Short- and long-term modulation of microvascular responses in streptozotocin-induced diabetic rats by glycosylated products.

Objective: This study aimed to determine the role of early and late glycation products in modulating inflammation in early diabetes.

Materials: Sprague-Dawley rats (130-170 g) were injected with streptozotocin (75 mg/kg, ip) and treated with daily aminoguanidine (AG, 25 mg/kg, ip) or vehicle for 2 or 4 weeks.

Methods: The base of a vacuum-induced blister raised on the hind paw was perfused with substance P (SP, 1 microM) and sodium nitroprusside (SNP, 100 microM).

Effects of diabetes on creatine kinase activity in streptozotocin-diabetic rats.

Objective: To study the effect of diabetes on the creatine kinase (CK) activity in different tissues of streptozotocin-induced diabetic rats.

Methods: Serum samples, heart, extensor digitorum longus, brain and bladder were collected from both streptozotocin-induced diabetic rat and control group. Ck was measured by enzymologic method.

Endothelin and free radicals modulate microvascular responses in streptozotocin-induced diabetic rats.

The quantitative contribution of endothelin and free radicals in modulating peripheral endothelial and smooth muscle-dependent vascular responses in 4 weeks streptozotocin-induced diabetic rats was investigated. Skin blood flow was monitored in base of blisters raised on the hind footpad. Smooth muscle-dependent vasodilation was tested using sodium nitroprusside (SNP).

Effect of chronic sciatic nerve lesion on the neurogenic inflammatory response in intact and acutely injured denervated rat skin.

A supersensitivity to the neuropeptide substance P (SP) has been shown to develop in post-terminal membranes of many denervated tissues. This study examined changes in the sensitivity of post-terminal vascular receptors to SP and calcitonin gene-related peptide (CGRP) in rat skin microvasculature following sciatic nerve section. In anaesthetised rats, 0.

Beta A4(25-35) modulates substance P effect on rat skin microvasculature in aged rats: pharmacological manipulation using SEC-receptor ligands.

The primary constituent of the senile plaque core in Alzheimer's disease (AD) is the beta-amyloid protein (beta A4). A discrete 11 amino acid fragment of the beta A4, beta A4(25-35), has been implicated in mediating in vitro neurotoxicity and an inflammatory response surrounding senile plaques in AD via interaction with the Serpin Enzyme Complex (SEC) receptor. Substance P (SP), a neuropeptide of the tachykinin family and a major mediator of neurogenic inflammation, shows sequence homology to beta A4(25-35) and has been shown to protect against the neurotoxicity of beta-amyloid.