{'fraction_non_alphanumeric': 0.03443708609271523, 'fraction_numerical': 0.016556291390728478, 'mean_word_length': 5.656387665198238, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Loss of flow mediated dilation accompanies endothelial dysfunction in the preconditioned state

To examine flow mediate dilation in the preconditioned state, terminal arteriolar junctions were observed in the hamster cheek pouch using intravital microscopy (pentobarbital 70mg/kg, N=28). Repeated occlusion of one downstream arteriolar branch induced dilation in both the unoccluded downstream branch B (where shear increased) and in the upstream feed F (where shear decreased). To test whether occlusion induced dilation was NO‐mediated, we applied nitro‐arginine (LNNA, 10‐5M) to either B or F (micropipette). LNNA prevented occlusion induced dilation in B (where shear increased) and not F. Thus dilation where shear increased is interpreted as flow mediated. To test whether occlusion induced dilation in F was propagated via gap junction (GJ) signals arising from B, 18‐alpha‐GA (10‐4M) was applied to either B or F. GJ inhibition blocked all dilation in F and none in B. Finally preconditioning induced pharmacologically with nitroprusside or b2‐adrenergic agonism (isoproterenol, ISO) caused endothelial dysfunction (bradykinin, acetylcholine). Occlusion in the preconditioned state caused the same flow changes in B or F, but no dilation. Local elevations in shear induce a local dilation and initiate a GJ mediated propagated dilation. Preconditioning inducing endothelial dysfunction includes absence of flow mediated dilation, and lack of GJ mediated propagated dilation. (NIH HL55492; AHA 0655908T)