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Biomedical subjects

Rolf Büttemeyer

Publications and source records attributed to Rolf Büttemeyer.

5 recordsLinked to original sources
PubMed2004

Re-endothelialization of punctured ePTFE graft: an in vitro study under pulsed perfusion conditions.

BACKGROUND: When used as arteriovenous (AV) shunts for haemodialysis, small diameter expanded polytetrafluoroethylene (ePTFE) grafts have a high failure rate in vivo. Attempts to improve graft patency are various, and focus on either improvement of implantation techniques or graft tissue engineering. The tissue engineering approach attempts to reproduce in grafts the properties of pristine vasculature. As shown in previous experiments, it is possible to grow on ePTFE grafts under shear stress in vitro an autologous endothelial cell layer, which will withstand physiological stress under in vivo conditions of blood flow. The aim of this study was to investigate in an in vitro model the regenerative potency of a tissue-engineered prosthetic vascular graft after repeated cannulation with a haemodialysis cannula. METHODS: Pig endothelial cells were harvested from an external jugular vein. Following processing of the endothelial cells, seven ePTFE grafts were coated with an inner cell layer and were kept under pulsed perfusion. Each graft was then cannulated three times with a standard shunt needle. The endothelium was then left to regenerate for a maximum of 48 h. The grafts were stained with haematoxylin/eosin before histological study. RESULTS: All grafts were endothelialized over the puncture sites within 48 h. Histological analysis revealed a confluent endothelial cell lining at each puncture site. Cell morphology and cell pattern over puncture sites were not different from randomly picked locations over the graft lumen. CONCLUSION: Our results underline the potential of endothelial tissue engineering in vascular shunt surgery. Vascular bio-hybrids that have the properties of pristine vascular endothelium may be a key step forward in maintaining angio-access in patients who require haemodialysis.

Animals↗
PubMed2003

Intraperitoneal administration of the angiogenesis inhibitor thalidomide does not impair anastomotic healing following large bowel resection in a rabbit model.

The effects of thalidomide after intraperitoneal instillation on the healing of colonic anastomoses are not known. A series of 40 New Zealand White rabbits underwent an end-to-end colonic anastomosis. The animals were randomized into four groups. Groups 1 (n = 10) and 2 (n = 10) were treated with dissolved thalidomide 200 mg/kg intraperitoneally, whereas groups 3 (n = 10) and 4 (n = 10) were treated only with the dissolver. Animals were sacrificed at day 3 (groups 1, 3) and day 7 (groups 2, 4). Anastomotic healing was tested by measuring the bursting pressure in vitro. Immunohistochemical staining of the anastomotic site was performed with polyclonal antibodies against CD31 and Mib-1, to determine a possible antiangiogenic or antiproliferative effect. Statistical analysis was performed using Spearman's log rank correlation and paired t-test. On postoperative day 3 (p > 0.19) and postoperative day 7 (p > 0.73), there was no difference in bursting pressure in the treatment and the control groups. Angiogenesis scores were reduced at day 3 in the thalidomide group (p < 0.05), but did not differ between the groups at day 7. White blood cell counts were decreased in the treatment groups at day 3 (p < 0.01) and day 7, compared to control groups (p < 0.01). There was no difference in the expression of Mib-1 in either group at day 3 or day 7. The intraperitoneal administration of thalidomide does not interfere with the healing of colonic anastomosis. Although the angiogenesis score is diminished at day 3, this did not lead to a reduced bursting pressure at day 3 or day 7.

Anastomosis, Surgical↗
PubMed2003

Epigallocatechin gallate can significantly decrease free oxygen radicals in the reperfusion injury in vivo.

OBJECTIVE: There is experimental evidence that oxygen-derived free radicals (Superoxide (O(2)(-))) play a key role in tissue damage in ischemia-reperfusion injury. Among various antioxidants tested in vitro, natural polyphenols like Epigallocatechine gallate (EGCG) show a 164-fold higher scavenging activity for O(2)(-) than ascorbic acid We therefore conducted an animal study in order to investigate the impact of EGCG on O(2)(-) production during reperfusion after defined periods of ischemia in the muscle tissue of the rat, using a recently developed cytochrome c-based biosensor for on-line in vivo monitoring of O(2)(-). MATERIALS AND METHODS: Femoral artery and vein were dissected below the inguinal ligament in male Wistar rats. The cytochrome c-based biosensor was placed in the gastrocnemius muscle. Ischemia was induced by clamping the femoral vessels. Ischemia times were either 60 (n = 14) or 120 (n = 14) minutes. Six animals in each group received 4 mg/kg body weight EGCG intravenously at the time of reperfusion, another six animals in each group served as controls (no treatment). Additionally, two animals in each group received the same volume of saline instead of EGCG. The current response of the biosensor corresponding to the O(2)(-) concentrations in vivo was recorded on a PC. The gastrocnemius muscles were harvested for histological evaluation. RESULTS: The average maximum O(2)(-) concentration after 60 minutes of ischemia was 188, 18 nmol/L (23 pA) compared to 90 nmol/L (11 pA) (P <.01) with EGCG application. The mean O(2)(-) value after 120 minutes was 220 nmol/L (27 pA) versus 135 nmol/L (16.5 pA) (P <.01) with EGCG, respectively. Histological analysis showed advanced muscle cell injury and neutrophil infiltration in the group without EGCG. No O(2)(-) reduction could be verified administering saline instead of EGCG. CONCLUSION: For the first time the scavenging activity of an antioxidant was verified in vivo on-line. EGCG significantly diminished O(2)(-) tissue concentrations after 60 or 120 minutes of ischemia by an average of nearly 50%, suggesting its therapeutic potential.

Animals↗
PubMed2002

In vivo measurement of oxygen-derived free radicals during reperfusion injury.

By use of an optimized cytochrome c-based biosensor, superoxide radical production was measured continuously in vivo. The aim of this study was the online detection of superoxide concentration during reperfusion after a variable time of ischemia. Measurements were performed by placing the detecting sensor into gastrocnemius muscle tissue. Ischemia was induced by clamping the vena and arteria femoralis. Current response of the sensor was recorded continuously as an equivalent for superoxide concentration. Ischemia times varied from 5 to 120 minutes. The minimum ischemia time to record superoxide production was 10 minutes. By inducing longer periods of ischemia, an increase in superoxide concentration reached its highest levels at 2 hours. Furthermore, the total time of superoxide production after reperfusion depended on the total time of ischemia.

Animals↗