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LETTERS TO THE EDITOR

Vasopressin and Postcardiopulmonary Bypass Refractory Hypotension

Division of AnesthesiologyUniversity HospitalCH-1211 Geneva 14, Switzerland

Overand and Teply (1) recently described a patient with intractable hypotension after cardiopulmonary bypass (CPB) who improved dramatically after the administration of vasopressin (VP). We wish to make a few comments regarding experimental and clinical data suggesting that VP is a promising therapeutic tool. First, in addition to its potent vasoconstricting effects, VP stimulates the endothelial release of prostaglandins and nitric oxide (NO) in the pulmonary, coronary, and mesenteric vascular beds (2,3). Hence, the regional heterogeneity in VP receptor density and the balanced relaxant/constrictive effects of VP contribute to maintain cardiac circulatory output with minimal risk of myocardial ischemia. Second, although deficient release of VP has been documented in some patients with septic shock or with a ventricular assist device, reversal of vasodilatory hypotension with VP has been achieved regardless of the plasma concentration of VP (4). Third, VP inhibits interleukin-1 _ß-induced NO production in vascular smooth muscle, leading to restoration of vascular reactivity to endogenous contractile mediators such as endothelin, thromboxane A₂, and catecholamines (5). Taken together, these data lend support to the hypothesis that VP can partially reverse the adrenergic hyporesponsiveness associated with sepsis and circulatory bypass. Likewise, because the renin-angiotensin system modulates the central release of VP (6), we hypothesize that the impaired adrenergic response often observed in patients chronically treated with angiotensin-converting enzyme inhibitors (7) can be normalized with subpressor doses of VP.

Finally, in the case of combined surgical procedure (aortic and mitral valve replacement) and prolonged CPB (>6 h), one may question whether ultrafiltration could prevent the occurrence of vasodilatory hypotension through attenuation of the systemic inflammatory response elicited by CPB and surgical trauma. Intraoperative ultrafiltration reduces the circulating levels of several biological markers of inflammatory cascade and could contribute to lesser postoperative blood loss, better hemodynamic control, and earlier extubation after cardiac surgery (8).

References

1. Overand PT, Teply JF. Vasopressin for the treatment of refractory hypotension after cardiopulmonary bypass. Anesth Analg 1998;86:1207–9.[Web of Science][Medline]
2. Garcia-Villalon AL, Garcia JL, Monge L, et al. Regional differences in the arterial response to vasopressin: role of nitric oxide. Br J Pharmacol 1996;118:1848–54.[Web of Science][Medline]
3. Martinez MC, Vila JM, Aldasoro M, et al. Relaxation of human isolated mesenteric arteries by vasopressin and desmopressin. Pharmacol 1994;113:419–24.
4. Argenziano M, Choudhry AF, Oz MC, et al. A prospective randomized trial of arginin vasopressin in the treatment of vasodilatory shock after left ventricular assist device placement. Circulation 1997;96 (Suppl II):286–90.
5. Kusano E, Tian S, Umino T, et al. Arginine vasopressin inhibits interleukin-1 beta-stimulated nitric oxide and cyclic guanosine monophosphate production via the V₁ receptor in cultured rat vascular smooth muscle cells. J Hypertens 1997;15:627–32.[Web of Science][Medline]
6. Muders F, Elsner D, Jandeleit K, et al. Chronic ACE inhibition by quinapril modulates central vasopressinergic system. Cardiovasc Res 1997;34:575–81.[Abstract/Free Full Text]
7. Licker M, Neidhart P, Lustenberger S, et al. Long-term angiotensin-converting enzyme inhibition attenuates adrenergic response without altering haemodynamic control in patients undergoing cardiac surgery. Anesthesiology 1996;84:789–800.[Web of Science][Medline]
8. Journois D, Israel-Biet D, Pouard P, et al. High-volume zero-balanced hemofiltration to reduce delayed inflammatory response to cardiopulmonary bypass in children. Anesthesiology 1996;84:965–76.[Web of Science][Medline]

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