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Studies on the mechanism of pulmonary vascular responses to miliary pulmonary embolism
Abstract:
The nature and mechanisms of pulmonary vascular responses which follow miliary pulmonary embolism were examined in intact dogs in which the isolated left lower lobe was perfused at constant blood flow. Embolization of the lung with plastic microspheres increased total pulmonary vascular resistance, whereas, in contrast, vascular resistance of the isolated perfused left lower lobe which was protected from embolization was decreased. This vasodilation was prevented by chronic denervation of the lobe and by ganglionic blockade. Cervical vagotomy also blocked the response but atropine failed to alter the vasodilation. The response, which appeared to be reflex in origin and involve efferent sympathetic pathways, was prevented by beta-adrenergic receptor blockade produced by propranolol. Since the lobar vascular response to norepinephrine was significantly enhanced by propranolol, it was concluded that embolization of the lung evokes pulmonary vascular reflex vasodilation which is mediated over the sympathetic nervous system via a beta-adrenergic receptor mechanism.
Insights
Pulmonary embolism triggers a reflex vasodilation in the lungs via sympathetic nervous system pathways. This response involves beta-adrenergic receptors and is crucial for regulating pulmonary vascular resistance during embolism.
Area of Science:
- Cardiovascular Physiology
- Pulmonary Circulation
- Autonomic Nervous System Regulation
Background:
- Miliary pulmonary embolism can significantly impact pulmonary vascular resistance.
- Understanding the body's compensatory mechanisms is vital for managing such conditions.
Purpose of the Study:
- To investigate the pulmonary vascular responses following miliary pulmonary embolism.
- To elucidate the neural and receptor mechanisms underlying these responses.
Main Methods:
- Isolated perfused canine lung lobe model.
- Induction of pulmonary embolism using plastic microspheres.
- Pharmacological blockade of neural pathways and receptors (denervation, ganglionic blockade, vagotomy, propranolol).
Main Results:
- Pulmonary embolism increased overall pulmonary vascular resistance.
- Protected lung lobes exhibited decreased vascular resistance (vasodilation).
- This vasodilation was abolished by denervation, ganglionic blockade, and vagotomy, but not atropine.
- Beta-adrenergic receptor blockade with propranolol prevented the vasodilation.
Conclusions:
- Pulmonary embolism elicits a reflex pulmonary vasodilation.
- This reflex is mediated by efferent sympathetic pathways.
- The mechanism involves beta-adrenergic receptors.