title: Viscerosomatic interaction induced by myocardial ischemia in conscious dogs.
abstract: Studies tested the hypothesis that myocardial ischemia induces increased paraspinal muscular tone localized to the T(2)-T(5) region that can be detected by palpatory means. This is consistent with theories of manual medicine suggesting that disturbances in visceral organ physiology can cause increases in skeletal muscle tone in specific muscle groups. Clinical studies in manual and traditional medicine suggest this phenomenon occurs during episodes of myocardial ischemia and may have diagnostic potential. However, there is little direct evidence of a cardiac-somatic mechanism to explain these findings. Chronically instrumented dogs [12 neurally intact and 3 following selective left ventricular (LV) sympathectomy] were examined before, during, and after myocardial ischemia. Circumflex blood flow (CBF), left ventricular contractile function, electromyographic (EMG) analysis, and blinded manual palpatory assessments (MPA) of tissue over the transverse spinal processes at segments T(2)-T(5) and T(11)-T(12) (control) were performed. Myocardial ischemia was associated with a decrease in myocardial contractile function and an increase in heart rate. MPA revealed increases in muscle tension and texture/firmness during ischemia in the T(2)-T(5) segments on the left, but not on the right or in control segments. EMG demonstrated increased amplitude for the T(4)-T(5) segments. After LV sympathectomy, MPA and EMG evidence of increased muscle tone were absent. In conclusion, myocardial ischemia is associated with significant increased paraspinal muscle tone localized to the left side T(4)-T(5) myotomes in neurally intact dogs. LV sympathectomy eliminates the somatic response, suggesting that sympathetic neural traffic between the heart and somatic musculature may function as the mechanism for the interaction.
authors.affiliation: Dept. of Integrative Physiology, Univ. of North Texas Health Science Center, 3500 Camp Bowie Blvd., Fort Worth, TX 76107, USA. gwirtzp@hsc.unt.edu
authors.forename: Patricia A
authors.initials: PA
authors.lastname: Gwirtz
authors.forename: Jerry
authors.initials: J
authors.lastname: Dickey
authors.forename: David
authors.initials: D
authors.lastname: Vick
authors.forename: Maurice A
authors.initials: MA
authors.lastname: Williams
authors.forename: Brian
authors.initials: B
authors.lastname: Foresman
mesh_terms: D000818:Animals; D002319:Cardiovascular System / Q000503:physiopathology; D023921:Coronary Stenosis / Q000503:physiopathology; D004285:Dogs; D004576:Electromyography; D005260:Female; D006321:Heart / Q000294:innervation / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D008297:Male; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology*; D009200:Myocardial Contraction / Q000502:physiology*; D017202:Myocardial Ischemia / Q000503:physiopathology*; D009475:Neurons, Afferent / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology / Q000601:surgery; D013904:Thoracic Vertebrae