HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): David N. Helman Mathew R. Williams Yoshifumi Naka Mehmet C. Oz Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Morales, D. L.S. Articles by Oz, M. C. Search for Related Content PubMed PubMed Citation Articles by Morales, D. L.S. Articles by Oz, M. C.

Ann Thorac Surg 2000;69:102-106
© 2000 The Society of Thoracic Surgeons

---

Original Articles

Arginine vasopressin in the treatment of 50 patients with postcardiotomy vasodilatory shock

^a Department of Surgery, Columbia University College of Physicians & Surgeons, New York, New York, USA
^b Department of Medicine, Columbia University College of Physicians & Surgeons, New York, New York, USA

Address reprint requests to Dr Morales, Department of Cardiothoracic Surgery, Columbia University College of Physicians & Surgeons, MHB 7-435, 177 Fort Washington, New York, NY 10032
e-mail: dlm36{at}columbia.edu

	Abstract

Top Abstract Introduction Material and methods Results Comment References

 
Background. The barroreflex-mediated secretion of arginine vasopressin has been found to be defective in a variety of vasodilatory shock states, such as postcardiotomy shock, and administration of the hormone markedly improves vasomotor tone and blood pressure. The high incidence of vasodilatory shock in patients undergoing left ventricular assist device (LVAD) implantation makes this population an ideal model in which to assess the risks and benefits of vasopressin.

Methods. The medical records of the 102 patients receiving LVADs at Columbia-Presbyterian Medical Center from January 1995 to August 1998 were reviewed. Fifty patients were eligible for study based on a history of arginine vasopressin administration in the operating room or intensive care unit within 24 hours of implantation.

Results. Despite LVAD implantation and the administration of vasopressors, patients were hypotensive with a mean arterial pressure less than 60 mm Hg. The administration of vasopressin (0.09 ± 0.05 U/min) increased mean arterial pressure (58 ± 13 to 75 ± 14 mm Hg; p < 0.001) while reducing norepinephrine administration (11.7 ± 13 to 7.9 ± 6.0 mcg/min; p = 0.023). There was no significant change in LVAD flow. The incidence of compromised regional perfusion was not different between LVAD patients who received vasopressin as compared to hemodynamically stable LVAD patients who did not receive vasopressin.

Conclusions. We have demonstrated vasopressin at low doses to be a safe and an effective vasopressor in 50 patients with postcardiotomy vasodilatory shock.

	Introduction

Top Abstract Introduction Material and methods Results Comment References

 
The hallmarks of vasodilatory shock are a triad of hypoperfusion, lactic acidosis, and profound vasodilatory hypotension unresponsive to catecholamine vasopressors [1–3]. This state occurs in postcardiotomy shock in which inflammatory mediators from cardiopulmonary bypass and the common use of vasodilatory inotropes (ie, phosphodiesterase inhibitors) in these patients contribute to this loss of vascular tone. Even though unsuccessful, catecholamine vasopressors have been the only drug therapy used to address this often premorbid state. With no alternative therapy available, a sustained systemic shock state occurs resulting in a high morbidity and mortality and is particularly prominent in patients after left ventricular assist device (LVAD) insertion [4, 5].

The need for an appropriate therapy for postcardiotomy vasodilatory shock in LVAD patients led us to investigate the role of arginine vasopressin (AVP) [4]. In 1997, we discovered that patients with post-LVAD vasodilatory shock had a deficiency in AVP and when treated with intravenous AVP, this shock resolved. A double-blinded, randomized study of 10 LVAD patients receiving standard treatment for post-LVAD vasodilatory shock with catecholamine vasopressors compared the effectiveness of AVP to placebo. Interestingly, the doses (0.1 U/min) of AVP employed had no significant pressor effect in normal subjects. However, in these LVAD recipients, AVP at these small doses significantly elevated systemic vascular resistance and arterial pressure, whereas the large doses of catecholamine pressors that were only maintaining a mean arterial pressure of 58 mm Hg were significantly reduced. In fact, AVP appeared to act synergistically with catecholamine vasopressors to make them effective in this clinical situation. Therefore, AVP deficiency in the plasma appears to contribute to the vasodilatory hypotension of postcardiopulmonary bypass (CPB) shock in LVAD recipients through a unique mechanism not addressed by standard therapies. Also, the replacement of this deficiency with small doses of exogenous AVP returns these patients to appropriate physiologic levels of AVP, resulting in an improved and stable hemodynamic state [4]. However to date, no reports of a large series with AVP resuscitation of vasodilatory shock and its potential complications have been published. Our prior findings and a high incidence of vasodilatory shock make the LVAD patient population an ideal model in which to assess the therapeutic value and morbidity of AVP in postcardiotomy vasodilatory shock. To this end, we report our overall experience with AVP as a treatment for post LVAD vasodilatory shock.

