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Results for “Vascular System Injuries”

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At least 37 records · Page 2Linked to original sources
PubMed1996

The somatostatin analog angiopeptin does not reduce chronic hypoxic pulmonary hypertension in rats.

Angiopeptin is an analog of somatostatin-14, which has been found to inhibit cellular proliferation in several models of systemic vascular injury. As proliferation plays a major role in pulmonary hypertension, we examined the hypothesis that angiopeptin would inhibit the development of chronic hypoxic pulmonary hypertension in the rat. Angiopeptin was infused intravenously (90-100 microg/kg/day) by minipumps in 10 rats during a 3-week exposure to hypobaric hypoxia and in six normoxic rats. Normal saline was infused in six hypoxic control rats and in seven normoxic control rats. Angiopeptin produced no significant difference in mean pulmonary arterial pressure and resistance, right ventricular weight, or medial thickness of small pulmonary vessels. Vasoconstrictor responses of isolated lungs to acute hypoxia were not affected by angiopeptin. We conclude that angiopeptin, at the high intravenous dose used, does not significantly reduce the development of chronic hypoxic pulmonary hypertension in rats.

Animals↗
PubMed2004

[Urgent partial sternotomy for the treatment of iatrogenic vascular injury to the thoracic outlet: a report of two cases].

Two patients underwent surgery for iatrogenic vascular injuries at the thoracic outlet. Injuries occurred during mediastinoscopy in one patient (male, aged 60 years) and removal of a Portovac catheter in the other (female, aged 49 years). We performed partial sternotomy in both cases to expose the proximal of a. carotis communis and vena cava superior, respectively. After distal and proximal control of the vessels, the injured vessel was primarily sutured in the first patient, and the tip of the catheter was removed through a venotomy incision in the latter. No postoperative complications occurred in both patients. Partial sternotomy incision provides an appropriate and quick access to the injured vessels and surrounding structures at the thoracic outlet.

Female↗
PubMed2006

The relationship of periodontal disease to cardiovascular diseases--review of literature.

Association of Oral and Systemic diseases has gained importance because the high occurrence of oral diseases is an extremely common source of infection. Epidemiological Studies have presented periodontal diseases as a risk factor for development of cardiovascular diseases. A chronic oral infection such as periodontitis is a constant potential source of infection and has now been considered as a separate risk factor for cardiovascular diseases, cerebrovascular diseases, peripheral arterial disease and respiratory diseases as well as delivery of low-birth-weight infants. The possible pathways linking oral infections to systemic diseases are metastatic infections, bacterial endotoxins, and systemic vascular injury. People with a history of periodontal disease and/or tooth loss were found at higher risk for Peripheral arterial disease (PAD) as compared to those without periodontal disease and/or tooth loss. All studies on the relationship of periodontal diseases to cardiovascular diseases are inconclusive and most of the data is based on epidemiological studies.

Cardiovascular Diseases↗
PubMed1984

Severe systemic vascular necrosis in cyclosporin-treated rabbits with acute serum sickness.

Rabbits given acute serum sickness (ASS) and treated with cyclosporin A (CyA) developed a severe, systemic vascular injury, which was not similar to that normally seen in ASS. Thirty-three NZW rabbits received a single intravenous injection of 250 mg/kg bovine serum albumen (BSA) with or without endotoxin (5 micrograms/kg), on day 0. Groups of rabbits were given intramuscular CyA as follows: 15 mg/kg/day from day -2 to +8, or 25 mg/kg/day from day -2 to +3 or day 0 to 5. Muscular arteries of the heart and splanchnic organs developed an arterial injury in which there was extensive fibrinoid necrosis of the vessel wall but little or none of the mononuclear cell reaction that is normally associated with the arteritis of ASS. A microvascular injury also occurred which led to interstitial haemorrhage in the gastric mucosa and multi-focal necrosis in the heart and liver. These lesions were seen with equal frequency in all groups of rabbits with serum sickness who received CyA, irrespective of whether they also received endotoxin. We suggest that CyA altered the host inflammatory response to the injury initiated by the BSA-anti-BSA immune complexes and this led to enhanced vascular injury. The inhibition by CyA of the perivascular cellular reaction suggests that this reaction may be mediated by T lymphocytes. This model should provide further insight into the pathogenesis of arteritis, as well as the mechanisms of cyclosporin toxicity.

Animals↗
PubMed1999

Percutaneous introducibility of the expandable vascular sheath system and injury potential of balloon-assisted thrombectomy: preliminary In vivo results.

PURPOSE: To test the percutaneous introducibility of the expandable vascular sheath (EVS) system and the safety of percutaneous balloon-assisted thrombectomy. METHODS: The EVS was inserted directly (n = 9) or through a 9.5 Fr regular vascular introducer sheath (n = 9) into the femoral arteries and veins and carotid arteries in four dogs (18-21 kg). Balloon-assisted thrombectomies were simulated in iliac arteries. Histologic examinations were done at sites of funnel deployment immediately (n = 4) and 25 days (n = 8) after the intervention. RESULTS: The EVS was successfully introduced into six of nine vessels by a direct percutaneous approach. Balloon-assisted thrombectomy using the EVS device caused localized intimal denudation, disruption of the internal elastic lamina, and mild hemorrhages into the media; one arterial dissection at the site of funnel deployment was seen. All indirect insertions and funnel deployments were successful. Twenty-five days after the experiments, intimal hyperplasia was noted in all cases. CONCLUSION: Percutaneous balloon-assisted thrombectomy may cause mild vascular injuries. Direct percutaneous introduction of the EVS device cannot be recommended yet.

