CARDIOPULMONARY INTERACTIONS OF SALBUTAMOL AND HYPOXEMIA IN HEALTHY-YOUNG VOLUNTEERS

Citation
Dg. Kiely et al., CARDIOPULMONARY INTERACTIONS OF SALBUTAMOL AND HYPOXEMIA IN HEALTHY-YOUNG VOLUNTEERS, British journal of clinical pharmacology, 40(4), 1995, pp. 313-318
Citations number
26
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
03065251
Volume
40
Issue
4
Year of publication
1995
Pages
313 - 318
Database
ISI
SICI code
0306-5251(1995)40:4<313:CIOSAH>2.0.ZU;2-Q
Abstract
1 Nebulised salbutamol is frequently used in the treatment of asthma a nd chronic obstructive pulmonary disease. Its effects on the cardiovas cular system have been extensively investigated although as yet little is known concerning its effects on the pulmonary circulation, particu larly during hypoxaemia. We have therefore examined the effects of neb ulised salbutamol on pulmonary haemodynamics to see if it modifies hyp oxic pulmonary vasoconstriction. 2 Eight healthy normal volunteers wer e studied on two separate occasions. After resting to achieve baseline haemodynamics patients were randomised to receive 5 mg salbutamol or placebo via a nebuliser. They were restudied after 30 min and then ren dered hypoxaemic by breathing an N-2/O-2 mixture to achieve an SaO(2) of 75-80%. Doppler echocardiography was used to measure mean pulmonary artery pressure (MPAP), cardiac output (CO) and hence pulmonary vascu lar resistance (PVR). 3 Treatment with salbutamol significantly increa sed MPAP during normoxaemia and hypoxaemia compared with placebo at 12 .0 +/- 1.2 vs 8.0 +/- 0.7 mm Hg and 28.6 +/- 0.9 vs 25.2 +/- 1.0 mm Hg , respectively (P < 0.05). Salbutamol caused a significant increase in heart rate compared with placebo and effects were additive to those o f hypoxia at 74 +/- 2 vs 67 +/- 3 beats min(-1) during normoxaemia and 84 +/- 3 vs 77 +/- 4 beats min(-1) during hypoxaemia, respectively (P < 0.05). Whilst systemic vascular resistance fell in response to salb utamol, PVR was unchanged by salbutamol during either normoxaemia or h ypoxaemia. Cardiac output was increased by salbutamol and by hypoxia. 4 Since PVR was not altered by salbutamol, this suggests that changes in CO rather than true pulmonary vasoconstriction were responsible for the observed increase in MPAP with salbutamol during normoxaemia and hypoxaemia. Thus, there appears to be no significant interaction betwe en salbutamol and hypoxia in the human pulmonary vasculature, although combined chronotropic effects may be important.