	Material and methods

Top Abstract Introduction Material and methods Results Comment References

 
The medical records of the 102 patients receiving LVADs at Columbia-Presbyterian Medical Center from January 1995 to August 1998 were reviewed. Fifty patients were eligible for study based on a history of AVP (Pitressin, Parke-Davis Morris Plains, NJ) administration in the operating room or intensive care unit (ICU) within 24 hours of implantation. This population represents our cumulative experience, including 8 patients that were previously reported [4]. The average age was 52 ± 15 (mean ± standard deviation) years, and 16% were women. Thirty-nine of these patients received a TCI (Thermo CardioSystems Incorporated, Woburn, MA) vented electric (VE) LVAD, whereas the remaining 11 received a TCI pneumatic LVAD. Our common recommended clinical dosing range for AVP (supplied in 20 U/2 cc vials) is 2 to 6 U/hour, although in our early experiences higher doses up to 15 U/hour were used.

All hemodynamic data and intravenous drug doses were recorded 15 minutes before and 15 minutes after initiation of AVP. The hemodynamic data included mean arterial pressure (mAP), LVAD flow, flow of the cardiopulmonary bypass machine, systemic vascular resistance (SVR), and mean pulmonary arterial pressure (PAP). Data on endpoints such as length of hospital stay, length of ICU stay, as well as morbidity and mortality, were collected. All complications recorded occurred during in-hospital LVAD support. Preimplantation end-organ insufficiency that did not worsen postoperatively, was not considered a complication. Right heart failure was defined as the need for inhaled nitric oxide (iNO) or a right ventricular assist device (RVAD). Postoperative hemorrhage was defined as the need to reoperate for clot-causing cardiac tamponade or for excessive bleeding. Infection was defined as a positive culture accompanied by an increased white blood cell count greater than 12,000/mm³ or a fever greater than 100.5°F that appeared clinically to require antibiotic therapy. Any stroke, transient ischemic attack (TIA), neuropathy, or encephalopathy was considered to be a neurological event. Any end-organ dysfunction caused by an embolus was considered to be a thromboembolic event. Any bleeding from the gastrointestinal tract that caused a drop in hematocrit greater than 3% and was associated with melena, hematochezia, or a bleeding source on endoscopy, was considered a gastrointestinal bleed. Any ventricular arrhythmia that required medical or surgical intervention was recorded. Liver insufficiency was defined as a change in prothrombin time (PT) greater than 3 seconds, or greater than 16.5 seconds, as well as an increase in alanine aminotransferase greater than 100 g/dL, or greater than 150 g/dL. Renal insufficiency was defined as a creatinine above 1.5 mg/dL, and recovery of full renal function was defined as the production of spontaneous urine and a creatinine below 1.5 mg/dL.

All results are reported as a mean ± the standard deviation. All data comparisons were done using a paired two-tailed Students’ t-test with p less than 0.05 being significant.

	Results

Top Abstract Introduction Material and methods Results Comment References

 
AVP was administered in all subjects for hypotension due to a decreased SVR, despite being supported on catecholamine vasopressors. The average starting dose of AVP was 0.09 ± 0.05 U/min. This dose resulted in a significant increase in SVR, causing an improvement in mAP (Table 1), whereas LVAD flow and inotropic support remained the same except for the mean norepinephrine dose, which was significantly decreased by 32% (Table 2). PAP was unchanged by AVP administration (Table 1).

