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Ann Thorac Surg 1989;47:575-579
© 1989 The Society of Thoracic Surgeons
Clinic for Cardiovascular Surgery, University Hospital, Zürich, Switzerland
Accepted for publication October 14, 1988.
* Address reprint requests to Dr von Segesser, Clinic for Cardiovascular Surgery, University Hospital, CH-8091 Zürich, Switzerland.
Internal mammary arteries (IMAs) are increasingly used for coronary artery revascularization. However, spastic reactions alter IMA-coronary artery anastomoses have been reported. Internal mammary artery flow and the effects of sudden hypovolemia, gradual hypovolemia, papaverine hydrochloride, nitrates, and epinephrine were evaluated in a canine model (n = 10) (body weight, 19 ± 5 kg) without interference from coronary artery resistance by dissecting the IMA as a pedicle, calibrating the flowmeter during free IMA flow, and anastomosing the IMA to the right atrium. Sudden hypovolemia (withdrawal of 20% of circulating blood volume over 90 seconds) caused significant modifications (p < 0.01) of the following hemodynamic variables: heart rate (+12%), right atrial pressure (–17%), pulmonary artery pressure (–20%), wedge pressure (–30%), aortic pressure (–49%), cardiac output (–33%), distal IMA pressure (–54%), and IMA flow (–85%). During hypovolemia, IMA flow could not be increased with topical application of papaverine, but baseline values were achieved after retransfusion of the withdrawn blood volume. Gradual hypovolemia and application of large doses of nitrates showed less dramatic effects, and injection of an epinephrine bolus under rormovolemic conditions increased aortic pressure and IMA flow. Under sever hypovolemia, however, administration of an epinephrine bolus provoked only a minimal increase in aortic pressure and a contrasting decrease in IMA flow. We conclude that sudden, severe hypovolemia can lead to disproportionate IMA flow reduction and that pharmacological interventions are delicate under these circumstances.
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