Interruption Of Arterial Blood Flow Research Articles

Pharmacotherapy of STEMI: a review of international guidelines

Introduction: ST-elevation myocardial infarction (STEMI) occurs as a result of plaque rupture, leading to interruption of arterial blood flow and subsequent myocardial necrosis. The incidence of hospital admission relating to STEMI in the UK is around 5 per 1000 people each year. The speed of access to reperfusion therapy in patients with STEMI cases […]

Efficacy of Thrombolytic, Laser, Anti-VEGF and Surgical Treatment in Retinal Artery Occlusion and Related Complications

Retinal artery occlusion (RAO) is characterized by the sudden interruption of arterial blood flow in the retinal circulation and subsequent ischemic retinal injury. Retinal artery occlusion is divided into sub-forms such as central retinal artery occlusion (CRAO) and branch retinal artery occlusion (BRAO). Patients with CRAO present with sudden, painless, and unilateral complete visual loss, while patients with BRAO present with partial or complete visual loss in relation to visual field damage. Thromboembolism is the non-arteritic form and the predominant mechanism in RAO; the form defined as arteritic RAO constitutes approximately 5% and is associated with inflammatory changes. Retinal artery occlusion is an ophthalmologic emergency where the most important factor in its treatment is time and the early interventions are very important. The conventional treatment methods aim to restore perfusion by reducing intraocular pressure or vasodilatation and to reduce ischemic damage. In order to achieve more accurate results in treatment, methods to directly open the obstruction caused by thromboembolism have been tried. These include thrombolytic therapy, laser, and surgical treatment. At the same time, studies on the efficacy of anti-VEGF treatment in emerging complications are ongoing.

Defining Characteristics and Related Factors of Decreased Cardiac Tissue Perfusion: Proposal of a New Nursing Diagnosis.

To identify the possible defining characteristics (DCs) and related factors of the nursing diagnosis (ND) decreased cardiac tissue perfusion. Cross-sectional study using medical charts of adults admitted to an emergency department with the chief complaint of chest pain in a hospital in São Paulo, Brazil. DCs identified: crushing chest pain, elevated markers of myocardial necrosis, ischemic electrocardiogram changes, sweating, nausea, and vomiting. Related factors identified: interruption of arterial blood flow and coronary spasm. This ND was clinically identified due to significant differences in the DCs of patients with and without the diagnosis. The clinical indicators identified in this study can be the starting point for the DCs for this ND.

Effect of Clopidogrel on Nitric Oxide Levels in an Ischemia Reperfusion Model

Ischemia and reperfusion injury is a pathologic process with serious consequences, arising due to interruption of arterial blood flow. Restored blood flow achieved after the ischemic period causes formation of oxygen radicals by activation of a variety of substances and systems. In this study, we investigated the effect of clopidogrel, an antithrombocyte agent, on tissue nitric oxide (NO) levels in an experimental ischemia reperfusion model. For this purpose, 6 hours of ischemia and 4 hours of subsequent reperfusion were applied to the right lower extremities of the subjects. Clopidogrel therapy was started in one of these groups 10 days before the process (study group). NO levels were measured in all groups in the muscle, lung, and liver tissues, and in plasma. Lung, plasma, and liver NO measurement values had statistically significant differences among the groups. There was no statistically significant difference in the measurements made on the muscle tissue. Clopidogrel, which has previously been reported to be suitable to be used as a preventive agent of ischemia reperfusion damage, has had a reducing effect on the NO levels in tissues in the ischemia reperfusion model created in our present study.

The role of ECA transection in the development of masticatory lesions in the MCAO filament model

In the intraluminal suture model of middle cerebral artery occlusion (MCAO) in the rat, lesions of the masticator muscles associated with impaired functional outcome occur. We evaluated the role of external carotid artery (ECA) transection. We assessed whether isolated interruption of an arterial or a venous connection to the ECA territory was sufficient to induce masticatory hypoperfusion and lesions. We also evaluated a direct access to the common carotid artery (CCA) with subsequent vascular closure with regard to its feasibility, frequency of masticatory lesions, complications, and cerebral ischemia. Cerebral and masticatory lesions and perfusion deficits were assessed by in vivo magnetic resonance imaging (MRI). Vessel patency was evaluated using computerized tomography angiography and histology. An interruption of arterial blood flow led to masticatory hypoperfusion. Masticatory lesions occurred in 6% of the rats. Access to and closure of the CCA were feasible in all animals, leading to moderate or severe vessel stenosis in 20%, and intraarterial thrombosis in 25% of the rats. Reproducible cerebral infarctions were obtained in all animals. In 24% of the rats, hyperintense MRI signal changes were observed in the ipsilateral temporal muscle. Thus, the induction of masticatory hypoperfusion and lesions by arterial transection supports the role of the ECA in this context. Direct access to the CCA with subsequent vessel closure led to stenosis in most animals. Preservation of ECA continuity was not suitable to fully prevent masticatory lesions.

Intraoperative complications in aneurysm surgery: a prospective national study.

