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5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
Published on: July 3, 2013
Effect of chronic renal insufficiency on the function and metabolic parameters of the isolated rat heart
M Tutterová1, H Vavrínková, M Bohdanecká
1Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
Insights
Chronic renal insufficiency (CRI) in rats impairs heart function but improves ischemic tolerance. Uremic hearts show reduced basal function but better recovery after ischemia, linked to increased myocardial glycogen.
Area of Science:
- Nephrology
- Cardiology
- Metabolic Research
Background:
- Chronic renal insufficiency (CRI) is linked to cardiovascular disease, but mechanisms are unclear.
- Understanding these links is crucial for managing cardiovascular risks in CRI patients.
Purpose of the Study:
- Investigate myocardial functions and metabolic changes in a rat model of CRI.
- Assess cardiovascular disease risk factors in subtotally nephrectomized rats.
Main Methods:
- Subtotal nephrectomy in rats to induce CRI.
- Measurement of blood pressure, left ventricular hypertrophy, hypertriglyceridemia, and glucose tolerance.
- Assessment of isolated perfused heart function and response to ischemia-reperfusion.
Main Results:
- Nephrectomized rats developed hypertension, left ventricular hypertrophy, hypertriglyceridemia, and impaired glucose tolerance.
- Uremic rat hearts showed 20-30% reduced basal function (coronary/aortic flow, stroke volume).
- Uremic hearts exhibited improved recovery of aortic flow and stroke volume post-ischemia, with 50% higher pre-ischemic myocardial glycogen.
Conclusions:
- CRI in rats leads to cardiovascular risk factors and altered myocardial function.
- Despite reduced basal function, uremic hearts show enhanced tolerance and recovery from ischemia.
- Increased myocardial glycogen may contribute to the improved ischemic tolerance in CRI.
Abstract:
Chronic renal insufficiency (CRI) is often associated with cardiovascular disease; however, its underlying mechanisms are not completely understood. Therefore, in the present study, myocardial functions and metabolic changes were investigated using an animal model of CRI in subtotally nephrectomized rats. In addition, some other parameters, considered risk factors of cardiovascular diseases, were determined. Subtotal nephrectomy led to an elevation in blood pressure (144 +/- 2.8 vs 114 +/- 2.5 mm Hg), left ventricular hypertrophy (290 +/- 12 vs 200 +/- 40 mg/100 g b.w.), hypertriglyceridaemia (2.96 +/- 0.31 vs 0.77 +/- 0.07 mmol/l), and impaired glucose tolerance (AUC 836 +/- 12.4 vs 804 +/- 10.4 mmol x l(-1) x 120 min). Isolated perfused hearts of uraemic rats exhibited diminished basal functions (coronary and aortic flow, stroke volume) by 20-30% compared with the controls. Interestingly, the tolerance of isolated heart to global 20-min no-flow ischaemia was improved in uraemic rats. The most marked differences in heart function recovery during reperfusion concerned aortic flow (90 +/- 2.3 vs 66 +/- 10%) and stroke volume (97 +/- 2.7 vs 68 +/- 5.6% of pre-ischaemic values). Pre-ischaemic myocardial glycogen content was distinctly increased (by 50%) in uraemic rats compared with the controls.