Of these 50 LVAD patients, 34 (68%) were transplanted, 13 (26%) expired, and 3 (6%) were explanted. Mean duration of LVAD support was 104 ± 112 days. No deaths occurred within the first 3 postoperative days. In the 13 patients who died with devices, the mean time to death was 66 ± 163 days with a median of 19 days and a range of 3 to 604 days. The average length of AVP infusion was 7 ± 12 days during which no tachyphylaxis was seen. The average ICU stay was 15 ± 12 days, thus patients on average received AVP for 47% of their ICU stay. Thirty-eight (76%) of these LVAD recipients who had been in vasodilatory shock were discharged from the ICU. Of these 38 patients, 29 had VE LVADs and were eligible for our outpatient program. Twenty-seven of these 29 patients (93%) were discharged from the hospital on postoperative day 32 ± 17 days. Complications are listed in Table 3. All complications resolved in the 37 patients successfully bridged to transplant or explant. The incidence of right heart failure and liver insufficiency in the 52 LVAD patients who did not receive AVP, 18 (35%) and 7 (13%) respectively, compared to those 50 patients who did receive AVP, 16 (32%) and 7 (14%) respectively, was similar.

	Comment

Top Abstract Introduction Material and methods Results Comment References

 
Hypotension (mAP < 60 mm Hg) post CPB is typically associated with a marked increase in AVP levels to concentrations of 100 to 200 pg/mL [4]. However, inappropriately low levels of AVP (8 to 34 pg/mL) often exist in post-LVAD implantation hypotension [4]. This relative deficiency in AVP correlates with episodes of vasodilatory shock [4, 5]. When this deficiency is corrected to the expected physiological concentration by administration of exogenous AVP, we have postulated that the patient should assume an improved hemodynamic state. This hypothesis is supported in this review of 50 LVAD recipients in vasodilatory shock following CPB. Despite LVAD implantation and all of these patients being on vasoconstrictive drugs, including norepinephrine, at an average dose of 11.7 mcg/min, patients were only able to maintain an average mAP of 58 mm Hg. The administration of pitressin at 0.09 U/min on average, known to have no pressor effect in normal subjects, effected a rise in mAP to 75 mm Hg without a significant change in LVAD flow or inotropic support except for a significant reduction in the norepinephrine dose. All patients in this study experienced a markedly improved hemodynamic state within 6 hours of AVP administration.

A central concern regarding the use of any vasopressor is the potential for compromising regional circulations (ie, pulmonary, coronary, and splanchnic) [6–8]. Pulmonary hypertension associated with AVP use was not identified as the PAP did not significantly change with the use of AVP. However, the high incidence of right heart failure (32%) required our frequent use of iNO (15 of 50, 30%). Of the 16 patients with right heart failure, only one necessitated an RVAD. Because the incidence of iNO administration in the 52 LVAD patients who did not receive AVP was 35%, we do not believe that AVP use increases the occurrence of right heart failure. Assessing coronary spasm secondary to AVP in LVAD patients is difficult, although no ischemic changes in the electrocardiogram were noted in any of these patients. Decreasing coronary blood flow and cardiac output is an often voiced concern by clinicians treating esophageal varices with AVP. These concerns perhaps stem from the initial research of the effect of AVP on the heart, which was done on normotensive dogs and did show decreased cardiac performance and coronary blood flow with AVP administration [9, 10]. Since then, this work has been repeated several times in hypotensive dogs, which is the clinical scenario in which we use the drug, and these have all shown an increase in coronary flow and cardiac output with AVP use [6, 7]. These studies have also demonstrated an overall increase in limb perfusion with AVP administration, calling into question whether limb ischemia seen clinically is due to the low flow state and multiple vasoconstrictors these patients are on or AVP [6, 7].

