Andrea Parmagnani

Medium term effects of a ketogenic diet and a Mediterranean diet on resting energy expenditure and respiratory ratio

Background Very low carbohydrate ketogenic type diets (VLCKD) have been shown to be more effective for body weight reduction and fat loss compared to balanced or low-calorie Mediterranean diets, at least in the short-medium term [1,2], although the underlying mechanisms of its efficacy are still not well understood. Despite being a diet in widespread use there are few data available regarding effects on respiratory ratio (RR) [3,4] and resting energy expenditure (REE) and, more specifically, there are no reports about the effects on RR following a return to a non ketogenic diet. The aim of this study was to compare the effects of a 20 day ketogenic Mediterranean diet with phytoextracts (KEMEPHY) and a low-calorie Mediterranean diet (MD) on RR and REE during and 20 days after finishing the ketogenic phase.

Flow and Volume Dependence of Rat Airway Resistance During Constant Flow Inflation and Deflation

Study ObjectivesThe aim of this study was to measure the flow and volume dependence of both the ohmic and the viscoelastic pressure dissipations of the normal rat respiratory system separately during inflation and deflation.MethodThe study was conducted in the Respiratory Physiology Laboratory in our institution. Measurements were obtained for Seven albino Wistar rats of both sexes by using the flow interruption method during constant flow inflations and deflations. Measurements included anesthesia induction, tracheostomy and positioning of a tracheal cannula, positive pressure ventilation, constant flow respiratory system inflations and deflations at two different volumes and flows.ResultsThe ohmic resistance exhibited volume and flow dependence, decreasing with lung volume and increasing with flow rate, during both inflation and deflation. The stress relaxation-related viscoelastic resistance also exhibited volume and flow dependence. It decreased with the flow rate at a constant lung volume during both inflation and deflation, but exhibited a different behavior with the lung volume at a constant flow rate (i.e., increased during inflations and decreased during deflations). Thus, stress relaxation in the rat lungs exhibited a hysteretic behavior.ConclusionsThe observed flow and volume dependence of respiratory system resistance may be predicted by an equation derived from a model of the respiratory system that consists of two distinct compartments. The equation agrees well with the experimental data and indicates that the loading time is the critical parameter on which stress relaxation depends, during both lung inflation and deflation.

The effect of angiotensin-converting enzyme inhibition by captopril on respiratory mechanics in healthy rats.

Context: Angiotensin stimulates smooth-muscle contraction. Accordingly, angiotensin-converting enzyme (ACE) inhibition is expected to decrease airway resistance. Objectives: To measure the effects of ACE inhibition on respiratory mechanics in healthy mammals. Materials and methods: We measured respiratory mechanics before and after i.p. ACE inhibitor captopril (100 mg/kg) in normal anaesthetised rats. The end-inflation occlusion method allowed the measurements of respiratory system elastance and ohmic and viscoelastic pressure dissipations. Respiratory system hysteresis and the elastic and resistive work of breathing were calculated. Results: Captopril induced a reduction of the ohmic and the total respiratory system resistances, while respiratory system hysteresis and elastance did not change. Accordingly, a reduction of the resistive and of the total work of breathing was observed. Conclusions: The captopril-induced reduction of airway resistance indicates that angiotensin modulates bronchomotor tone in basal conditions. ACE inhibition may positively affect respiratory system mechanics and work of breathing.

Body metabolic rate and electromyographic activities of antigravitational muscles in supine and standing postures

We measured metabolic (oxygen uptake, carbon dioxide production, respiratory ratio), cardio-circulatory (heart rate, systolic and diastolic arterial blood pressure, rate-pressure product, an index of myocardial oxygen consumption calculated by multiplying heart rate by systolic pressure) and electromyographic (integrated electromyographic activities of two antigravitational muscles of the lower limb, soleus and gastrocnemius) variables on 12 young healthy subjects in supine and standing positions at rest. We found statistically significant increments of oxygen uptake, carbon dioxide production, heart rate and integrated electromyographic activities in standing versus supine position. Rate-pressure product increased but not significantly, and no other significant changes were detected. We conclude that postural changes influence metabolic rate, antigravitational muscle reflex activities, and heart rate. A significant positive correlation was found between oxygen uptake and carbon dioxide production and integrated electromyographic activities of antigravitational muscles, while the same was not found for cardio-circulatory variables. These results suggest that the increased metabolic rate in standing position is, at least in part, due to antigravitational muscle tone.

Hippocampal cellular loss after brief hypotension

Brief episodes of hypotension have been shown to cause acute brain damage inanimal models. We used a rat hemorrhagic shock model to assess functionaloutcome and to measure the relative neuronal damage at 1, 4 and 14 dayspost-injury (3 min of hypotension). All rats underwent a neurological assessmentincluding motor abilities, sensory system evaluation and retrograde memory atpost-hypotensive insult. Brains were harvested and stained for Fluorojade C andNissl. Stereology was used to analyze Fluorojade C and Nissl stained brainsections to quantitatively detect neuronal damage after the hypotensive insult.Statistical analysis was performed using Graphpad Prism 5 with the Bonferronitest at a 95% confidence interval after ANOVA. A Mixed Effect Model was usedfor the passive avoidance evaluation. Stereologically counted fluorojadepositive cells in the hippocampus revealed significant differences in neuronalcell injury between control rats and rats that received 3 min of hypotension oneday after insult. Quantification of Nissl positive neuronal cells showed asignificant decrease in the number hippocampal cells at day 14. No changes infrontal cortical cells were evident at any time, no significative changes inneurological assessments as well. Our observations show that brief periods ofhemorrhage-induced hypotension actually result in neuronal cell damage inSprague–Dawley rats even if the extent of neuronal damage that wasincurred was not significant enough to cause changes in motor or sensorybehavior.

