Francesca Iacobellis1,2, Teresa Segreto3, Daniela Berritto3, Francesca Nettuno3, Santolo Cozzolino4, Daniele Di Napoli4, Marco Montella5, Raffaele Natella3, Salvatore Cappabianca3, Luca Brunese6, Roberto Grassi3. 1. Department of Radiology, University of Campania "L. Vanvitelli", Piazza Miraglia 2, 80138, Naples, Italy. iacobellisf@gmail.com. 2. Biotechnology's Center, "A. Cardarelli" Hospital, Via Cardarelli 9, 80131, Naples, Italy. iacobellisf@gmail.com. 3. Department of Radiology, University of Campania "L. Vanvitelli", Piazza Miraglia 2, 80138, Naples, Italy. 4. Biotechnology's Center, "A. Cardarelli" Hospital, Via Cardarelli 9, 80131, Naples, Italy. 5. Division of Pathology, Department of Public, Clinic and Preventive Medicine, Second University of Naples, Piazza Miraglia 2, 80138, Naples, Italy. 6. Department of Radiology, University of Molise, Via Francesco de Sanctis, 1, 86100, Campobasso, Italy.
Abstract
AIM: To create an animal model of acute renal ischemia induced by systemic hypoperfusion, controllable and reproducible to study, in real time, hemorrhagic shock changes with micro-imaging. ANIMALS AND METHODS: Hemorrhagic shock was induced in rats activating a syringe pump setup to remove 1 mL/min of blood, through the femoral artery catheter. The withdrawal was continued until the mean arterial pressure (MAP) dropped to 25-30 mmHg. For the next 60 min, the MAP was maintained at a constant pressure value, by automatic pump infusion and withdrawal. Micro-ultrasound imaging was performed using the Vevo 2100 system with the MS250 transducer (13-24 MHz). Renal size, morphology and echogenicity were evaluated in B-mode. Renal blood flow was evaluated using color and PW-Doppler. RESULTS: After 1 h of ischemia, B-mode images documented slight changes in kidney echogenicity. Color and PW-Doppler analysis showed a reduction in renal blood flow in kidneys during the hypoperfusion with a progressive and significant change from baseline values of resistive index (RI). At the histological evaluation, 60 min of hypoperfusion resulted in ischemic changes in the kidneys. CONCLUSIONS: The results of this experimental study encourage the use of the described model to study acute renal ischemia trough severe hypoperfusion. The histological data confirmed that the model was able to produce injury in renal parenchyma. It can be used to assess acute ischemic damage not only in the kidney but also in other organs by using all available dedicated small animals imaging techniques.
AIM: To create an animal model of acute renal ischemia induced by systemic hypoperfusion, controllable and reproducible to study, in real time, hemorrhagic shock changes with micro-imaging. ANIMALS AND METHODS: Hemorrhagic shock was induced in rats activating a syringe pump setup to remove 1 mL/min of blood, through the femoral artery catheter. The withdrawal was continued until the mean arterial pressure (MAP) dropped to 25-30 mmHg. For the next 60 min, the MAP was maintained at a constant pressure value, by automatic pump infusion and withdrawal. Micro-ultrasound imaging was performed using the Vevo 2100 system with the MS250 transducer (13-24 MHz). Renal size, morphology and echogenicity were evaluated in B-mode. Renal blood flow was evaluated using color and PW-Doppler. RESULTS: After 1 h of ischemia, B-mode images documented slight changes in kidney echogenicity. Color and PW-Doppler analysis showed a reduction in renal blood flow in kidneys during the hypoperfusion with a progressive and significant change from baseline values of resistive index (RI). At the histological evaluation, 60 min of hypoperfusion resulted in ischemic changes in the kidneys. CONCLUSIONS: The results of this experimental study encourage the use of the described model to study acute renal ischemia trough severe hypoperfusion. The histological data confirmed that the model was able to produce injury in renal parenchyma. It can be used to assess acute ischemic damage not only in the kidney but also in other organs by using all available dedicated small animals imaging techniques.