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1 Howard Florey Institute
2 University of Newcastle
3 University of Melbourne
* To whom correspondence should be addressed. E-mail: rmca{at}florey.edu.au.
The sympathetic actions of medullary raphé neurons on heart rate (HR), atrioventricular conduction, ventricular contractility and rate of relaxation were examined in 9 urethane-anesthetized (1-1.5 g/kg i.v.), artificially ventilated rats that had been adrenalectomized and given atropine methyl nitrate (1mg/kg i.v.). Mean arterial pressure (MAP), ECG and left ventricular pressure were recorded. The peak rates of rise and fall in left ventricular pressure (LVdP/dtmax, LVdP/dtmin) and the stimulus-R interval ($-R) were measured during brief periods of atrial pacing at 8.5 Hz before and after ventral medullary raphé neurons were activated by d,l-homocysteic acid (DLH, 0.1M) or inhibited by GABA (0.3M) in local microinjections (90nl). LVdP/dtmax values were corrected for the confounding effect of MAP, determined at the end of experiments after giving propranolol (1 mg/kg i.v.) to block sympathetic actions on the heart. DLH microinjections into the ventral medullary raphé region increased HR by 44±2bpm, LVdP/dtmax by 1055±156mmHg/s and the negative value of LVdP/dtmin by 729±204 mmHg/s (all P<0.001), while shortening $-R interval by 2.8±0.8ms (P<0.01). GABA microinjections caused no significant change in HR, LVdP/dtmax or $-R interval, but reduced LVdP/dtmin from -5974±93 to -5548±171 mmHg/s and MAP from 115±4 to 105±5 mmHg (both P<0.01). Rises in tail skin temperature confirmed that GABA injections effectively inhibited raphé neurons. When activated, neurons in the ventral medullary raphé region thus enhance atrioventricular conduction, ventricular contractility and relaxation in parallel with HR, but they provide little or no tonic sympathetic drive to the heart.
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