Myocardial Microcirculation in the Beating Heart — In Vivo Microscopic Studies

Author(s):  
H. Tillmanns ◽  
H. Leinberger ◽  
F. J. Neumann ◽  
M. Steinhausen ◽  
N. Parekh ◽  
...  
Author(s):  
Narendar Dudhipala ◽  
Arjun Narala ◽  
Dinesh Suram ◽  
Karthik Yadav Janga

The objective of this present study is to develop a semisolid dispersion (SSD) of zaleplon with the aid of self-emulsifying lipid based amphiphilic carriers (TPGS E or Gelucire 44/14) addressing the poor solubility of this drug. A linear relationship between the solubility of drug with respect to increase in the concentration of lipid surfactant in aqueous medium resulting in AL type phase diagram was observed from phase solubility studies. Fusion method was employed to obtain semisolid dispersions (SSD) of zaleplon which showed high content uniformity of drug. The absence of chemical interactions between the pure drug, excipients and formulations were conferred by Fourier transmission infrared spectroscopic examinations. The photographic images from polarized optical microscopic studies revealed the change in crystalline form of drug to amorphous or molecular state. The superior dissolution parameters of zaleplon from SSD over pure crystalline drug interpreted from in vitro dissolution studies envisage the ability of these lipid surfactants as solubility enhancers. Further, the caliber of TPGS E or Gelucire 44/14 in encouraging the GI absorption of drug was evident with the higher human effective permeability coefficient and fraction oral dose of drug absorbed from SSD in situ intestinal permeation study. In conclusion, in vivo studies in Wister rats demonstrated an improvement in the oral bioavailability of zaleplon from SSD over control pure drug suspension suggesting the competence of Gelucire 44/14 and TPGS E as conscientious carriers to augment the dissolution rate limited bioavailability of this active


Cornea ◽  
1993 ◽  
Vol 12 (5) ◽  
pp. 369-378 ◽  
Author(s):  
Hideji Ichijima ◽  
W Matthew Petroll ◽  
James V. Jester ◽  
Patricia A. Barry ◽  
Peter M. Andrews ◽  
...  

Development ◽  
1978 ◽  
Vol 46 (1) ◽  
pp. 119-133
Author(s):  
Janet Heasman ◽  
C. C. Wylie

Primordial germ cells (PGCs) of Xenopus laevis have been isolated from early embryos and kept alive in vitro, in order to study the structural basis of their motility, using the transmission and scanning electron microscope. The culture conditions used mimicked as closely as possible the in vivo environment of migrating PGCs, in that isolated PGCs were seeded onto monolayers of amphibian mesentery cells. In these conditions we have demonstrated that: (a) No significant differences were found between the morphology of PGCs in vitro and in vivo. (b) Structural features involved in PGC movement in vitro include (i) the presence of a filamentous substructure, (ii) filopodial and blunt cell processes, (iii) cell surface specializations. These features are also characteristic of migratory PGCs studied in vivo. (c) PGCs in vitro have powers of invasion similar to those of migrating PGCs in vivo. They occasionally become completely surrounded by cells of the monolayer and, in this situation, bear striking resemblance to PGCs moving between mesentery cells to the site of the developing gonad in stage-44 tadpoles. We conclude that as far as it is possible to assess, the behaviour of isolated PGCs in these in vitro conditions mimics their activities in vivo. This allows us to study the ultrastructural basis of their migration.


1992 ◽  
Vol 263 (5) ◽  
pp. H1537-H1545
Author(s):  
C. Delcayre ◽  
D. Klug ◽  
V. T. Nguyen ◽  
C. Mouas ◽  
B. Swynghedauw

