Aortic depressor nerve myelinated fibers in acute and chronic experimental diabetes.
BACKGROUND
Preliminary data from our laboratory have demonstrated baroreflex dysfunction as early as 5 days after the onset of experimental diabetes in rats. The aim of the present study was to determine the morphologic alterations of the aortic depressor nerve of rats submitted to acute (15 days) or chronic (12 weeks) experimental diabetes.


METHODS
Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) 15 days or 12 weeks before the experiments. Time control animals received vehicle. Under pentobarbital anesthesia the aortic depressor nerves were identified by means of electroneurographic recording simultaneously with the recording of arterial pressure. After identification, the aortic depressor nerves were prepared for light microscopy and our analysis only included the myelinated fibers.


RESULTS
Five of 10 aortic depressor nerves from animals with acute diabetes showed clear signs of axonal atrophy with significantly smaller average diameter of myelinated fibers (1.9 +/- 0.1 microm) and their axons (1.0 +/- 0.1 microm) than the time control (2.1 +/- 0.1 microm and 1.2 +/- 0.1 microm, respectively). Histograms of the G-ratio (ratio between axon diameter and total fiber diameter--an index of axonal atrophy) distribution of acute diabetic animal nerves were shifted to the left. All aortic depressor nerves from animals with chronic diabetes showed signs of axonal atrophy with the average diameter of myelinated fibers (2.3 +/- 0.1 microm) and their axons (1.2 +/- 0.1 microm) also being significantly smaller than the time control (2.6 +/- 0.2 microm and 1.5 +/- 0.1 microm, respectively).


CONCLUSIONS
These findings provide morphologic support for an impaired baroreflex during acute and chronic experimental diabetes.
Fazan
Valéria Paula Sassoli
VP
Department of Surgery and Anatomy, School of Medicine of Ribeirão Preto, USP, Ribeirão Preto, São Paulo, Brazil. vpsfazan@fmrp.usp.br
Salgado
Helio Cesar
HC
Barreira
Amilton Antunes
AA
D000208:Acute Disease; D000818:Animals; D001011:Aorta / Q000294:innervation* / Q000473:pathology; D001284:Atrophy; D001369:Axons / Q000473:pathology; D017704:Baroreflex / Q000502:physiology*; D002908:Chronic Disease; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000503:physiopathology*; D004195:Disease Models, Animal; D008297:Male; D009413:Nerve Fibers, Myelinated / Q000502:physiology* / Q000648:ultrastructure; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013311:Streptozocin / Q000633:toxicity
D013311:Streptozocin