Animals↗
PubMed2005

Controlled survival study of the effects of Tisseel or a combination of FloSeal and Tisseel on major vascular injury and major collecting-system injury during partial nephrectomy in a porcine model.

PURPOSE: We report the results of a controlled survival study in a porcine model investigating Tisseel or a combination of FloSeal and Tisseel in dealing with vascular and collecting-system injury during partial nephrectomy. MATERIALS AND METHODS: We performed an open right lower-pole partial nephrectomy on 15 large female pigs. The defect was repaired using standard open techniques (N = 5; controls), Tisseel only (N = 6; group I), or FloSeal followed by Tisseel (N = 4; group II). A Jackson-Pratt drain was placed. Nephrectomy and retrograde pyelography were performed at 1 week. RESULTS: Operative times were shorter in both study groups, achieving statistical significance in group I (P = 0.008). Warm-ischemia times were significantly improved in both study groups (P = 0.029 and P = 0.00005 in groups I and II, respectively). Time to hemostasis was significantly shorter in group II only (P = 0.002) but approached significance in Group I as well (P = 0.09). Estimated blood loss was not significantly different from the controls in either group. When Tisseel was placed alone after hilar control, hematoma formation under the Tisseel was noted on release of the hilar clamp. After 1 week, there was one urinoma and three urine leaks in the control group. In group I, there was one urinoma and four urine leaks, and there was only one urine leak and no urinomas in group II. There were no hematomas in any of the groups. CONCLUSIONS: Tisseel alone is not adequate for either hemostasis or management of major collecting-system injury. FloSeal capped with Tisseel appears sufficient to control major vascular and collecting-system injuries without adjunctive surgical measures. A proposed technique for laparoscopic partial nephrectomy without reconstructive techniques is presented that warrants clinical study.

Animals↗
PubMed1998

The Xylum Clot Signature Analyzer: a dynamic flow system that simulates vascular injury.

The Xylum Clot Signature Analyzer (CSA) is an automated, user-friendly, benchtop analyzer that assesses platelet function and coagulation in non-anticoagulated whole blood under physiological flow and temperature conditions. From blood drawn in a single venipuncture, the CSA measures: a) the time for platelets to occlude holes "punched" in a blood conduit (platelet hemostasis time or PHT); b) collagen-induced thrombus formation (CITF) as blood flows in a channel containing a collagen fiber; and c) clotting time (CT). Micrographs show platelet-rich thrombi in the punched holes and on the collagen surface after a run. PHT and CITF increased at lower shear rate, suggesting that shear activation of platelets is involved in hole closure and in collagen-induced thrombus formation. In blood mixed with anti-von Willebrand's factor (vWF) antibodies, anti-GPIb antibodies, aurin tricarboxylic acid (ATA), or anti-GPIIb-IIIa, PHT and CITF were prolonged, further supporting the reflection of platelet function by those parameters. At low shear rate (<1000 sec(-1)), native blood and blood treated with anti-vWF did not have significantly different PHTs or CITFs. At high shear rate (>6000 sec(-1)), the PHT and CITF of the anti-vWF-treated sample were significantly greater than those of the untreated sample. This supports the inhibition of shear-induced activation of platelets by anti-vWF in the CSA. Heparin-treated blood showed significantly longer CT, indicating that coagulation of blood under flow is inhibited by heparin. The CSA thus assess multiple aspects of hemostasis under near-physiological conditions.

Biological Assay↗
PubMed1994

Pharmacological reduction of the systemically damaging effects of local ischaemia.

Many patients with intermittent claudication are encouraged to exercise. However, transient exercise-induced muscle ischaemia results in systemic vascular endothelial injury associated with increased vascular permeability manifest as an increase in urinary albumin excretion. Repetitive systemic vascular endothelial injury leads to accelerated atherogenesis and may explain the high cardiovascular mortality rate of claudicants. Oxpentifylline, a haemorheological agent, has recently been shown to prevent vascular endothelial injury in animal models. A double-blind, placebo-controlled, cross-over trial was undertaken to determine the effect of oxpentifylline on exercise-induced systemic vascular endothelial injury in 20 claudicants. Urinary albumin, expressed as a creatinine ratio (ACR), was measured before and 1 and 2 hours after standardised exercise following 1 week treatment with either active drug or placebo. Oxpentifylline reduced the median (range) 1 hour post exercise increase in ACR from 0.35 (-0.46-12.72) to 0.02 (-6.00-14.10) mg/mmol. (p = 0.030, z = 2.2 Wilcoxon rank sign test). These results confirm that local ischaemia is associated with a potentially deleterious systemic effect and that it may be possible to attenuate this pharmacologically. The clinical significance of this is yet to be determined.

Aged↗