Single- versus multiple-stage catheter-directed thrombolysis for acute iliofemoral deep venous thrombosis does not have an impact on iliac vein stent length or patency rates.

BACKGROUND: Incomplete venous thrombolysis and residual nonstented iliac vein disease are known predictors of recurrent deep venous thrombosis (DVT). Controversy exists as to whether the number of thrombolysis sessions affects total stent treatment length or stent patency. The goal of this study was to evaluate the outcomes of patients who underwent single vs multiple catheter-directed lysis sessions with regard to stent extent and patency. METHODS: Consecutive patients who underwent thrombolysis and stenting for acute iliofemoral DVT between 2007 and 2018 were identified and divided into two groups on the basis of the number of treatments performed (one vs multiple sessions). Operative notes and venograms were reviewed to determine the number of lytic sessions performed and stent information, including size, location, total number, and length treated. End points included total stent length, 30-day and long-term patency, and post-thrombotic syndrome (Villalta score ≥5). The χ2 comparisons, logistic regression, and survival analysis were used to determine outcomes. RESULTS: There were 79 patients who underwent lysis and stenting (6 bilateral interventions; mean age, 45.9 ± 17 years; 48 female). Ten patients (12 limbs) underwent single-stage treatment with pharmacomechanical thrombolysis, and the remaining 69 (73 limbs) had two to four operating room sessions combining pharmacomechanical and catheter-directed thrombolysis. Patients who underwent a single-stage procedure were older and more likely to have a malignant disease. These patients received less tissue plasminogen activator compared with the multiple-stage group (17.2 ± 2.2 mg vs 27.6 ± 11.6 mg; P = .008). Average stent length was 8.8 ± 5.2 cm for the single-stage group vs 9.2 ± 4.6 cm for the multiple-stage group (P = .764). Patients who underwent a single-stage procedure had no difference in average length of stay from that of patients who underwent multiple sessions (8.5 days vs 5.9 days; P = .269). The overall 30-day rethrombosis rate was 7.3%. Two-year patency was 72.2% and 74.7% for the single and multiple stages, respectively (P = .909). The major predictors for loss of primary patency were previous DVT (hazard ratio [HR], 5.99; P = .020) and incomplete lysis (HR, 5.39; P = .014) but not number of procedures (HR, 0.957; P = .966). The overall post-thrombotic syndrome rate was 28.4% at 5 years and was also not associated with the number of treatment sessions. CONCLUSIONS: Single- vs multiple-stage thrombolysis for DVT is not associated with a difference in extent of stent coverage. Patency rates remain high for iliac stenting irrespective of the number of lytic sessions, provided lysis is complete and the diseased segments are appropriately stented.

Renal and femoral venous blood flows are regulated by different mechanisms dependent on α-adrenergic receptor subtypes and nitric oxide in anesthetized rats.

Venous and arterial walls are responsive to sympathetic system and circulating substances, nevertheless, very few is known about the venous blood flow regulation simultaneously to arterial vascular beds. In this study, we compared the venous and arterial blood flow regulation in visceral and muscular beds upon injection of different doses of vasoactive drugs which act in arterial vascular beds. Anesthetized adult male Wistar rats underwent to right femoral artery and vein cannulation for hemodynamic recordings and infusion of drugs. Doppler flow probes were placed around the left renal artery and vein, and left femoral artery and vein to evaluate the changes in flood flow. Phenylephrine (PHE) injection (α1-adrenergic receptor agonist) elicited vasoconstriction in all arteries and veins. Intravenous prazosin (PZS) (1mg/kg, α1-adrenergic receptor blocker) caused renal artery vasodilation, but not in the other beds. Vasoconstrictor effect of PHE was abolished by PZS in all vascular beds, except in femoral vein. Phentolamine (PTL) injection (1mg/kg, α1/α2-adrenergic receptor blocker) produced renal artery vasodilation with no change in other beds. After PTL, the vasoconstriction evoked by PHE was abolished in all vascular beds. Sodium Nitroprusside (SNP), a nitric oxide donor, elicited vasodilation in all beds, and after PTL but not post PZS injection, SNP enhanced the vasodilatory effect in femoral vein. Our findings suggest that the vasoconstriction in renal and femoral veins is mediated by different subtypes of α-adrenoceptors. The nitric oxide-dependent vasodilation in femoral vein enhances when α2-adrenoceptors are not under stimulation, but not in the other vascular beds investigated.

