Reduced neurogenic inflammation in streptozotocin-diabetic rats due to microvascular changes but not to substance P depletion.
The effect of streptozotocin treatment (65 mg/kg i.v.) on plasma protein extravasation, nociception, and the content of substance P immunoreactivity (SP-IR) and somatostatin immunoreactivity (SOM-IR) was investigated in the rat. Twelve days after treatment, the neurogenic plasma extravasation induced by 5% mustard oil was reduced by 67% in the skin of the hind paw. Extravasation caused by SP, a putative mediator of neurogenic inflammation, was also reduced by 61% in the abdominal skin. While calcitonin gene-related peptide (CGRP) potentiated the SP-induced extravasation in control rats, no potentiation was observed in diabetic rats. Thermonociception or chemonociception was unchanged after streptozotocin treatment. The content of SP-IR and SOM-IR in sensory nerves or spinal ganglia was also not altered. These results indicate that the impairment of neurogenic inflammation in diabetic rats is not the result of depletion of neurogenic mediators like SP. Changes of the microvasculature at the leakage site appear to account for the effects observed.
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D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D005260:Female; D007249:Inflammation / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation; D009419:Nerve Tissue Proteins / Q000502:physiology; D009619:Nociceptors / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D013004:Somatostatin / Q000502:physiology*; D013373:Substance P / Q000502:physiology*
D001786:Blood Glucose; D009419:Nerve Tissue Proteins; D013373:Substance P; D013004:Somatostatin