Blood flow to the liver and bowel has been experimentally shown in both normotensive and hypotensive states to be compromised by AVP use [6, 7]. However, in our experience there was no clinical evidence of ischemic bowel. There was a 14% incidence of liver insufficiency in this cohort. However, this is not significantly different than the 13% incidence of liver insufficiency in the 52 patients who received LVADs but not AVP during the study period. The 44% incidence of pre-LVAD renal insufficiency in our study cohort was corrected in 82% of cases with LVAD implantation. This recovery also may have been associated with the use of AVP. AVP receptors in the renal vasculature are concentrated in the efferent arterioles in contrast to catecholamine receptors, which are concentrated on the afferent arterioles [11]. Therefore, unlike catecholamine vasoconstriction that causes a decreased filtration fraction [12], AVP causes an increase in the filtration fraction and perhaps in the urinary output as well [11, 13]. This may explain why only 1 of 50 patients in vasodilatory shock without preexisting renal insufficiency developed sustained renal failure postoperatively. Also, all patients who did not expire regained full renal function (Table 4).

The salutary benefits we believe AVP has on renal function muddy the issues surrounding the weaning protocol of AVP. At times, even after AVP has resulted in hemodynamic stabilization without the need for other vasoactive medications, AVP is often continued on patients with renal insufficiency at 0.03 U/min to maintain an improved filtration fraction and urine output. Once renal function begins to recover, AVP is weaned over 12 hours. This institutional bias helps explain why patients were on AVP for 47% of their ICU stay. If no renal insufficiency exists, then AVP is weaned over 2 to 3 hours once the catecholamine requirement normalizes (1 to 3 mcg/min of norepinephrine) and physiological parameters such as acidosis correct.

AVP does not increase blood pressure under normotensive conditions. This is demonstrated by the syndrome of inappropriate release of antidiuretic hormone, in which a significant elevation of plasma AVP from unregulated hormone release, does not cause hypertension [14]. In marked contrast, when the arterial pressure is threatened, AVP is involved in the maintenance of blood pressure and administration of exogenous hormone increases the pressure significantly [6, 15, 16]. This data suggests that the sensitivity to AVP is regulated, and that the role of the hormone on blood pressure control increases as cardiovascular function is compromised [15, 16].

The ability of AVP to affect the vasculature of patients in vasodilatory shock, and not in normotensive patients, is unique [13, 17]. This is an indication that AVP probably does not function through the same mechanisms as other vasoconstrictors. Catecholamine vasopressors are presently the only drug therapy available for the management of vasodilatory hypotension. They cause vasoconstriction by opening voltage-gated channels that allow an influx of Ca²⁺ into the smooth muscle cell, increasing the cytoplasmic concentration of Ca²⁺. This allows actin and myosin coupling to occur, resulting in smooth muscle contraction of the vessel wall and vasoconstriction. However, in late vasodilatory shock, characterized by lactic acidosis secondary to hypoperfusion, this mechanism appears interrupted since catecholamines become ineffective vasoconstrictors [3, 18].

Mechanistically, this interruption most likely occurs by cellular acidosis secondary to hypoperfusion opening adenosine-triphosphate sensitive potassium (K⁺_ATP) channels in myocytes [19]. This allows the efflux of K⁺ resulting in the hyperpolarization of the myocytes, which prevents voltage-gated Ca²⁺ channels from opening; this halts Ca²⁺ influx into the myocytes [19, 20]. We hypothesize that this interruption of the catecholamine vasoconstrictor mechanism is the reason for the catecholamines’ ineffectiveness in vasodilatory shock. Also, vasodilatory shock increases the endothelial production of the known vasodilator nitric oxide, a mechanism unaffected by catecholamines [21]. The profound loss of vascular tone in vasodilatory shock and its resistance to catecholamines is probably from a combination of nitric oxide production and the hyperpolarization of the myocyte by the K⁺_ATP channel.

When AVP binds to its vascular receptors, three pathways are activated. First, AVP activates the second messenger system of inositol triphosphate (IP₃) and diacylglycerol (DAG) in vascular smooth muscle cells causing a rise in cytoplasmic Ca²⁺. This results in the contraction of the actin and myosin filaments, and thus vasoconstriction [22]. Second, AVP inhibits NO induced accumulation of cyclic guanosine monophosphate in vascular smooth muscle, which inhibits the vasodilatory effect of NO [23]. Third, AVP closes K⁺_ATP channels if open, halting the efflux of K⁺ and promoting myocyte depolarization. This depolarization enables Ca²⁺ to enter the myocyte and cause contraction [24].

