Search PubMed⌕ Search

Biomedical subjects

Catherine S H Sassoon

Publications and source records attributed to Catherine S H Sassoon.

6 recordsLinked to original sources

Early effects of mechanical ventilation on isotonic contractile properties and MAF-box gene expression in the diaphragm.

This study aimed to determine the time-dependent effects of diaphragmatic inactivity on its maximum shortening velocity (V(max)) and the muscle atrophy F-box (MAF-box, atrogin-1) gene expression during controlled mechanical ventilation (CMV). Twenty-four New Zealand White rabbits were grouped into 1 day, 2 days, and 3 days of CMV and controls in equal numbers. The in vitro isotonic contractile properties of the diaphragm were determined. In addition, myosin heavy chain protein and mRNA, myosin light chain, MAF-box mRNA, and volume density of abnormal myofibrils were measured. Tetanic force decreased, and V(max) increased from control of 6.4 to 6.6, 7.7, and 8.1 muscle lengths per second after 1, 2, and 3 days of CMV, respectively (P < 0.02). The increased V(max) compensated for the decreased tetanic force; consequently, compared with the controls, maximum power output was unchanged after 3 days of CMV. V(max) correlated with the volume density of abnormal myofibrils [y = 0.1x + 5.7 (r = 0.87, P < 0.01)]. In the diaphragm, MAF-box was overexpressed (355% of control) after 1 day of CMV, before the evidence of structural myofibril disarray. In conclusion, CMV produced a time-dependent increase in V(max) that was associated with the degree of myofibrillar disarray and independent of changes in myosin isoform expression. Furthermore, CMV produced an increase in MAF-box mRNA levels that may be partially or completely responsible for the degree of myofibrillar disarray resulting from CMV.

Animals↗

Potential advantages of patient-ventilator synchrony.

During conventional mechanical ventilation, fixed set pressure, flow, and tidal volume result in a mismatch between patient and ventilator inspiratory time and in a patient's inability to adapt to changing ventilatory demand. Synchrony between the patient and ventilator improves neuromuscular coupling and the ability to adapt to increased ventilatory demand or loading. The sensation of dyspnea prevents ineffective inspiratory efforts and attenuates periodic breathing during sleep.

Humans↗

Assist-control mechanical ventilation attenuates ventilator-induced diaphragmatic dysfunction.

Controlled mechanical ventilation induced a profound diaphragm muscle dysfunction and atrophy. The effects of diaphragmatic contractions with assisted mechanical ventilation on diaphragmatic isometric, isotonic contractile properties, or the expression of muscle atrophy factor-box (MAF-box), the gene responsible for muscle atrophy, are unknown. We hypothesize that assisted mechanical ventilation will preserve diaphragmatic force and prevent overexpression of MAF-box. Studying sedated rabbits randomized equally into control animals, those with 3 days of assisted ventilation, and those with controlled ventilation, we assessed in vitro diaphragmatic isometric and isotonic contractile function. The concentrations of contractile proteins, myosin heavy chain isoform, and MAF-box mRNA were measured. Tetanic force decreased by 14% with assisted ventilation and 48% with controlled ventilation. Maximum shortening velocity tended to increase with controlled compared with assisted ventilation and control. Peak power output decreased 20% with assisted ventilation and 41% with controlled ventilation. Contractile proteins were unchanged with either modes of ventilation; myosin heavy chain 2X mRNA tended to increase and that of 2A to decrease with controlled ventilation. MAF-box gene was overexpressed with controlled ventilation. We conclude that preserving diaphragmatic contractions during mechanical ventilation attenuates the force loss induced by complete inactivity and maintains MAF-box gene expression in control.

Actins↗

Effects of CPAP therapy on cardiovascular variability in obstructive sleep apnea: a closed-loop analysis.

To determine the long-term effects of continuous positive airway pressure (CPAP) therapy on cardiovascular variability, we measured R-R interval (RR), systolic blood pressure (SBP) and respiration (DeltaV) in 13 awake, supine patients with moderate-to-severe obstructive sleep apnea (OSA), before and after ~6 mo of treatment. Using these data, we estimated the dynamics of the following components of a closed-loop circulatory control model: 1) the baroreflex component, 2) the neural coupling of DeltaV to RR or respiratory sinus arrhythmia (RSA), 3) the mechanical effects of respiration (MER) on SBP, and 4) the circulatory dynamics (CID) component, which is responsible for the feedforward effect of RR fluctuations on SBP. Baroreflex and RSA gains increased whereas MER and CID gains decreased in compliant subjects whose average CPAP use was >3 h/night. In contrast, baroreflex, RSA, and MER gains remained unchanged and CID gain increased in noncompliant subjects. Other summary measures were unchanged in both groups, except for mean RR, which increased in compliant patients. Closed-loop analysis provides a simple but sensitive means for quantitatively assessing cardiovascular control in OSA by using data collected from a single, nonintrusive test procedure.

Adult↗

Altered diaphragm contractile properties with controlled mechanical ventilation.

This study shows that, over time, diaphragm inactivity with controlled mechanical ventilation (CMV) decreases diaphragm force and produces myofibril damage contributing to the reduced force. We measured in vivo and in vitro diaphragm contractile and morphological properties in 30 sedated rabbits grouped (n = 6) as follows: 1 or 3 days of CMV, 1 or 3 days of 0 cmH(2)O continuous positive airway pressure, and control. The CMV rate was set sufficient to suppress diaphragm electrical activity. Compared with the control group, phrenic-stimulated maximum transdiaphragmatic pressure did not decrease with continuous positive airway pressure but decreased to 63% after 1 day of CMV and to 49% after 3 days of CMV. The in vitro tetanic force decreased to 86% after 1 day of CMV and to 44% after 3 days of CMV. After 3 days of CMV, significant myofibril damage occurred in the diaphragm but not in the soleus. The decrease in tetanic force correlated with the volume density of abnormal myofibrils. We conclude that CMV had a detrimental effect on diaphragm contractile properties.

Anatomy, Cross-Sectional↗