Endothelial, renal and hepatic variables in Wistar rats treated with Vancomycin.

Vancomycin (VCM) is indicated in combat against Gram-positive infections, but it is not considered a first-choice drug because of its adverse effects. It is believed that oxidative stress is the primary mechanism of endothelial injury and the consequent VCM toxicity, which varies from phlebitis to nephrotoxicity. Moreover, dose recommendations, dilution, rates and types of infusion are still controversial. The aim of this study was to determine the effect of different VCM dilutions in endothelial, liver and kidney injuries by biochemical parameters and histopathological analysis. Wistar rats were randomly divided into six groups and subjected to femoral vein cannulation for drug administration. Control groups received 0.9 ml of saline and the others received VCM (10mg/Kg/day) at dilutions of 5.0 and 10.0 mg/mL for 3 and 7 days. Homocysteine, hs-CRP, AST, ALT, GGT, urea, creatinine, lycopene, alpha-tocopherol, beta-carotene and retinol were analyzed. Kidney, liver and cannulated femoral vein fragments were collected.This study showed alterations in ALT which featured hepatotoxicity. However, drug dilutions were not able to show changes in other biochemical parameters. In contrast, kidney and endothelium pathological changes were observed. More studies are needed to characterize VCM induced kidney and endothelium toxicity and biochemical markers able to show such morphological modifications.

Involvement of the AT1 receptor in the venoconstriction induced by angiotensin II in both the inferior vena cava and femoral vein.

Although angiotensin II-induced venoconstriction has been demonstrated in the rat vena cava and femoral vein, the angiotensin II receptor subtypes (AT(1) or AT(2)) that mediate this phenomenon have not been precisely characterized. Therefore, the present study aimed to characterize the pharmacological receptors involved in the angiotensin II-induced constriction of rat venae cavae and femoral veins, as well as the opposing effects exerted by locally produced prostanoids and NO upon induction of these vasomotor responses. The obtained results suggest that both AT(1) and AT(2) angiotensin II receptors are expressed in both veins. Angiotensin II concentration-response curves were shifted toward the right by losartan but not by PD 123319 in both the vena cava and femoral vein. Moreover, it was observed that both 10(-5)M indomethacin and 10(-4)M L-NAME improve the angiotensin II responses in the vena cava and femoral vein. In conclusion, in the rat vena cava and femoral vein, angiotensin II stimulates AT(1) but not AT(2) to induce venoconstriction, which is blunted by vasodilator prostanoids and NO.

Role of adenosine on intestinal ischemia-reperfusion injury in rabbits.

To study if the treatment with adenosine (ADO), an agonist of adenosine receptors, attenuates intestinal dysfunction caused by ischemia (I) and reperfusion (R), we treated rabbits with ADO (15 mg x kg(-1), intravenously) or saline solution (SS) to I (60 minutes) before occlusion of superior mesenteric artery and/or R (120 min). After I or I/R, isolated jejunal segments (2 cm) were mounted in an organ bath to study nerve-mediated contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained (hematoxylin and eosin) for analysis by optical microscopy. Compared to the sham group, the jejunal contractions were similar in I + ADO, but reduced in I + SS, I/R + SS, and I/R + ADO groups. We concluded that the jejunal enteric nerves were damaged in I + SS, I/R + SS, and I/R + ADO, but not in I + ADO group. These results suggested that ADO attenuated intestinal dysfunction due to I, but not to R.