We hypothesize that extended or marked periods of hypotension caused by hemorrhage, sepsis, or the cardiopulmonary bypass machine causes central nervous system exhaustion of AVP [5, 25]. This relative deficiency in AVP accompanied by sustained hypotension, hypoperfusion, and lactic acidosis results in NO production and hyperpolarization of myocytes. Now resistant to catecholamines, the patient enters a downward spiral of worsening vasodilatory hypotension, hypoperfusion, and lactic acidosis. However, the administration of exogenous AVP returns AVP to appropriate physiological levels, which repolarizes myocytes and inhibits NO production [23]. This now allows catecholamines to synergistically work with AVP to return the patient to a sustained normotensive and stable hemodynamic state.

In summary, we have demonstrated vasopressin to be an effective vasoconstrictor for postcardiotomy vasodilatory shock in 50 patients when standard therapies failed. We have also observed that the use of vasopressin infrequently compromised regional perfusion of the viscera, heart, or lung in this cohort and may aid in the recovery of renal function. The study of vasopressin has introduced the K⁺_ATP channel and its central role in vascular tone regulation into the clinical realm, leading us to a novel way of conceptualizing and treating shock. Arginine vasopressin should become an important weapon in the armamentarium of managing postcardiotomy vasodilatory shock.

	References

Top Abstract Introduction Material and methods Results Comment References

 

1. Bond R.F., Johnson G., III Vascular adrenergic interactions during hemorrhagic shock. Fred Proc 1985;44:281-289.
2. Bond R.F., Manley E.S.J., Green H.D. Cutaneous and skeletal muscle vascular responses to hemorrhage and irreversible shock. Am J Physiol 1967;212:488-497.[Free Full Text]
3. Mellander S., Lewis D.H. Effect of hemorrhagic shock on the reactivity of resistance and capacitance vessels and on capillary filtration transfer in cat skeletal muscle. Circ Res 1963;13:105-118.[Abstract/Free Full Text]
4. Argenziano M., Choudhri A.F., Oz M.C., et al. A prospective randomized trial of arginine vasopressin in the treatment of vasodilatory shock after left ventricular assist device placement. Circulation 1997;96(Suppl):II286-II290.
5. Argenziano M., Chen J.M., Choudhri A.F., et al. Management of vasodilatory shock after cardiac surgery. J Thorac Cardiovasc Surg 1998;116:973-980.[Abstract/Free Full Text]
6. Ericsson B.F. Hemodynamic effects of vasopressin during haemorrhagic hypotension in the anesthetized dog. Acta Chir Scand 1972;138:227-233.[Medline]
7. Ericsson B.F. The effect of vasopressin on the distribution of cardiac output in the early phase of hemorrhagic shock in the anesthetized dog. Acta Chir Scand 1972;138:119-123.[Medline]
8. Foreman B.W., Dai X.Z., Bache R.J. Vasoconstriction of canine coronary collateral vessels with vasopressin limits blood flow to collateral-dependent myocardium during exercise. Circ Res 1991;69:657-664.[Abstract/Free Full Text]
9. Wakim K.G., Denton C., Essex H.E. Certain cardiovascular effects of vasopressin (pitressin). Amer Heart J 1954;47:77.
10. Ericsson B.F. Effect of vasopressin on the distribution of cardiac output and organ blood flow in the anesthetized dog. Acta Chir Scand 1971;137:729-738.[Medline]
11. Edwards R.M., Rinza W., Kinter L.B. Renal microvascular effects of vasopressin and vasopressin antagonist. Am J Physiol 1989;256(2 Pt 2):F274-F278.[Abstract/Free Full Text]
12. Edwards R.M. Segmental effects of norepinephrine and angiotensin II on isolated renal microvessels. Am J Physiol 1983;244:F526-F534.[Abstract/Free Full Text]
13. Wagner H.N., Jr, Braunwald E. The pressor effect of the antidiuretic principle of the posterior pituitary in orthostatic hypotension. J Clin Invest 1956;35:1412-1418.
14. Padfield P.L., Brown J.J., Lever A.F., Moron J.J., Robertson J.I.S. Blood pressure in acute and chronic vasopressin excess. N Eng J Med 1981;304:1067-1070.[Abstract]
15. Linder K.H., Prengel A.W., Brinkmann A., et al. Vasopressin administration in refractory cardiac arrest. Ann Intern Med 1996;124:1061-1064.[Abstract/Free Full Text]
16. Landry D.W., Levin H.R., Gallant E.M., et al. Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation 1997;95:1122-1125.[Abstract/Free Full Text]
17. Graybiel A., Glendy R.E. Circulatory effects following the intravenous administration of Pitressin in normal persons and in patients with hypertension and angina pectoris. Am Heart J 1941;21:481-489.
18. Thiemermann C., Szabo C., Mitchell A., Vane J.R. Vascular hyporeactivity to vasoconstrictor agents and hemodynamic decompensation in hemorrhagic shock is mediated by nitric oxide. Proc Natl Acad Sci USA 1993;90:267-271.[Abstract/Free Full Text]
19. Landry D.W., Oliver J.A. The ATP-sensitive K⁺ channel mediates hypotension in endotoxemia and hypoxic lactic acidosis in dog. J Clin Invest 1992;89:2071-2074.
20. Szabo C., Salzman A.L. Inhibition of ATP-activated potassium channels exerts pressor effects and improves survival in a rat model of severe hemorrhagic shock. Shock 1996;5:391-394.[Medline]
21. Kilbourn R.G., Gross S.S., Jubran A., et al. Ng-methyl-L-arginine inhibits tumor necrosis factor-induced hypotension. Proc Natl Acad Sci USA 1990;87:3629-3632.[Abstract/Free Full Text]
22. Howel J., Wheatley M. Molecular pharmacology of V1a vasopressin receptors. Gen Pharmacol 1995;25:1143-1152.
23. Tetsuka T., Nakaya Y., Inoue I. Arginine vasopressin inhibits interleukin-1beta-stimulated nitric oxide and cyclic guanosine monophosphate production via the V1 receptor in cultured rat vascular smooth muscle cells. J Hyper 1997;15:627-632.
24. Salzman A.L., Vromen A., Denenberg A., Szabo C. K_ATP-channel inhibition improves hemodynamics and cellular energetics in hemorrhagic shock. Am J Physiol 1997;272(2 Pt 2):H688-H694.[Abstract/Free Full Text]
25. Errington M.L., Rocha M., Silva E. The secretion and clearance of vasopressin during the development of irreversible haemorrhagic shock. Proc Physiol Soc 1971;217:43P-45P.

