Abstract Background: This study aimed to explore the possible role and mechanism of venous hypertension (VH) in the occurrence and development of arteriovenous malformations (AVMs) and to study the therapeutic effect of VH regulation on AVMs to provide insight into AVM pathogenesis and explore new treatments. Methods: Maxillofacial VH models were established by cervical vascular anastomosis. Osteogenesis and angiogenesis in the model rats were analysed by imaging and histology, and the inhibitory effects of intraperitoneal (ip) sirolimus injection on angiogenesis were detected. The effect of sirolimus on the biological behaviour of human umbilical vein endothelial cells (HUVECs) cultured in vitro and mechanism of sirolimus were detected by cytology. Result: The local microvessel density increased, the vessels showed tortuous dilation, and mRNA and protein levels of angiogenesis-related genes were increased in venous hypertension environment. These phenomena were alleviated or eliminated by ip injection of a sirolimus solution. Sirolimus inhibited proliferation, tubule formation, migration, invasion, angiogenesis-related gene transcription and translation, and phosphorylation of mammalian target of rapamycin (mTOR) and its downstream substrate proteins S6K1 and 4EBP1. Conclusions: Abnormal angiogenesis caused by VH is related to abnormal activation of the mTOR pathway, which is important in regulating local angiogenesis; sirolimus inhibited hypertension-induced excessive angiogenesis in vivo and in vitro through the mTOR signalling pathway. This study provides a basis for further mechanistic study of AVM formation and insight into sirolimus as a possible target drug for AVM management.
Objective Attempting to find a reliable method for assessing the patient's ability to tolerate carotid artery occlusion. Methods The temporary balloon occlusion (TBO) test of carotid artery was performed for 20 patients who might have carotid artery manipulated or permanently occluded. Transfemoral artery Seldinger's catheterization was used to introduced the temporary balloon occlusion catheters into the vessels of the concern. Neurologic testing was performed continuously by the attending neurologist. Transcranial Doppler ultrasonography (TCD) and carotid artery stump pressure (SP) were measured contiuously during the TBO. The collateral circulation of Willis circle was observed with DSA. Results Out of the 20 cases, one failed during the TBO because of CCA dissection caused by catheterization, another one failed because of a neurologic defect occurring before the balloon was inflated, the others went through the test uneventfully. Two cases finished the test before the approved schedule because neurologic defects appeared 34 min and 27 min after the vascular occlusion, respectively. These two patients were proved unable to tolerate carotid artery sacrifice. The other 16 cases passed the 45 minutes TBO. Their mean velocity of ipsilateral middle cerebral artery fell 36%±18%. Their SP is (53.76±21.49) mmHg(30-87). Adequate collateral circulation in Willis circle was observed by DSA in all cases except the two who failed with the TBO. Conclusions TBO is a safe and reliable method for assessing the patient's ability to tolerate carotid artery occlusion. We suggest it should be a routine examination prior to carotid manipulations.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
'/%3e%3cuse xlink:href='%23a' transform='rotate(144 450 300)'/%3e%3cuse xlink:href='%23a' transform='rotate(216 450 300)'/%3e%3cuse xlink:href='%23a' transform='rotate(288 450 300)'/%3e%3c/svg%3e)