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Piglet Model (piglet + model)
Selected AbstractsMorphological and hemodynamic magnetic resonance assessment of early neonatal brain injury in a piglet modelJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 1 2004Berit H. Munkeby MD Abstract Purpose To investigate the utility of functional and morphological magnetic resonance imaging (MRI) to assess the extent of brain injury in a hypoxia-ischemia (HI) piglet model and further to validate that the desired ischemic injury was successfully induced. Materials and Methods MRI was performed at 1.5 T in anesthetized piglets (N = 10, age = 12-36 hours). Relative cerebral blood flow (rCBF), time-to-peak (TTP) contrast, and apparent diffusion coefficient (ADC) were estimated at different time points pre-, during, and post-HI. The effect following bilateral clamping of the carotid arteries was assessed by contrast-enhanced MR angiography (MRA) and phase contrast MR angiography (PCA) (N = 4). Results A linear correlation was observed between relative cerebral perfusion reduction and cerebral ADC during HI (r2 = 0.85, P < 0.05). There was no correlation between rCBF reduction during 30 minutes of HI and cerebral ADC after 30 or 150 minutes of reperfusion/reoxygenation (RR). Conclusion The combination of morphological and functional (perfusion and diffusion) MRI enabled consistent assessment of both the presence and absence of complete occlusion as well as the functional significance of the occlusion. J. Magn. Reson. Imaging 2004;20:8,15. © 2004 Wiley-Liss, Inc. [source] Protective ventilation to reduce inflammatory injury from one lung ventilation in a piglet modelPEDIATRIC ANESTHESIA, Issue 4 2010MARY C. THEROUX MD Summary Objectives:, To test the hypothesis that protective ventilation strategy (PVS) as defined by the use of low stretch ventilation (tidal volume of 5 ml·kg,1 and employing 5 cm of positive end expiratory pressure (PEEP) during one lung ventilation (OLV) in piglets would result in reduced injury compared to a control group of piglets who received the conventional ventilation (tidal volume of 10 ml·kg,1 and no PEEP). Background:, PVS has been found to be beneficial in adults to minimize injury from OLV. We designed the current study to test the beneficial effects of PVS in a piglet model of OLV. Methods:, Ten piglets each were assigned to either ,Control' group (tidal volume of 10 ml·kg,1 and no PEEP) or ,PVS' group (tidal volume of 5 ml·kg,1 during the OLV phase and PEEP of 5 cm of H2O throughout the study). Experiment consisted of 30 min of baseline ventilation, 3 h of OLV, and again 30 min of bilateral ventilation. Respiratory parameters and proinflammatory markers were measured as outcome. Results:, There was no difference in PaO2 between groups. PaCO2 (P < 0.01) and ventilatory rate (P < 0.01) were higher at 1.5 h OLV and at the end point in the PVS group. Peak inflating pressure (PIP) and pulmonary resistance were higher (P < 0.05) in the control group at 1.5 h OLV. tumor necrosis factor-alpha (P < 0.04) and IL-8 were less (P < 0.001) in the plasma from the PVS group, while IL-6 and IL-8 were less (P < 0.04) in the lung tissue from ventilated lungs in the PVS group. Conclusions:, Based on this model, PVS decreases inflammatory injury both systemically and in the lung tissue with no adverse effect on oxygenation, ventilation, or lung function. [source] Hypercapnic acidosis and compensated hypercapnia in control and pulmonary hypertensive piglets,PEDIATRIC PULMONOLOGY, Issue 2 2003K. Jane Lee MD Abstract Low tidal volume/inspiratory pressure ventilator strategies result in hypercapnia, which has been shown to increase pulmonary vasomotor tone. This may be particularly detrimental in infants and children with preexistent pulmonary hypertension. In this study, a piglet model of chronic hypoxia-induced pulmonary hypertension was used to test the hypotheses that: 1) the effects of hypercapnic acidosis are exaggerated by preexistent pulmonary hypertension; and 2) the pulmonary hemodynamic effects of hypercapnic acidosis are attenuated by normalizing pH. Pulmonary hypertension was induced by 2 weeks of hypoxia. Hemodynamic responses were measured in control and pulmonary hypertensive piglets during both normoxia and hypoxia under normocapnic, hypercapnic acidotic, and compensated hypercapnic conditions. We found that: 1) hypercapnic acidosis increased both normoxic and hypoxic pulmonary vascular resistance index (PVRI) in control piglets; 2) the pressor effects of hypercapnia were not attenuated by infusing bicarbonate to normalize the pH; and 3) piglets with chronic hypoxia-induced pulmonary hypertension had elevated baseline normoxic and hypoxic PVRI, but responded to hypercapnic acidosis and compensated hypercapnia in a similar way to control piglets. These data suggest that acute hypercapnic acidosis may have deleterious effects on the pulmonary hemodynamics of normal and pulmonary hypertensive subjects which may not be acutely reversed by buffering the pH. Pediatr Pulmonol. 2003; 36:94,101. © 2003 Wiley-Liss, Inc. [source] |