With increasing use of endovascular procedures, the number of aneurysms treated surgically will decline. In this study the authors review complications related to the surgical treatment of aneurysms and address the issue of maintaining quality standards on a national level. A prospective, nonselected amalgamation of every aneurysm case treated in five of six neurosurgical centers in Sweden during 1 calendar year was undertaken (422 patients; 7.4 persons/100,000 population/year). The treatment protocols at these institutions were very similar. Outcome was assessed using clinical end points. In this series, 84.1% of the patients underwent surgery, and intraoperative complications occurred in 30% of these procedures. Poor outcome from technical complications was seen in 7.9% of the surgically treated patients. Intraoperative aneurysm rupture accounted for 60% and branch sacrifice for 12% of all technical difficulties. Although these complications were significantly related to aneurysm base geometry and the competence of the surgeon, problems still occurred apparently at random and also in the best of hands (17%). The temporary mean occlusion time in the patients who suffered intraoperative aneurysm rupture was twice as long as the temporary arrest of blood flow performed to aid dissection. The results obtained in this series closely reflect the overall management results of this disease and support the conclusion that surgical complications causing a poor outcome can be estimated on a large population-based scale. Intraoperative aneurysm rupture was the most common and most devastating technical complication that occurred. Support was found for a more liberal use of temporary clips early during dissection, regardless of the experience of the surgeon. Temporary regional interruption of arterial blood flow should be a routine method for aneurysm surgery on an everyday basis. A random occurrence of difficult intraoperative problems was clearly shown, and this factor of unpredictability, which is present in any preoperative assessment of risk, strengthens the case for recommending neuroprotection as a routine adjunct to virtually every aneurysm operation, regardless of the surgeon's experience.

Therapeutic efficacy of two‐route chemotherapy using cis‐diamminedichloroplatinum(II) and its antidote, sodium thiosulfate, combined with the angiotensin‐II‐induced hypertension method in a rat uterine tumor

To enhance the therapeutic effect of conventional TRC using intra-arterial (i.a.) DDP plus simultaneous i.v. STS, we combined the AT-II-induced hypertension method with TRC and evaluated its efficacy for a rat uterine tumor, using the simulation of intra-arterial chemotherapy for human uterine tumors. During interruption of arterial blood flow by vascular manipulations, DDP plus AT-II were injected for 10 min through the abdominal aorta in the direction of the uterus. Then STS was administered i.v. for a further 5 min and all the arterial restrictions were released. This modified TRC using AT-II showed a much higher anti-tumor effect than that seen in conventional TRC without AT-II and was free from DDP-induced renal damage. On the other hand, severe nephrotoxicity was unavoidable in the rats given the delayed i.v. administration of STS to i.a. DDP alone. The feasibility of post-administration of STS without obvious nephrotoxicity in modified TRC was explained by transient inhibition of DDP delivery to the kidney during the AT-II-induced hypertension. The loss of body weight and the decrease in the number of leukocytes after this therapy were tolerable. Modified TRC showed a higher anti-tumor effect and a lower nephrotoxicity compared with other treatments, as follows: DDP i.a. with or without AT-II; i.v. infusion of DDP alone. Such a superior anti-tumor effect of modified TRC consists of the following 2 factors: (i) the post-administration of STS leading to the delayed neutralization of DDP at the tumor site; (ii) the selective enhancement of DDP delivery to the tumor tissue during AT-II-induced hypertension.

Chemoembolisation hepatozellulärer Karzinome - computertomographische Verlaufsbeobachtung

The prognosis of unresectable hepatocellular carcinomas is bad. Untreated, survival is 1.6 to 2.5 months. Systemic chemotherapy has little effect and is associated with marked side effects. Tumour cells are supplied almost exclusively by the hepatic artery, whereas normal liver tissue is supplied by the hepatic artery and portal vein. Consequently, interruption of arterial blood flow results in damage to the carcinoma without affecting the rest of the liver. Lipiodol is an oily contrast medium which is taken up selectively by the tumour and can be demonstrated in tumour, in the interstitium and in blood vessels. We used lipiodol emulsified with cisplatin and epirubicin successfully in 22 patients with inoperable liver cell carcinomas. The treatment was well tolerated, apart from some nausea and mild upper abdominal discomfort. Survival time from first diagnosis and the first embolisation was ten months longer than expected survival or that following systemic chemotherapy.

Intrinsic regulation of the blood flow to the endocrine and exocrine parts of the rat pancreas.

To evaluate possible differences in the local regulation of blood flow between the endocrine and exocrine pancreatic parenchyma, the blood perfusion of the pancreas and the pancreatic islets has been measured after a 90-second period of anoxia or a 5-min period of increased venous pressure. After anoxia, caused by interruption of arterial blood flow, there was a significant increase (P less than 0.01) in islet blood flow (IBF) while whole pancreatic blood flow (PBF) remained unchanged. Arterial occlusion also increased the serum glucose (P less than 0.01) and serum insulin concentrations (P less than 0.001). Vagotomy prevented the increase in IBF but did not affect the increase in serum glucose or serum insulin concentration, which suggests that the increase in IBF was due to the increased serum glucose concentration. An increased venous pressure in the portal vein did not affect IBF, PBF, serum glucose or serum insulin concentrations. It is concluded that, in the rat pancreas, the local control of PBF and IBF is of minor importance in the regulation of blood flow.

Diabetogenic action of alloxan following temporary interruption of arterial blood flow to pancreas in rats.

Ligation of the superior mesenteric and the superior pancreatico-duodenal arteries just prior to alloxan treatment and their release ten minutes after treatment did not protect rats against development of alloxan diabetes. Prior incubation of alloxan in vitro for a period of ten minutes at a physiological pH value and 37° C. resulted in loss of diabetogenic activity. Identical blood flow interruption without alloxan treatment did not produce elevated blood glucose levels. After the intravenous injection of alloxan, a substance giving a fluorescence product with alloxan reagent was detected in blood over four hours. The substance remained at higher levels when animals, prior to alloxan treatment, were injected with reduced glutathione. There was also a prolonged detection of alloxan during incubation in whole blood and in buffer containing reduced glutathione. The production of alloxan diabetes following temporary interruption of arterial blood flow is discussed in the light of the present results.