Antidromic stimulation of the sensory nerve to the rabbit eye produces pupillary meiosis, supposedly by release of prostaglandins into the aqueous humour. The analogy between this phenomenon and neurogenic inflammation is drawn. It is shown that aspirin and indomethacin, known blockers of prostaglandin synthesis and release, fail to block the meiosis thus produced.

Type 2 diabetes is associated with chronic systemic inflammation and the recruitment of immune cells. In this study, we postulated that CD11c positive cells, a specific subset of lymphocytes, are increasingly expressed with age in perivascular adipose tissues from diabetic mice. Homozygous Type 2 diabetic (db/db) and heterozygous control (DbHET) mice from the same strain were purchased from Jackson Laboratory, and divided into four age groups: 6‐10, 12‐16, 18‐22, and greater than 24 weeks. Epididymal (EAT), mesenteric (MAT), pericardial (PCAT), and periaortic (PAAT) adipose tissues were collected from the db/db and DbHET mice along with spleen, thoracic aortas (TA), mesenteric (MA), and left anterior descending coronary (LAD) arteries. All samples were used to detect CD11c m RNA level using quantitative real‐time PCR. Our data show an age‐dependent increase in CD11c expression of EAT, MAT, PCAT and PAAT adipose tissues from db/db mice. In contrast, CD11c expression remained constant among all four age groups of DbHET mice. Within each age group, higher adipose tissue CD11c levels were observed in db/db mice, compared to those of the DbHET mice. No significant changes of CD11c expression were detected in spleen, TA, MA or LAD. Overall, our data support the conclusion that in a mouse model of Type 2 diabetes, CD11c positive cells accumulate in a duration of diabetes‐dependent manner in the perivascular adipose tissues, rather than in the vascular wall. The impact of these cells on vascular function therefore likely occurs through paracrine regulated mechanisms. Grant Funding Source: NIH HL085119