ADP-induced fibrinogen receptor exposure. (3) Receptor exposure by both ADP and chilling is independent of platelet shape. (4) Increased cyclic AMP inhibits the shape change induced by ADP but not that caused by chilling. (5) EDTA and low pH prevent aggregation by interfering with the binding of fibrinogen to exposed receptors. (6) Receptor mobility may be as important as fibrinogen binding in supporting platelet aggregation.

Membrane structure of nonactivated and activated human blood platelets as revealed by freeze-fracture: evidence for particle redistribution during platelet contraction.

The distribution of intramembrane particles of nonactivated and activated human blood platelets was studied by freeze-fracture under various experimental conditions to see whether morphological evidence for a structural coupling between the platelet actomyosin system and the fibrin network in a retracting clot could be established. Membrane particles were evenly distributed in nonactivated platelets; the total number (E + P faces) was approximately 1,500/micrometers 2 of membrane, and there were two to three times more particles present on the E face than on the P face. Transformation of discoid platelets to "spiny spheres" by cooling did not change the particle distribution. Platelet activation and aggregation by serum or ADP caused no change in membrane particle density or distribution. Particle distribution was not changed in Ca2+-activated platelets fixed immediately before fibrin formation, but after fibrin formation and during clot retraction, particles were sometimes most frequent on the P face and tended to form distinct clusters, and aggregates of E face pits were observed. Blood platelets contain contractile proteins that are distinct as filaments in platelets in retracting clots. We suggest that the redistribution of particles seen in activated platelets during clot retraction reflects the esablishment of mechanical transmembrane links between the platelet actomyosin system and the fibrin net. The P-face particle clusters may represent sites of force transmission between actin filaments bonded to the inside of the membrane and the fibrin network at the outside. Thus, whereas membrane particles may not be directly involved in the attachment of actin filaments to membranes, the transmission of the force of the contractile system to an exterior substrate apparently involves the intramembrane particles.

Movement of sodium into human platelets

Addition of ADP induces platelets in plasma to undergo shape change from a disc to a spiny sphere and to develop adhesiveness, i.e. to aggregate. The aggregation of human platelets by ADP is associated with a net uptake of Na +. The present experiments demonstrate that the induction of shape change by ADP in acidified or EGTA-treated plasma conditions which inhibit aggregation, is also associated with a movement of Na + into platelets. When ADP-induced platelet shape change and aggregation is inhibited by prostaglandin E 1 Na + uptake is also blocked. Platelets aggregated by epinephrine do not take up Na +. In a manner analogous to the effect of ADP, polylysine also induces Na + uptake during aggregation. Vasopressin, in a manner analogous to epinephrine, induces aggregation without Na + uptake. The increase in platelet Na + resulting from ouabain inhibition of Na + efflux induces an increase in the aggregation response to ADP and to epinephrine.

Relationship of ADP-Induced Fibrinogen Binding to Platelet Shape Change and Aggregation Elucidated by Use of Colchicine and Cytochalasin B

ADP causes human, aspirin-treated, gel-filtered platelets to change from their native discoid shape to spiny spheres with pseudopods, bind 125I-labeled fibrinogen, and aggregate if shaken with sufficient fibrinogen. After destruction of the added ADP with the enzyme apyrase, the platelets revert to a disc shape and lose much of their bound fibrinogen. Colchicine (208 muM or 83 microgram/ml) added to ADP-treated platelets before apyrase prevented restoration of the discoid shape but not the loss of bound fibrinogen. It did not inhibit ADP-induced shape change, aggregation, or fibrinogen binding. Cytochalasin B (0.02--0.2 muM or 0.01--0.10 microgram/ml) prevented ADP-induced shape change but not ADP-induced fibrinogen binding or aggregation. Thus, these findings support earlier studies with thrombasthenic and EDTA-treated platelets and with normal platelets at low pH, or in the presence of EDTA to indicate that fibrinogen binding is associated with aggregability but not with platelet shape.

Shape change and the percentage of sialic acid removed by neuraminidase from human platelets.

SummaryThe sialic acid of human gelfiltered platelets was studied before and after ADP-induced shape change. Neuraminidase cleaved 47% of the total sialic acid from both discoid control platelets and platelets that had become spiny spheres after treatment with 5 μM ADP.We are grateful to the following colleagues for materials used in these experiments: Thomas H. Finlay, Ph.D., for the radiolabeled TAMe, Joel U. Harris, Ph.D., for the radiolabeled fibrinogen, Henriette Lackner, M. D., for the connective tissue suspension, and John Fenton, II, Ph.D. for the purified human thrombin.

