Use of rheolytic thrombectomy in the treatment of feline distal aortic thromboembolism

The purpose of this prospective clinical trial was to evaluate the safety and efficacy of a commercially available rheolytic thrombectomy system in the treatment of naturally occurring feline aortic thromboembolic disease. All 6 cats enrolled in the investigation were affected at the level of the distal aorta and had signs of the disease affecting both pelvic limbs. Cats were anesthetized and an arteriotomy was performed on 1 carotid artery to gain access to the arterial system. Selective arterial angiography was used to confirm the presence of thromboembolic disease. The thrombectomy system was advanced to the level of the thrombus using fluoroscopic guidance. Repeat angiography was used intermittently to assess progress of thromboembolus dissolution throughout the procedure. The use of the rheolytic thrombectomy system resulted in successful thrombus dissolution in 5 of 6 cats. Three of 6 cats survived to discharge. Both of these results compare favorably with conventional therapies used in the treatment of this disease. Feline distal aortic thromboembolism is a frustrating disease that warrants a guarded to poor prognosis. Rheolytic thrombectomy may provide veterinarians with an alternative therapy in the treatment of thromboembolic diseases, including feline distal aortic thromboembolism.     

Dexamethason enhanced aorta-derived CD105+ mesenchymal stem cells to differentiate into adipocytes

AIM: To investigate whether aorta-derived CD₁₀₅⁺ cells show characteristics of mesenchymal stem cells, and if dexamethason enhances this kind of CD₁₀₅⁺ cells to differentiate into adipocytes. METHODS: The distribution of CD105 in aorta was assessed by imunohistochemistry. The aorta wall cells were isolated and immunophenotypes were identified by FACS. CD₁₀₅⁺ cells were sorted using MACS CD105 micromagnetic beads. The differentiation of CD₁₀₅⁺ cells into adipocytes and osteoblasts was induced under different conditions and indicated by staining of Oil red O, detecting of alkaline phosphatase activity, calcium accumulation stained with silver nitrate and transmission electron microscope analysis, respectively. RESULTS: The endothelial cells, a part of medial smooth muscle cells and adventital fibrblasts were CD105 positive. The isolated aortic arch cells were positive for CD105, CD106, CD44, CD29, and negative for CD45, CD11a, CD11b and HLADR. The CD₁₀₅⁺ cells differentiated into adipocytes contained Oil-Red-O-positive lipid droplets, the osteocytes with calcium deposition and alkaline phosphatase activity. Ultrastructurally, it was observed that some needle-shaped crystal calcium deposition similar to bone spicules was inside the cytoplasm of induced osteocytes. When the dexamethason was absent in the adipogenic medium, there were no adipocytes with lipid droplets. CONCLUSION: The results demonstrated that CD₁₀₅⁺ cells showed characters of MSCs reside in aortic wall, and was able to differentiate into adipocytes and osteocytes in vitro. Dexamethason enhanced aorta-derived CD₁₀₅⁺ with characters of MSCs to differentiate into adipocytes. These suggested that MSCs might be related with atherosclerosis.     

The disturbance of calcium metabolism of vascular smooth muscle in the late phase of septic shock and the underlying mechanism

AIM: To evaluate the alterations in calcium metabolism of the vascular smooth muscle in the late phase of septic shock and test the hypothesis that nitric oxide might be involved in sepsis-induced vascular hyporeactivity. METHODS: Male Sprague-Dawley rats were subjected to sepsis by cecal ligation and puncture (CLP). 18 hours post CLP, rat aortic rings were employed for measurement of contractile responses by using organ bath technique. RESULTS: In endothelium-denuded aortic rings from CLP rats, concentration-contraction curves to phenylephrine (PE) and KCl were significantly decreased when compared to that from sham control rats. The transient contraction induced by PE in calcium-free Krebs solution and the concentration-dependent contraction to CaCl₂ in KCl-depolarized medium were also markedly reduced. The hyporeactivity was partially reversed by treatment with aminoguanidine, a selective inducible nitric oxide synthase inhibitor. CONCLUSION: An impairment in calcium handling in vascular smooth muscle is involved in the vascular hyporeactivity during the late phase of septic shock, in which an excessive nitric oxide production might be the major mechanism.     

Change of Gαq/11-mediated signal transduction pathway in aorta of spontaneously hypertensive rats

AIM: To investigate the changes of Gαq/11and phospholipase C(PLC) of the aorta and to evaluate the role of signal transduction pathway mediated by Gαq/11in the pathogenesis of spontaneous hypertension. METHODS: Blood pressure was measured by intubation of carotid, and the level of plasma angiotension Ⅱ was measured by radioimmunoassay. In addition, Gαq/11and PLC contents in aorta were determined by Western blot analysis. RESULTS: Arterial blood pressure was not changed in 4-week-old spontaneously hypertensive rats(SHR), but it was increased markedly in12-week-old SHR. The Gαq/11expression of aorta in 4-week-old SHR was increased by 69.2%(P<0.05) The levels of PLCβ/₃ of aorta in 4-and12-week-old SHR were increased by 66.9% and 85.1%(P<0.05), respectively, compared with their age-matched WKY rats.CONCLUSION: The up-regulation of Gαq/11-mediated signal transduction pathway of aorta may contribute to the initiation and maintenance of spontaneous hypertension.     

