Effect of bariatric surgery on renal hemodynamics in obese rats

医学 肾血流 糖尿病 袖状胃切除术 血压 肾动脉 肥胖 外科 内科学 肾功能 泌尿科 减肥 内分泌学 胃分流术
作者
Sumit R. Monu
出处
期刊:Physiology [American Physiological Society]
卷期号:38 (S1)
标识
DOI:10.1152/physiol.2023.38.s1.5734598
摘要

Background: Obesity per se increases the risk of renal disease, and the true number is likely much higher after including obesity-associated diseases such as diabetes and hypertension. A previous study from my lab showed that higher glomerular capillary pressure (PGC), as a result of renal autodysregulation in obese Zucker rats (OZR), may play a central role in initiating glomerular damage in obesity. Bariatric surgery is one of the most effective treatments to maintain long-term weight loss and improve hypertension and diabetes. Recent evidence also indicates that obesity-related renal complications are significantly improved after bariatric surgery. However, whether bariatric surgery improves renal damage by normalizing renal autodysregulation is not clear. Hypothesis: In obese Zucker rats, bariatric surgery reduces renal damage in part by normalizing glomerular autoregulation by decreasing PGC and renal blood flow. Methods: 16 weeks old OZR were anesthetized with isoflurane, and the femoral artery was cannulated to continuously measure mean arterial pressure (MAP). Lean Zucker rats (LZR) served as a control. A midline incision was performed to expose the stomach and the left kidney. The left kidney was placed in a kidney cup to stabilize its movement. A laser flow probe was inserted in the renal cortex to continuously measure cortical blood flow (CBF). The blood glucose level was measured by a tail vein nick every 10 minutes. After 30-45 minutes of equilibration, bariatric surgery was performed using the vertical sleeve gastrectomy method. In a separate group of rats, in similar experimental settings, PGC was measured using the stop-flow pressure method by in vivo renal micropuncture instead of renal-CBF before and after bariatric surgery. Stop-flow pressure was used as an index of PGC. Results: Bariatric surgery (BS) did not change MAP in either LZR (before BS: 100.98±4.89 vs. after BS: 102.61±5.59 mmHg, n=3, p > 0.05) or OZR (before BS: 109.89±10.40 vs. after BS: 114.73±12.81 mmHg, n=3, p > 0.05). In LZR, renal CBF remained unchanged after bariatric surgery. However, in OZR, renal CBF was 36.4% decreased (n=3, p<0.05) after bariatric surgery. Similarly, PGC remained unchanged in LZR after bariatric surgery (before BS: 34.28±1.39 vs after BS: 32.08±1.73 mmHg, n=3, p > 0.05). However, in OZR, PGC was significantly reduced after bariatric surgery (before BS: 41.18±2.69 vs after BS: 32.02±1.73 mmHg, n=3, p<0.05). There was no change in blood glucose values in either LZR or OZR after bariatric surgery. Conclusion and Perspective: We conclude that bariatric surgery significantly decreases glomerular capillary pressure and renal cortical blood flow without affecting either blood pressure or blood glucose, at least in acute settings. This is the first study showing the direct effect of bariatric surgery on glomerular capillary pressure and renal cortical blood flow and may explain in part lower renal damage observed upon bariatric surgery. Henry Ford Institutional support This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

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