Repetitive intraperitoneal caspase-3 inhibitor and anesthesia reduces neuronal damage.

Caspase inhibitors are usually administered intracranially. There’s very limited evidence showing that they can be used intraperitoneally, and still have a beneficial effect. We tested the hypothesis that, during focal cerebral ischemia, caspase inhibitors when used in combination with an anesthetic agent results in a significantly reduction in the neuronal damage. Male Sprague Dawley rats were randomly divided into six different groups: control, Isoflurane, Propofol, Isoflurane and Caspase-3 inhibitor intraperitoneally (IP), propofol and Caspase-3 inhibitor IP and only caspase-3 inhibitor, during post-ischemia. Neurological evaluation and histochemical analysis was assessed post-ischemia. The treatment proposed, resulted in a significant decrease in the cerebral infarction volume. Combination of treatments, and caspase-3 inhibitor alone significantly decreased the number of TUNEL and cleaved caspase-3 positive cells in the boundary area of cortical infarction. IP administration appears to reach cerebral targets similarly to intracerebral model. This combination reduces the neurological damage caused by focal cerebral ischemia.

Daily variations of spirometric indexes and maximum expiratory pressure in young healthy adults.

In order to document possible variations in the main spirometric indexes in young healthy adults due to the time of the day, we performed standard and complete spirometric measurements at three different hours of the same day (8 am, 4 pm and 12 am) in 33 healthy, non-smoking young volunteers of both sexes. An index of airway resistance was also calculated. We confirm a general worsening of spirometric indexes at night-time compared to daily hours. This result also includes the main effort-independent indexes which were not previously measured. Maximum expiratory pressure does not show daily variations, while an index of respiratory system resistance exhibits a progressive increase from morning to night.

Daily variations in lung volume measurements in young healthy adults

Lung volume measurements were performed on 30 healthy young volunteers of both genders at three different times of the day (8 am, 4 pm, and 12 am). They included total lung capacity, functional residual capacity (FRC), vital capacity, residual volume (RV), inspiratory and expiratory reserve volumes, and inspiratory capacity, and were technically performed according to well-known, recently stated, international standards.We found statistical increments of the mean values of total lung capacity, FRC, and RV at 4 pm with respect to both 8 am and 12 am The possible mechanisms explaining these findings are addressed, including daily variations of respiratory system compliance, alveolar surfactant activity, and abdominal wall and diaphragmatic muscle tonic activity.

Metabolic and ventilatory effects of oral glucose load at rest and during incremental aerobic muscular work in young healthy adults

We measured respiratory ratio (RR), pulmonary ventilation (VE) and end-tidal carbon dioxide partial pressure (ETPCO2) at rest and during cycling aerobic workloads (20%, 40%, 60% of estimated maximal oxygen uptake). Measurements were taken after overnight fasting and after an oral glucose load. RR, VE and ETPCO2 increased with workload. Glucose load caused RR and VE increments at rest (0.75 ± 0.01 vs. 0.86 ± 0.02, p < 0.01, and 10.8 ± 0.43 vs. 12.1 ± 0.49 l/min, p < 0.01, respectively) and for each workload (20% estimated maximal oxygen uptake: 0.77 ± 0.01 vs. 0.855 ± 0.02, p < 0.01, and 16.2 ± 0.73 vs. 17.7 ± 0.8 l/min, p < 0.01; 40% estimated maximal oxygen uptake: 0.76 ± 0.02 vs. 0.82 ± 0.01, p < 0.01, and 25.9 ± 1.1 vs. 28.3 ± 1.3 l/min, p < 0.05; 60% estimated maximal oxygen uptake: 0.85 ± 0.02 vs. 0.91 ± 0.02, p < 0.01, and 37.4 ± 1.7 vs. 40.9 ± 1.9 l/min, p < 0.05) but ETPCO2 did not change. The differences in RR before and after glucose load became smaller as the workload increased. Linear regression analysis of VE and carbon dioxide output yielded virtually identical results for both fasting and glucose load conditions. We have concluded that: a) for the metabolic carbon dioxide load increment due to glucose-induced RR increment, the physiological response is an increase of VE at all workloads. This response modulates constant ETPCO2 values; b) on workload increment, skeletal muscle increasingly utilises more and more glycogen stores, regardless of the blood glucose availability. This reduces the usefulness of dietary manipulations decreasing carbon dioxide metabolic load during muscular work in respiratory failure; c) the absolute value of metabolic carbon dioxide load exerts a role in ventilation regulation at rest and during aerobic exercise.