A study of the relationship between the platelet shape and it's function

It is widely accepted that the platelet which is originally discoid is deformed into spiny spheres by ADP, thrombin or collagen (viscous metamorphosis) and forms thrombus by its function-adhesiveness and aggregation. But we have hardly achieved the quantative analysis of the morphological changes and disclosed the relationship between the deformed platelets and their functions.In order to clarify this relationship, we examined the influences of the following procedures on human platelets.1) preservation (non-anticoagulated whole blood, citrated whole blood), 2) stirring (the same blood samples), 3) preservation after stirring (citrated whole blood) and 4) surgical operation with laparotomy on 10 patients with various diseases.After fixing the platelets by 1% glutaraldehyde, the platelets were classified into disc, hemisphere, sphere and the other form, and checked for pseudopod formation under a light microscope. As a platelet function, platelet retention rate was measured by a modified Hellem-II method.Platelet shape was easily changed and pseudopods issued by preservation and stirring. These morphological changes were brought about more strikingly by stirring than by preservation. The retension rate decreased when spherification and pseudopod formation had prominently advanced. However, it increased when the incidences of non-discoids and the pseudopods increased to some degree, e. g. when citrated blood was preserved up to 60min. at room temperature and when it was stirred for 1min. These phenomena were similarly observed in vivo condition (during operation).These results suggested that some relationship existed between the platelet shape and its function and that halfly deformed platelets were in an activated phase and prominently deformed platelets were rather in a refractory phase. This relationship was probably derived fromnot only extra-platelet factors such as activation of plasma coagulation factors (contact factor and prothrombin) but also from internal factors (or character) of platelets. The latter factors were considered to be more important because both shape change and the increase of retention rate were demonstrated in some experiments to occur before the silicon PTT became shortened.

ELECTRON MICROSCOPE STUDIES ON THE MORPHOLOGICAL CHANGES IN RABBIT PLATELETS INDUCED BY ADENOSINE DIPHOSPHATE (ADP), METABOLIC INHIBITORS OR INHIBITORS OR PLATELET AGGREGATION

The shape changes in rabbit platelets induced by ADP, NEM, KCN, PGE, , aspirin or distilled water were investigated using Born's method and electron microscopy. The following results were obtained : 1) The optical density of EDTA-PRP was increased rapidly after the addition of ADP, NEM or distilled water. ADP-induced increase in optical density has been thought to be resulted from the shape change of platelets. It could be confirmed by electron microscopy that the change in optical density was due to the morphological change in platelets.2) When ADP was added to PRP, platelets changed their shape from “disc” to “spiny sphere” with a marked pseudopodia formation. Both microtubules and granules were concentrated in the center of platelet. This type of morphological change was followed by the platelet aggregation.3) The platelets treated with NEM became also spherical and posessed several number of pseudopodia. As compared to ADP-induced changes, however, the pseudopodia were much shorter, microtubules were destroyed and granules were not concentrated. This kind of morphological change was not followed by the platelet aggregation. The same kind of change was introduced by the addition of distilled water.4) The optical density of PRP was also increased by addition of KCN and PGE1, but no significant change in platelet morphology was found by electron microscopy.5) Aspirin also induced no changes in the shape of platelets.6) From these results, the relationship between platelet shape change and aggregation of platelets was discussed, and it was suggested that the contractile proteins in the platelets might play an important role in such a shape change as well as the aggregation of platelets.

Effects of Anti-Adhesive Agents on the Ultrastructure of Rabbit Blood Platelets in Vitro

SummaryThe in vitro effects of two anti-adhesive agents, designated as substances “86” and BLR-743, on the ultrastructure of rabbit blood platelets were examined. When compared with control platelet preparations, it was found that these agents, over a 10 min period, induced platelets to become spiny spheres. Vacuoles of the surface connected system inside platelets tended to enspherulate, also. No change in structure or location of form-maintaining structures such as microtubules were observed in treated platelets. Neither were changes observed in the structure or location of mitochondria. While the distribution within platelets of α-granules and vacuoles containing 5-hydroxytryptamine granules seemed to be little affected by treatement of platelets with these agents, 5-hydroxytryptamine granules were reduced in number and α-granules expressed variable degrees of electron density suggesting variable degrees of extraction of materials from these granules. It is concluded on the basis of the morphologic changes in platelets observed that the anti-adhesive agents have a primary action on the plasma membrane and other membrane bound structures of blood platelets.