{'fraction_non_alphanumeric': 0.02102803738317757, 'fraction_numerical': 0.008566978193146417, 'mean_word_length': 5.406483790523691, '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}}
Chronic fluid and electrolyte imbalance contributes to brain inflammation and the development of cardiovascular complications in streptozotocin‐treated diabetic rats

We previously showed specific microglial activation within cardiovascular control centers, in the brains of streptozotocin (STZ) diabetic rats. Microglial activation within the PVN of STZ diabetic rats was not evident until the 6th week after STZ treatment, and was preceded by neuronal activation in the PVN and associated with chronic dehydration and electrolyte imbalance (1). Furthermore, giving STZ diabetic rats 1% saline to drink after the induction of diabetes increased blood pressure (BP) (2). Therefore, we sought to investigate the complex relationships among PVN microglial activation, the development of diabetic cardiovascular complications and the effect of saline intake. Male Sprague‐Dawley rats were given a single injection of STZ via the tail vein to induce diabetes. Throughout the experiment fluid intake and BP parameters were monitored in control rats and diabetic rats given tap water or saline to drink. Echocardiography was used to measure cardiac function and tail cuff was used to record BP. Microglial morphology was quantified using immunohistochemistry for CD11b (1). Here we show that, two weeks after the induction of diabetes in STZ diabetic rats drinking 1% saline, BP was elevated and microglial activation was prominent in the PVN in comparison to diabetic rats drinking tap water. However, by week 6, STZ diabetic rats given tap water to drink showed elevated polydipsia, blood parameters consistent with dehydration, activation of PVN microglia, and functional signs of cardiomyopathy, whereas STZ diabetic rats drinking 1% saline did not, suggesting a delicate balance between electrolyte intake and electrolyte loss in these animals. In a separate set of experiments STZ diabetic rats were given 0.9% saline,+/‐20 mM KCl or 1 mM MgCl to drink. At the second week after the induction of diabetes, rats drinking 0.9% saline showed no elevations in blood pressure; whereas STZ diabetic rats drinking saline + 20 mM KCl or 1 mM MgCl showed BP elevations. All STZ diabetic rats were given low level insulin supplementation to prevent dehydration and showed no sign of cardiomyopathy even after 10 weeks of diabetes. We conclude that neuroinflammation in the PVN and other cardiovascular control centers, secondary to chronic fluid and electrolyte imbalances may contribute to the development of diabetic complications and preventing dehydration may be therapeutic