Recent reports have indicated that platelet aggregation is enhanced in some diabetics who have proliferative retinopathy and that platelet function is a altered by glucose loading. But the mechanism is not clarified yet. Arachidonic acid, the precursor of prostaglandin endoperoxide, plays a major role on platelet aggregation. Blood samples were collected with sodium citrate at 0, 30, 60, 120 and 300 minutes after 100 g glucose loading. Platelet-rich plasma was obtained by centrifugation and platelet aggregation was studied photometrically adding ADP. Platelet was obtained by further centrifugation and was kept freeze-dried. Platelet samples were extracted and transesterificated and separated by gas liquid chromatography. The quantitative regulation of arachidonic acid in platelets was measured by the composition ratio of arachidonic acid (C20-4)/linoleic acid (C18-2)=AL index. The results of platelet aggregation after glucose loading were as follows; platelet aggregation was not changed remarkably in normal subjects, but was enhanced at 30 and 60 and suppressed at 120 minutes in diabetics.AL index is as fol lows:prior to glucose loading, AL index of diabetics (4.6 ± 1.2) was higher than that of normal subjects (3.5 ± 0.5). After glucose loading, no significant change was observed in normal subjects, but AL index was increased at 30 (4.8 ± 1.4) and 60 (4.9 ± 1.4) and decreased at 120 minutes (4.1 ± 0.9) in diabetics. The results indicates that there is a certain relationship between quantitative regulation of arachidonic acid in platelet and platelet aggregation and that hyperaggregation may be induced by abnormal prostaglandin metabolism in diabetes.
A 3-day-old alpaca cria presented for progressive weakness and dyspnea since birth. Complete bloodwork, thoracic radiographs, and endoscopic examination of the nasal passages and distal trachea revealed no significant findings. Echocardiogram and contrast study revealed a single artery overriding a large ventricular septal defect (VSD). A small atrial septal defect or patent foramen ovale was also noted. Color flow Doppler and an agitated saline contrast study revealed bidirectional but primarily right to left flow through the VSD and bidirectional shunting through the atrial defect. Differential diagnosis based on echocardiographic findings included common arterial trunk, Tetralogy of Fallot, and pulmonary atresia with a VSD. Postmortem examination revealed a large common arterial trunk with a quadricuspid valve overriding a VSD. Additionally, defect in the atrial septum was determined to be a patent foramen ovale. A single pulmonary trunk arose from the common arterial trunk and bifurcated to the left and right pulmonary artery, consistent with a Collet and Edwards' type I common arterial trunk with aortic predominance. Although uncommon, congenital cardiac defects should be considered in animals presenting with clinical signs of hypoxemia, dyspnea, or failure to thrive.
•Large interatrial communications in dogs are rare.•When indicated, surgical closure of an interatrial communication is possible.•When indicated, surgical repair of the atrioventricular valve is possible.•Multimodal imaging aids surgical planning in cardiac surgeries of dogs.
A 13-year-old neutered female Labrador retriever had inspiratory dyspnea secondary to bilateral laryngeal paralysis. Radiographically, there was pectus excavatum with a mediastinal shift to the right. Arytenoid lateralization was performed, relieving the upper respiratory obstruction, and the sternal deformity also resolved. Chronic upper respiratory obstruction should be considered in dogs with pectus excavatum. Furthermore, correction of upper respiratory obstruction has the potential to result in resolution of pectus excavatum.
Aortic thromboembolism (ATE) occurs in cats with cardiomyopathy and often results in euthanasia due to poor prognosis. However, the underlying predisposing mechanisms leading to left atrial (LA) thrombus formation are not fully characterised. von Willebrand Factor (vWF) is a marker of endothelium and shows increased expression following endothelial injury. In people with poor LA function and LA remodelling, vWF has been implicated in the development of LA thrombosis. In this study we have shown (1) the expression of endocardial vWF protein detected using immunohistofluorescence was elevated in cats with cardiomyopathy, LA enlargement (LAE) and clinical signs compared to cats with subclinical cardiomyopathy and control cats; (2) vWF was present at the periphery of microthrombi and macrothrombi within the LA where they come into contact with the LA endocardium and (3) vWF was integral to the structure of the macrothrombi retrieved from the atria. These results provide evidence for damage of the endocardial endothelium in the remodelled LA and support a role for endocardial vWF as a pro-thrombotic substrate potentially contributing to the development of ATE in cats with underlying cardiomyopathy and LAE. Results from this naturally occurring feline model may inform research into human thrombogenesis.