Pressure overload in vivo induces an increase in cardiac protooncogene and stress protein expression that may initiate the long-term genetic changes observed in hypertrophy. To known whether mechanical stimulus is linked to specific gene transcription, expression of immediate early genes and synthesis of total proteins and myosin heavy chains (MHCs) were studied in beating and KCl-arrested isolated rat hearts perfused for 2 h under various coronary pressures. The main result of this study is that in the beating heart an augmentation of aortic pressure from 60 to 120 mmHg results in a pronounced enhancement of the synthesis of MHC (+59%) and of the expression of the beta-MHC isomyosin mRNA (iso-mRNA; +104%). Also, total protein synthesis and the amounts of poly-(A)+, c-fos, c-myc, and heat-shock protein HSP68 mRNAs were increased. To arrest the heart at 60 mmHg has no effect on total protein synthesis and on the amounts of poly(A)+, alpha-MHC and beta-MHC iso-mRNAs, and mRNAs coding for oncoproteins, but the synthesis of MHC decreased by 24%. By contrast with what we have observed in the beating heart, the augmentation of the coronary pressure in the arrested heart stimulates total protein synthesis and increases the amount of poly(A)+, c-fos, c-myc, and HSP68 mRNAs but has no effect on the expression of both MHC iso-mRNAs. In conclusion, the activation of myosin synthesis by high coronary pressure in this model has mainly a pretranslational origin when the heart is beating.(ABSTRACT TRUNCATED AT 250 WORDS)


2007 ◽  
Vol 16 ◽  
pp. S24-S25
Author(s):  
John F. Fraser ◽  
G. Scalia ◽  
J. Keys ◽  
B. Garlick ◽  
C. McDonald ◽  
...  
Keyword(s):  

Blood ◽  
1974 ◽  
Vol 43 (6) ◽  
pp. 831-836 ◽  
Author(s):  
Carl R. Kjeldsberg ◽  
John Swanson

Abstract Platelet adherence to polymorphonuclear leukocytes, or so-called platelet satellitism, has, to our knowledge, been reported in only four patients. We had the opportunity to study this phenomenon in two patients. Platelet satellitism was only seen in EDTA anticoagulated blood, and the platelets were seen to surround polymorphonuclear leukocytes only. Electron microscopic studies demonstrated focally opposed regions of platelet and neutrophil plasma membranes. Phagocytosis of platelets was also observed. In vivo and in vitro platelet functions were normal. Platelet satellitism is an in vitro phenomenon, the cause of which is unknown. We are unable to relate it to functional abnormalitles of the blood, the clinical condition of the patient, or to drugs. This phenomenon has some clinical importance in that it causes spurious thrombocytopenia.


2011 ◽  
Vol 4 (7) ◽  
pp. 1167-1176 ◽  
Author(s):  
Alkiviadis Tsamis ◽  
Wolfgang Bothe ◽  
John-Peder Escobar Kvitting ◽  
Julia C. Swanson ◽  
D. Craig Miller ◽  
...  

1969 ◽  
Vol 112 (3) ◽  
pp. 269-274 ◽  
Author(s):  
C. N. Murty ◽  
T. Hallinan

1. Phospholipid-rich membranous contaminants are present in free polysomes from rat liver isolated on discontinuous sucrose gradients. 2. Electron-microscopic studies indicate that the membranous contaminants are mainly agranular with very occasional granular membranes. This is confirmed by the study of their sedimentation behaviour and their initial rate of labelling with radioactive glucosamine in vivo. 3. Conventional ribosome-purification methods fail to remove the contaminants, whereas deoxycholate effectively solubilizes the membranous contaminants with little breakdown of polysomes. 4. Amino acid-incorporation studies show that these membranous contaminants may seriously interfere in assessment of the functional capacity of free polysomes in protein biosynthesis in vivo.


1967 ◽  
Vol 33 (2) ◽  
pp. 255-263 ◽  
Author(s):  
Philip W. Brandt ◽  
Enrique Lopez ◽  
John P. Reuben ◽  
Harry Grundfest

In cross-sections of single fibers from the frog semitendinosus muscle the number of thick myofilaments per unit area (packing density) is a direct function of the sarcomere length. Our data, derived from electron microscopic studies, fit well with other data derived from in vivo, low-angle X-ray diffraction studies of whole semitendinosus muscles. The data are consistent with the assumption that the sarcomere of a fibril maintains a constant volume during changes in sarcomere length. The myofilament lattice, therefore, expands as the sarcomere shortens. Since the distance between adjacent myofilaments is an inverse square root function of sarcomere length, the interaction of the thick and the thin myofilaments during sarcomere shortening may occur over distances which increase 70 A or more. The "expanding-sarcomere, sliding-filament" model of sarcomere shortening is discussed in terms of the current concepts of muscle architecture and contraction.


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