Reflex sympathetic tachycardia during intravenous infusions in chronic spinal cats.
The reflex tachycardia elicited by rapid intravenous infusions of a blood substitute was studied in 21 chronic cats with spinal sections at C8. All animals could breath spontaneously. The day after section the average resting heart rate (HR) and arterial pressure (AP) were 109 beats/min and 98/67 mmHg, respectively. Vagal blockade with atropine (0.5-0.7 mg/kg iv) was performed prior to each infusion, increasing the average HR To 127 beats/min. In 39 infusions in 21 cats the average increase in HR was 10 beats/min (range from -6 to +22 beats/min). A tachycardia was observed in all but five trials, four of which were obtained in two cats that subsequently responded with a tachycardia. In seven animals the neural circuit mediating the response was partially or totally interrupted by section of several thoracic dorsal roots (T1-T4 or T1-T6) and of the spinal cord at the inferior level of these sections (between T6 and T7). The tachycardia response was progressively reduced and finally abolished by these procedures. These experiments indicate that spinal neural mechanisms are likely to contribute to the phenomenon first described by Bainbridge.
Reflex sympathetic tachycardia during intravenous infusions in chronic spinal cats. The reflex tachycardia elicited by rapid intravenous infusions of a blood substitute was studied in 21 chronic cats with spinal sections at C8. All animals could breath spontaneously. The day after section the average resting heart rate (HR) and arterial pressure (AP) were 109 beats/min and 98/67 mmHg, respectively. Vagal blockade with atropine (0.5-0.7 mg/kg iv) was performed prior to each infusion, increasing the average HR To 127 beats/min. In 39 infusions in 21 cats the average increase in HR was 10 beats/min (range from -6 to +22 beats/min). A tachycardia was observed in all but five trials, four of which were obtained in two cats that subsequently responded with a tachycardia. In seven animals the neural circuit mediating the response was partially or totally interrupted by section of several thoracic dorsal roots (T1-T4 or T1-T6) and of the spinal cord at the inferior level of these sections (between T6 and T7). The tachycardia response was progressively reduced and finally abolished by these procedures. These experiments indicate that spinal neural mechanisms are likely to contribute to the phenomenon first described by Bainbridge.