Alteration of aortic function from streptozotocin-diabetic rats with Kilham's virus is associated with inducible nitric oxide synthase

Kilham's rat virus (KRV) is a parvovirus commonly known to affect laboratory rats. Qualitative immunohistochemical analysis revealed that aorta isolated from KRV-infected streptozotocin (STZ)-induced diabetic adult rats expressed markedly greater levels of inducible nitric oxide synthase (iNOS) than aorta from KRV-infected controls. In contrast with the prevailing literature, nitric oxide-mediated endothelium-dependent relaxation to acetylcholine was not blunted by STZ-diabetes, but was comparable to relaxations of aorta from controls. However, with increasing ex vivo duration, a decreased response to acetylcholine was observed in the STZ-diabetic aorta. In addition, whereas contraction responses to phenylephrine were not significantly altered over time in control tissue, aorta from STZ-diabetic rats developed increased tensions. The data suggest that increased iNOS-derived nitric oxide masks expected acetylcholine-mediated relaxation deficits as a result of KRV-infection, and that the deficit is unmasked by iNOS turnover ex vivo.     

Insulin influences the vasoconstriction caused by endothelin-1 in the hyperglycemic rat

AIM: To investigate the effects of insulin on aortic constriction caused by endothelin-1(ET-1) in normal and hyperglycemic rats. METHODS: Hyperglycemic rat models were prepared. Two aortic rings were immersed in the Krebs-Hensleit fluid with and without insulin (40 mIU/L) and the responses of rings to 10^-9 mol/L ET-1 were observed. RESULTS:ET-1 induced more obvious aortic ring constriction in normal rats than those in hyperglycemic rats ( P< 0.01). Rings constriction caused by ET-1 were attenuated in normal rats if the rings were immersed in the KH fluid with insulin ( P< 0.01), but no obvious changes were found in hyperglycemic rats.CONCLUSION: (1) the vasoconstriction of aortic rings caused by ET-1 can be reduced by hyperglycemia. (2) Insulin can attenuate the aortic response to ET-1. (3) Insulin can not attenuate the vasoconstriction caused by ET-1 in hyperglycemic rats. These results suggest that insulin may affect vasoconstriction caused by ET-1, which may be involved in the pathogenesis of vascular complication in diabetic or insulin resistance condition.     

Ante-mortem diagnosis of persistent truncus arteriosus in an 8-year-old asymptomatic dog

Persistent truncus arteriosus (PTA) was diagnosed in an 8-year-old neutered male Poodle referred for echocardiographic examination prior to anesthesia for surgical correction of bilateral cataract. A single large artery limited by a bicuspid valve and overriding both ventricles was observed with 2 distinct pulmonary arteries arising from the common arterial trunk. A large size interventricular septal defect was associated with a low velocity bidirectional shunt. The lesion was identified as a Type 3 PTA according to Collett and Edwards' classification. Although no clinical signs were reported, the dog presented polycythemia (packed cell volume = 68%) at the time of diagnosis. To our knowledge, this is the first report of an echocardiographic diagnosis of PTA in the dog. Until now, the ante-mortem diagnosis of this congenital heart disease has only been described in the cat. This case is also of interest because of the age of the animal and the total absence of cardio-respiratory signs at the time of diagnosis.     

Effects of cholecystokinin octapeptide on changes in rabbit thoracic aortic reactivities induced by lipopolysaccharides in vitro

AIM and METHODS: To elucidate the mechanism of anti-endotoxic shock of cholecystokinin octapeptide(CCK-8), the effects of CCK-8 on changes in rabbit thoracic aortic reactivities induced by lipopolysaccharides(LPS) in vitro were studied, and the ultrastructure of the endothelial cells was observed under scanning electron microscope. RESULTS: Incubation of thoracic aortic rings(TARs) with LPS(100 mg/L) resulted in an time-dependent impairment of the endothelium-dependent relaxations to acetylcholine(incubation for 3, 7, 14 h), a reduction of contractive response to phenylphrine(incubation for 14 h) and ultrastructural injury in endothelial cells(incubation for 7 h), all of which were alleviated by concomitant incubation with CCK-8(1 mg/L). In contrast, neither the vascular contractions nor the relaxations were affected by CCK-8 (1 mg/L) alone. CONCLUSION: CCK-8 improved the vascular reactivities in the presence of LPS, which may be one of the anti-endotoxic shock mechanisms of CCK.