title: Effect of acute anaesthesia on synthesis of contractile and non-contractile proteins of heart muscle and mixed proteins of types I and II fibre rich skeletal muscles of rat.
abstract: OBJECTIVE
  The aim of the study was to determine whether the deleterious effects of anaesthesia on cardiac muscle function were due to disturbance of protein synthesis. Comparative investigations were made on anaerobic and aerobic skeletal muscles, and plasma insulin and growth hormone levels were also measured to see if these were mediating factors.
  
  
  METHODS
  Rats were subjected to acute methoxyfluorane anaesthesia for 10 min. At the end of the study they were killed and plasma growth hormone and insulin were measured. Rates of cardiac and skeletal muscle protein synthesis were also determined with a flooding dose of L[4-3H]phenylalanine.
  
  
  METHODS
  Muscle samples were obtained from male Sprague-Dawley rats, weight 191-222 g.
  
  
  RESULTS
  Anaesthesia reduced the fractional rate of myocardial mixed protein synthesis and synthesis relative to RNA (p less than 0.05). The anaesthesia induced decrease in the synthesis rates of cardiac contractile proteins (p less than 0.05) was greater than the decrease in the non-contractile protein fractions (p greater than 0.05). Soleus (aerobic, Type I) and plantaris (anaerobic, Type II) muscle rates of protein synthesis were unaltered in response to anaesthesia (p greater than 0.05). Plasma insulin concentrations increased in response to acute anaesthesia (p less than 0.05), but the insulin effect was depressed by the flooding dose of phenylalanine (p less than 0.05). Plasma growth hormone levels were not altered in response to anaesthesia (p greater than 0.05). Thus, the changes in cardiac protein synthesis could not be ascribed to these hormones.
  
  
  CONCLUSIONS
  Synthesis of cardiac contractile proteins is selectively sensitive to the effects of acute anaesthesia even in the presence of high plasma insulin concentrations. The fall in cardiac protein synthesis may be a result of the negative inotropic effects of general anaesthesia.
authors.affiliation: Department of Cardiology, King's College School of Medicine and Dentistry, London, United Kingdom.
authors.forename: T
authors.initials: T
authors.lastname: Siddiq
authors.forename: P J
authors.initials: PJ
authors.lastname: Richardson
authors.forename: I A
authors.initials: IA
authors.lastname: Hashim
authors.forename: V R
authors.initials: VR
authors.lastname: Preedy
mesh_terms: D000768:Anesthesia, General; D000818:Animals; D003864:Depression, Chemical; D013006:Growth Hormone / Q000097:blood; D007328:Insulin / Q000097:blood; D008297:Male; D008733:Methoxyflurane; D009124:Muscle Proteins / Q000096:biosynthesis*; D009132:Muscles / Q000378:metabolism*; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D007328:Insulin; D009124:Muscle Proteins; D008733:Methoxyflurane; D013006:Growth Hormone