Advantages of longer compression intervals during Basic Life Support.
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Biomedical subjects
Publications and source records attributed to Christian Friedrich.
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UNLABELLED: We studied the influence of placenta growth factor (PlGF) on arteriogenesis and tested the role of bone marrow (BM)-derived cells on PlGF-depleted vascular growth. METHODS: Right femoral artery was occluded in wild type (+/+), PlGF k.o. (-/-) and (-/-) mice receiving BM from (+/+) mice (-/- BM). Blood supply in paws was assessed by laser-Doppler imaging (LDI) measurements before, immediately after, as well as 3, 7, 14, 21 and 28 days after surgery. Seven and 28 days after occlusion, hindlimbs were perfusion fixed and filled with contrast medium. Angiograms were evaluated, collateral arteries were analysed histologically and morphometrically. RESULTS: Seven days after occlusion the blood flow and collateral growth in (-/-) were delayed in comparison to the (+/+) group. BM transplantation from +/+ donors prevented this delay. After 3 weeks the (-/-) mice reached values similar to the +/+ control. CONCLUSION: PlGF is an important promoter of arteriogenesis. BM transplantation abolishes inhibition of arteriogenesis in PlGF -/- mice.
Endothelial cell swelling is one of the earliest hallmarks of arteriogenesis, the growth and maturation of collaterals. Mibefradil was found to block endothelial Cl(-) channels that control the volume of endothelial cells. Thus the authors investigated whether the blockade of volume-controlling endothelial cell channels would translate into an inhibition of arteriogenesis. In BALB/c mice, the right femoral artery was ligated and the animals received either mibefradil or solvent (phosphate-buffered saline [PBS]) via osmotic minipumps. Laser Doppler perfusion ratio (R/L) of ligated versus nonligated distal hindlimb increased from 0.06 +/- 0.01 (immediately after ligation) to 0.25 +/- 0.02 (day 7) in the PBS group and only from 0.07 +/- 0.02 to 0.13 +/- 0.02 in the mibefradil group (p <.01). Collateral artery diameters were significantly smaller in the mibefradil group (61 +/- 4.7 microm) versus controls (77.3 +/- 0.9 microm) (p <.05). Relative hemoglobin oxygen saturation measurements confirmed these findings (p <.02). The inhibition of arteriogenesis in the mibefradil group suggests that endothelial Cl(-) channels are involved in the initiation of arteriogenesis.
UNLABELLED: The goal of this study was to examine the mechanisms of vascular growth that lead to the restoration of perfusion in a peripheral vascular disease model in mice. We monitored blood flow recovery and measured vascular growth in inbred strains of mice following femoral artery occlusion. Acute collateral blood flow to the hindlimb was lowest in Balb/C mice, causing intense ischemia, and showed a slower recovery (more than 21 days to 50% normal) than C57Bl/6 which had a 7-fold higher acute collateral flow and a fast recovery (3 days). Collateral vessels were enlarged by proliferation of ECs and SMCs. Capillary density increased in the lower limbs of Balb/Cs (1.7-fold) and of sv129s. Tissue oxygen saturation recovered faster than flow in all strains. Morphometry of mature collaterals showed a diameter increase of 2.1-2.4 fold. The increase in total vessel wall area exceeded that of the femoral artery by 1.4-fold and the common lumenal area by 1.6-fold. Infusion of the growth factor peptide FGF-2 by osmotic minipump accelerated arteriogenesis but inhibited the angiogenic response probably because it prevented ischemia. CONCLUSION: the speed of arteriogenesis is inversely related to the intensity of ischemia, and arteriogenesis is by far the most efficient mechanism to increase blood flow after femoral artery occlusion. De novo arteriogenesis was not observed.