Function of canine diaphragm with hypovolemic shock and beta-adrenergic blockade

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Abstract
The effects of hypovolemia and .beta.-adrenergic stimulation on the decrease in force generation by the diaphragm [transdiaphragmatic pressure (Pdi)] during electrical stimulation of the phrenic nerves for 1 h was studied in anesthetized mongrel dogs. In 7 normovolemic dogs with arterial pressure (Pa) of .apprx. 125 Torr, Pdi fell .apprx. 48% from an initial value of 35 .+-. 4.8 Torr. In dogs made moderately hypovolemic, Pdi was actually higher than with normovolemia (P < 0.01). In dogs made severely hypovolemic, Pa .apprx. 50 Torr, Pdi at the start of pacing was less than with normovolemia (25 .+-. 1.5 Torr) and remained so during phrenic nerve stimulation. When .beta.-adrenergic blockade with propranolol was added to moderate hypovolemia, the values of Pdi became similar to those of severe hypovolemia. Analysis of the relative contributions of gastric pressure and pleural pressure revealed that the factor responsible for maintaining Pdi with moderate hypovolemia was pleural pressure. Changes in thoracic gas volume and chest wall configuration did not explain the changes seen in diaphragm function. Analysis of the relationship between rib cage motion and pleural pressure confirmed the finding of the greater pleural pressure generation with sympathetic stimulation that accompanies hypovolemia. These studies demonstrated that severe hypovolemia impaired diaphragm function, diaphragm function was maintained with moderate hypovolemia by .beta.-adrenergic stimulation, and with hypovolemia-associated sympathetic stimulation there was an increase in force generation by the intercostal muscles.