Chronic traumatic thoracic aortic aneurysms-results of endovascular treatment. Fourteen-year single-center experience.

AIM: Chronic traumatic thoracic aneurysms are results of blunt trauma of the chest during motorcar accident. Treatment of choice is the endovascular procedure with stent-graft. METHODS: Between 2000-2012 in General and Thoracic Surgery Department 30 patients with post-traumatic aneurysms were operated. In all cases aneurysm was located below left subclavian artery and in 63% developed during road traffic accident. RESULTS: All patients were operated on with 100% technical success and no device failure was noticed. None of patients died during the endovascular procedure and no serious complications like spinal cord ischemia was observed. In one (3%) case, where left subclavian artery was covered, stroke was diagnosed treated conservatively. CONCLUSION: At long-term follow-up, one endoleak type IA was found, solved with balloon-plasty. Two patients died due to cardiac diseases.

Severity of chronic venous disease and anatomic distribution of valvular incompetence.

AIM: The aim of the study was to examine the association between anatomical patterns of valvular incompetence and the severity of venous insufficiency in patients with chronic venous disease. METHODS: A total of 211 consecutive patients (70% females) were referred from the vascular clinic to undergo a Doppler ultrasound examination. The extent and anatomical pattern of valvular incompetence was noted using CEAP criteria. Clinical classes C1-6 for each patient were expressed as a string of binary digits and translated into a clinical ordinal score. In this way, higher grade signs were not obscuring lower grade signs and non-parametric analysis could include a wider range of clinical data. RESULTS: Varicose veins were the main complaint in 33% of the patients. 54% had at least one incompetent deep vein, 80% had incompetent perforators. Clinical severity increased with age, but was not related with gender. The presence of deep venous incompetence did not account for significant increase in signs. Superficial incompetence, especially if involving two or more segments, was most commonly seen in patients with severe signs. A linear regression model for clinical ordinal score identified non-saphenous superficial reflux and small saphenous vein reflux as the strongest predictors of clinical severity. CONCLUSION: CEAP clinical classes can be translated into a clinical ordinal score, which is useful for data analysis. In a group with chronic venous disorders, clinical status is associated mostly with the condition of superficial and calf perforating veins.

Dependence of basal cerebral blood flow and cerebral vascular resistance in spontaneously hypertensive rats upon vasoconstrictor prostanoids.

The effects of indomethacin (inhibitor of cyclooxygenase), imidazole (inhibitor of thromboxane A2 synthase) and SQ 29548 (antagonist of TxA2/PGH2 receptors) on basal CBF and CVR were studied in normocapnic and normoxic SHR and WKY rats. CBF was measured by the intracarotid 133Xe technique. CVR was calculated as ratio of mean arterial blood pressure and CBF. Resting CBF did not differ between SHR and WKY. MABP and CVR were significantly higher (p < 0.01) in SHR than in WKY. Indomethacin (6 mg/kg, i.v.) produced a significant long-lasting decrease of CBF and increase of CVR in both strains, although these effects were more pronounced (p < 0.01) in WKY. Imidazole (20 mg/kg, i.v.) had no effect on measured variables in either strain. SQ 29548 (1 mg/kg, i.v.) produced a significant increase of CBF in SHR (p < 0.001) but not in WKY. CVR decreased in SHR parallel to the increase of CBF but remained unchanged in WKY. Our results demonstrate that, in contrast to WKY, basal CBF and CVR in SHR depend upon vasoconstricting prostanoids which act on TxA2/PGH2 receptors but are distinct from thromboxane A2.

Hormonal dependence of the effects of metabolic encephalopathy on cerebral perfusion and oxygen utilization in the rat.

Previous studies have demonstrated that in adult rats with chronic hyponatremia, both symptoms of encephalopathy and mortality largely depend upon the gender of the animal and the presence of elevated plasma levels of vasopressin (AVP). Since effects of AVP on blood vessels may be gender dependent, the present study was designed to compare the effects of chronic (4 days) hyponatremia on cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and cerebral perfusion index (CPI) in adult male and female rats. CBF (intra-arterial 133Xe injection method) and CMRO2 (arteriovenous difference of cerebral oxygen contentxCBF) were measured in normonatremic and hyponatremic (hyponatremia induced with 140 mmol/L glucose and either AVP or desmopressin [dDAVP], plasma sodium = 100 to 110 mmol/L) adult rats of both genders. The CPI was assessed from magnetic resonance imaging of the transit of magnetic susceptibility contrast agent through the brain. Female rats with AVP-induced chronic hyponatremia had a 36% decrease in CBF and a 60% decrease in CMRO2. In male animals, both parameters were not different from control values. AVP-induced hyponatremia resulted in a 45% decrease in CPI in female rats, but hyponatremia induced with dDAVP did not affect CPI in either male or female rats. Chronic (4 days) administration of AVP did not affect CPI in either male or female normonatremic rats. When rats with AVP-induced chronic hyponatremia were pretreated with estrogen, the CPI in males was not different from that in females. Our results demonstrate that during AVP-induced chronic hyponatremia in female rats, there is significant depression of both oxygen utilization and blood flow in the brain.

Effects of endothelium-derived nitric oxide on cerebral circulation during normoxia and hypoxia in the rat.

The aim of this study was to determine the effects of endogenous nitric oxide (NO) on cerebral blood flow (CBF) and cerebrovascular resistance (CVR) under conditions of normoxia and hypoxia. Experiments were performed on anesthetized, mechanically ventilated Wistar rats. CBF was measured using the intracarotid 133Xe injection technique. NO formation was inhibited by NG-monomethyl-L-arginine (L-NMMA). Administration of L-NMMA (100 mg kg-1 i.v.) during normoxia resulted in an increase in mean arterial blood pressure from 113 +/- 4 to 145 +/- 4 mm Hg (p less than 0.001), a decrease in CBF of 21% (from 91 +/- 4 to 75 +/- 5 ml 100 g-1 min-1, p less than 0.001), and an increase in CVR of 53% (from 1.3 +/- 0.1 to 2.0 +/- 0.2 mm Hg ml-1 100 g min, p less than 0.001). These effects were reversed by i.v. administration of 300 mg kg-1 of L-arginine but not D-arginine. Moreover, the administration of L-NMMA abolished the enhancement of CBF and the diminution in CVR observed during intracarotid infusion of acetylcholine (ACh). The increase in CBF and decrease in CVR during hypoxia in the group of rats that received L-NMMA were similar to that in the control group, although CBF and CVR levels attained during hypoxia in both groups were different. The results show that NO is involved in the maintenance of basal CBF and CVR, and is responsible for the ACh-elicited increase in CBF and the decrease in CVR in rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence against participation of V2 receptors in the increase of cerebral blood flow during hypoxemia in the rat.

Cerebral blood flow (CBF) and cerebral utilization of oxygen (CMRO2) were studied in anesthetized and artificially ventilated rats during normoxemia and hypoxemia before and during intravenous infusion of a selective blocker of V2 vasopressinergic receptors (d(CH2)5 [D-Ile2,Abu4] AVP, 15 micrograms/kg per hour i.v.). CBF was measured by means of the intracarotid 133-Xe injection method. CMRO2 was calculated from the oxygen arteriovenous difference using the Fick principle. Infusion of V2 antagonist did not influence CBF, CMRO2 or blood pressure (BP) during normoxia. It also did not change the response of cerebral circulation to hypoxemia. Increase in CBF and decrease in cerebrovascular resistance (CVR) during hypoxemia were similar during the infusion of V2 blocker or without it. However, the decrease in BP observed during hypoxemia in the control group of rats was prevented in the group of animals which were infused with V2 blocker.