Electrolytic lesions of the ventrolateral medulla, coinciding with the A1 catecholamine cells of the conscious rabbit (A1 lesions) cause acute hypertension and bradycardia and in some animals, pulmonary oedema. We have assessed the change in cardiac performance after an A1 lesion, the role of cardiac autonomic effectors in this change; and the mechanism of the pulmonary oedema. Following A1 lesions there was a profound (over 100%) rise in total peripheral resistance and a fall in cardiac output which was mainly due to a fall in stroke volume since it occurred even in animals in which the heart rate was held constant by atrial pacing. This reduced stroke volume occurred despite a 40% increase in myocardial contractility (peak LV dP/dt) and elevation of left ventricular end diastolic pressure. p-Adrenoceptor blockade with propranolol abolished the rise in peak LV dP/dt, while vagal blockade with methylscopolamine abolished the bradycardia and combined blockade with propranolol and methylscopolamine abolished the rise in peak LV dP/dt and reduced the bradycardia. In rabbits which developed pulmonary oedema, left ventricular end diastolic pressure rose to 35 ± 3.5 compared to 16 ± 2.7 mmHg in those which did not, suggesting that the pulmonary oedema was due to raised left ventricular filling pressure.
|Number of pages||8|
|Journal||Journal of Hypertension|
|Publication status||Published - Aug 1984|
- A1 lesions
- Cardiac performance
- Myocardial contractility
- Pulmonary oedema