Control of acute aortic dissection.
An experimental model of acute aortic dissection has been designed in an effort to examine myocardial contractility and systolic arterial pressure as factors influencing the progression of dissection. Thirty mongrel dogs divided into three experimental groups underwent left thoracotomy and construction of a standard intimal tear in the proximal descending aorta. Nine of ten animals in the control group showed progression of the aortic dissection a mean of 81.5 percent of the distance from the aortotomy to the celiac axis. Group II consisted of ten dogs pretreated with propranolol. The myocardial contractility (dp/dt) was significantly depressed in this group without change in systolic pressure. However, progression of dissection occurred in nine of ten animals as in the control group. In Group III, ten dogs were pretreated with trimethaphan lowering the systolic blood pressure to 90 mm. Hg and depressing the dp/dt to levels equal to those of Group II. There was no progression of aortic dissection in any of the animals in this group. The results indicate that, under these experimental conditions, depression of myocardial contractility alone has no inhibitory effect on the progression of dissection. When controlled hypotension is added to myocardial depression, aortic dissection is inhibited completely.
D000818:Animals; D001011:Aorta / Q000601:surgery; D001014:Aortic Aneurysm / Q000188:drug therapy* / Q000628:therapy; D001794:Blood Pressure / Q000187:drug effects*; D003864:Depression, Chemical; D004195:Disease Models, Animal; D004285:Dogs; D007022:Hypotension / Q000139:chemically induced; D007023:Hypotension, Controlled; D009200:Myocardial Contraction / Q000187:drug effects*; D011292:Premedication; D011433:Propranolol / Q000494:pharmacology / Q000627:therapeutic use; D014294:Trimethaphan / Q000494:pharmacology / Q000627:therapeutic use
D014294:Trimethaphan; D011433:Propranolol