Effects of hypercapnia on myocardial contractility in piglets.
The effects of acute hypercapnia on cardiac contractility and their dependence on adrenergic pathways were studied in 27 piglets anesthetized with pentobarbital (30 mg/kg, ip). Aortic pressures and flow, and heart rate were held constant; atropine was used to produce parasympathetic blockade. Hypercapnia was achieved by addition of CO2 to the respirator. In the control group (N = 7) the first derivative of left ventricular (LV) pressure (dP/dtmax) increased significantly following induction of severe hypercapnia (PaCO2 greater than 80 mm Hg; pH less than 7.00). There were no significant changes in LV end diastolic pressure. The magnitude of the positive inotropic responses was unaltered by ganglionic blockade with tetraethylammonium chloride (100 mg) (N = 5). In contrast, no change in LV dP/dtmax was observed during hypercapnia in piglets (N = 15) subjected to beta-adrenoreceptor blockade with practolol (4 mg/kg). Our findings indicate that the increased cardiac contractility during acute severe hypercapnia is not dependent upon the integrity of the neural reflex system. Rather, it is due to adrenal release of catecholamines into the circulation. These animals are highly resistant to the intrinsic cardiac depressant action of hypercapnic acidosis.
D000138:Acidosis / Q000503:physiopathology; D000313:Adrenal Medulla / Q000502:physiology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002395:Catecholamines / Q000502:physiology; D002415:Cats; D005260:Female; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D013552:Swine
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D002245:Carbon Dioxide; D010100:Oxygen