Thin-film nickel titanium demonstrates reduced bacterial adherence in vitro compared with commercially available endograft materials

Vol. 209, No. 3S, 2009

Thin-film nickel titanium demonstrates reduced bacterial adherence in vitro compared with commercially available endograft materials Allan Wiley Tulloch MD, Youngjae Chun MS, Anthony Chau BS, Komindar P Mohanchandra PhD, Greg P Carman PhD, Peter F Lawrence MD, David A Rigberg MD, FACS University of California, Los Angeles, Los Angeles, CA INTRODUCTION: We have previously demonstrated the novel use of thin-film nickel titanium (TFN) to cover stents. This study was aimed at evaluating the potential infectivity of TFN compared with currently available endograft materials. METHODS: TFN was created using a sputter deposition technique to a uniform thickness of 5 microns. TFN, woven polyester, and polytetrafluoroethylene (PTFE) were incubated in a 107 suspension of E coli for 24 hours at 37 degrees Celsius, at which point samples were washed to remove nonadherent organisms. Samples were either fixed and prepared for electron microscopy or ultrasonically oscillated at 20 kHz for 5 minutes to dislodge adherent organisms. Quantitative culture of the sonication effluent on agar plates was used to calculate bacterial adherence. RESULTS: TFN demonstrated an approximate 10-fold decrease in the number of colony-forming units per cm2 of material compared with both woven polyester and PTFE. These results were corroborated by electron microscopic findings demonstrating greater bacterial adherence on the commercially available stent materials. CONCLUSIONS: We demonstrate that TFN is more resistant to E coli adherence in vitro. These preliminary findings suggest that TFN may represent a superior material to resist endograft infection.

Microvascular acclimatization to chronic hypoxia is dependent on altered mast cell function Alfred J Casillan MD, PhD, John G Wood PhD, Norberto C Gonzalez MD, Michael Moncure MD, James H Thomas MD University of Kansas Medical Center, Kansas City, KS INTRODUCTION: Mast cell degranulation plays a key role in the development of the rapid microvascular inflammation during systemic hypoxia (Hx) characterized by increased leukocyte adherence and emigration; however, during chronic Hx, this inflammation resolves. Our goal was to investigate the role of altered mast cell function in microvascular acclimatization to chronic Hx, as well as the underlying mechanism.

Surgical Forum Abstracts

S141

both LA and MCD during Hx in AC rats. The oxidant H2O2 increased LA and MCD in NA but not AC rats. The iNOS inhibitor L-NIL increased these responses in AC rats during Hx. Platelet activating factor (PAF) increased LA but not MCD in NA but not AC rats. iNOS levels were increased within mast cells of AC rats. Nonacclimatized Rats

Treatment

Leukocyte Adherence

Mast Cell Degranulation

Acclimatized Rats Leukocyte Adherence

Mast Cell Degranulation

Normoxia

0.6 ⫾ 0.2

1.00

0.4 ⫾ 0.2

Hypoxia

8.8 ⫾ 0.8ⴱ

1.32 ⫾ 0.14ⴱ

0.3 ⫾ 0.1†

1.02 ⫾ 0.4†

Vehicle

0.6 ⫾ 0.2

1.00

0.2 ⫾ 0.1

1.00

H2O2 (100 ␮M)

9.8 ⫾ 1.4ⴱ

1.48 ⫾ 0.14ⴱ

0.2 ⫾ 0.1†

1.06 ⫾ 0.04†

Normoxia ⫹ L-NIL

0.8 ⫾ 0.3

1.04 ⫾ 0.02

0.4 ⫾ 0.1

1.05 ⫾ 0.03

Hypoxia ⫹ L-NIL

9.2 ⫾ 0.6ⴱ

1.38 ⫾ 0.12ⴱ

4.4 ⫾ 0.4ⴱ

1.26 ⫾ 0.11

Vehicle

0.4 ⫾ 0.2

1.00

0.6 ⫾ 0.3

1.00

PAF (20 nM)

8.6 ⫾ 1.8ⴱ

1.00 ⫾ 0.04

1.6 ⫾ 0.4†

1.05 ⫾ 0.04

1.00

Values are means ⫾ standard errors. n ⫽ 5 or 6 rats in each group. ⴱIndicates p ⬍ 0.05 vs corresponding control group. †Indicates p ⬍ 0.05 vs nonacclimatized rats.

CONCLUSIONS: These results demonstrate that mast cell function is altered through upregulation of iNOS after hypoxic acclimatization. These results also indicate that other mechanisms are involved in this process. Since tissue hypoxia occurs in many surgical settings, a better understanding of acclimatization may lead to novel interventions to reduce microvascular inflammation.

Exercise induces a systemic inflammatory response with and without chronic unilateral hind-limb ischemia Robert S Crawford MD, Hassan Albadawi MD, Alessandro Robaldo MD, Michael Peck MD, Christopher Abularrage MD, Glenn LaMuraglia MD, Mark Conrad MD, Virendra Patel MD, Michael Watkins MD, FACS Massachusetts General Hospital, Boston, MA INTRODUCTION: Demand limb ischemia following exercise, ie, claudication is associated with substantial morbidity in vascular beds outside of the ischemic limb. Experiments were designed to determine whether exercise and limb ischemia modulate the systemic inflammatory response and vascular injury in remote vascular beds.

METHODS: Leukocyte adherence (LA) and mast cell degranulation (MCD) were measured in mesenteric microcirculation of anesthetized rats using intravital microscopy. Rats were acclimatized to hypobaric Hx for 3 weeks at a level equivalent to 10% inspired O2. Immunocytochemistry was used to detect inducible nitric oxide synthase (iNOS). Responses were compared in nonacclimatized (NA) and acclimatized (AC) rats.

METHODS: Aged C57BL6 mice underwent carotid artery ligation alone (CAL), or in combination with femoral artery ligation (CAL ⫹ FAL). At day 14, both the CAL and CAL ⫹ FAL groups were divided into a sedentary and an exercise group. Basal limb perfusion and demand ischemia for FAL animals was quantified using laser Doppler imaging (LDI) and an established scale of neurological function. At day 14, animals in the exercise groups underwent daily treadmill exercise through day 28; thereafter, serum was harvested for measurement of KC (keratinocyte chemoattractant), MCP-1 (monocyte chemoattractant protein-1), VEGF (vascular endothelial growth factor), and MIP-2 (macrophage inflammatory protein-2). All CAL specimens were harvested for measurement of intimal medial ratio.

RESULTS: As shown in the table, Hx increased LA and MCD in NA but not AC rats. However, the iNOS inhibitor L-NIL increased

RESULTS: All measured serum proteins (Table) were significantly increased in CAL mice subjected to exercise alone as compared with