Ultrastructural Changes of the Tissue Thromboplastin after Intravenous Injection in Rabbits

1978 ◽  
Vol 39 (01) ◽  
pp. 201-209 ◽  
Author(s):  
Hiroshi Hasegawa ◽  
Hiroshi Nagata ◽  
Makoto Murao
Keyword(s):  
Intravenous Injection ◽  
Vascular Endothelium ◽  
Model Experiment ◽  
Venous Return ◽  
Ultrastructural Changes ◽  
Membrane Structures ◽  
Tissue Thromboplastin ◽  
Short Time ◽  
Sheet Membrane

SummaryAttempts were made to demonstrate ultrastructural changes of the tissue thromboplastin after intravenous injection, as a model experiment on the pulmonary microthrombi formation induced by the tissue thromboplastin circulating from venous return.Concentrically arranged membrane structures of the injected thromboplastin disappeared in extremely short time after the injection of the thromboplastin in rabbits. The long sheet membrane of the injected thromboplastin was frequently seen as adhered to the vascular endothelium or to the surface of blood corpuscles. Furthermore, fibrin fibres were formed in contact with the long sheet membrane of the thromboplastin. Membrane structures were not found anywhere in the control rabbits.

Single-Patch Fold-Back Technique for Augmentation of the Superior Vena Cava in Sinus Venosus Atrial Septal Defect Associated with Partial Anomalous Pulmonary Venous Return

2015 ◽  
Vol 17 (6) ◽  
pp. 282
Author(s):  
Suguru Ohira ◽  
Kiyoshi Doi ◽  
Takeshi Nakamura ◽  
Hitoshi Yaku
Keyword(s):  
Atrial Septal Defect ◽  
Superior Vena Cava ◽  
Septal Defect ◽  
Venous Return ◽  
Superior Vena ◽  
Pulmonary Veins ◽  
Vena Cava ◽  
Sinus Venosus ◽  
Right Atrial ◽  
Anomalous Pulmonary Venous Return

Sinus venosus atrial septal defect (ASD) is usually associated with partial anomalous pulmonary venous return (PAPVR) of the right pulmonary veins to the superior vena cava (SVC), or to the SVC-right atrial junction. Standard procedure for repair of this defect is a patch roofing of the sinus venosus ASD and rerouting of pulmonary veins. However, the presence of SVC stenosis is a complication of this technique, and SVC augmentation is necessary in some cases. We present a simple technique for concomitant closure of sinus venosus ASD associated with PAPVR and augmentation of the SVC with a single autologous pericardial patch.

Transport: blood and circulation

2017 ◽  
Author(s):  
Derek Burton ◽  
Margaret Burton
Keyword(s):  
Carbon Dioxide ◽  
Blood Cells ◽  
Venous Return ◽  
White Blood Cells ◽  
Nutrient Transport ◽  
Blood System ◽  
Fluid Component ◽  
Nucleated Red Blood Cells ◽  
Ventral Aorta ◽  
Osmotic Effects

The blood system transports nutrients, oxygen, carbon dioxide and nitrogenous wastes; other functions include defence. Fish have a closed, single circulation in which blood is pumped by a contractile heart via a ventral aorta to the gills, then via the dorsal aorta to vessels supplying the tissues and organs, with a venous return to the heart. Large venous sinuses occur in elasmobranchs. Air-breathing fish have modifications of the circulation. Complex networks of narrow blood vessels can occur as red patches, retia, maximizing transfer of nutrients, oxygen or heat. Most fish have nucleated red blood cells (erythrocytes) with haemoglobin. The types of white blood cells (leucocytes) are similar to those of other vertebrates but there are thrombocytes rather than platelets. Nutrient transport is in the plasma, the fluid component of the blood, which may also carry antifreeze agents and molecules (e.g. urea in elasmobranchs) which counteract deleterious osmotic effects

scholarly journals Repair of total anomalous pulmonary venous return (TAPVR) with pulmonary artery (PA) Stenosis in adult

2015 ◽  
Vol 10 (S1) ◽  
Author(s):  
Fuad Z Abdullayev ◽  
Imadaddin M Bagirov ◽  
Nigar J Kazimzade ◽  
Larisa S Shikhiyeva
Keyword(s):  
Pulmonary Artery ◽  
Venous Return ◽  
Anomalous Pulmonary Venous Return

Computer simulation of experiments in responses to intravenous and inhaled CO2

1981 ◽  
Vol 50 (4) ◽  
pp. 835-843 ◽  
Author(s):  
W. S. Yamamoto
Keyword(s):  
Venous Return ◽  
Neural Signal ◽  
Set Point ◽  
Ventilatory Responses ◽  
Operating Level ◽  
Excitatory State ◽  
Co2 Level ◽  
Neural Excitation ◽  
Low Levels ◽  
Hypercapnic Response

A simulation of ventilatory responses to infused and inhaled CO2 at controlled cardiac output and high and low levels of neural excitation mimics comparable experiments in animals. The model suggests that at low levels of endogenous and exogenous CO2 load the alert quiescent animal will show hyperpnea to both test states associated with hypercapnia. The nonalert quiescent animal simulated will show an isocapnic response to endogenous load and hypercapnic response to exogenous load. The explanation of this behavior lies in the model formulation, which allows the neural signal from metabolically active sources to drive the proportional component of the controller below an operating level established by its set point. By this reasoning the excited but metabolically inactive animal should be paradoxically less sensitive to small changes in CO2, whether exogenous or endogenous, than the quiescent animal. The model demonstrates further that a neural "exercise" signal in proportion to venous return better simulates observations in which CO2 load and venous return are dissociated than one in which the neural signal is computed from metabolism. The use of delta V/delta P slopes as estimates of sensitivity go awry in experiment and simulation when blood flow, CO2 level, and neural excitatory state are dissociated. This is particularly true when the organism is operating at and below the hypothesized set point.

scholarly journals Prostanoids and pulmonary venous return

1992 ◽  
Vol 103 (3) ◽  
pp. 596-597
Author(s):  
Thomas Z. Lajos ◽  
Joseph Venditti ◽  
Rocco Venuto
Keyword(s):  
Venous Return
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