This article has been cited by other articles:

				S. Maier, W. Hasibeder, W. Pajk, C. Hengl, H. Ulmer, H. Hausdorfer, B. Wurzinger, and H. Knotzer Arginine-vasopressin attenuates beneficial norepinephrine effect on jejunal mucosal tissue oxygenation during endotoxinaemia Br. J. Anaesth., November 1, 2009; 103(5): 691 - 700. [Abstract] [Full Text] [PDF]

				N. Mongardon, A. Dyson, and M. Singer Pharmacological optimization of tissue perfusion Br. J. Anaesth., July 1, 2009; 103(1): 82 - 88. [Abstract] [Full Text] [PDF]

				J. A. Russell, K. R. Walley, J. Singer, A. C. Gordon, P. C. Hebert, D. J. Cooper, C. L. Holmes, S. Mehta, J. T. Granton, M. M. Storms, et al. Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock N. Engl. J. Med., February 28, 2008; 358(9): 877 - 887. [Abstract] [Full Text] [PDF]

				N. M. Katz The emerging specialty of cardiothoracic surgical critical care: the leadership role of cardiothoracic surgeons on the multidisciplinary team. J. Thorac. Cardiovasc. Surg., November 1, 2007; 134(5): 1109 - 1111. [Full Text] [PDF]

				M. Egi, R. Bellomo, C. Langenberg, M. Haase, A. Haase, L. Doolan, G. Matalanis, S. Seevenayagam, and B. Buxton Selecting a Vasopressor Drug for Vasoplegic Shock After Adult Cardiac Surgery: A Systematic Literature Review Ann. Thorac. Surg., February 1, 2007; 83(2): 715 - 723. [Abstract] [Full Text] [PDF]

				H. Knotzer, W. Pajk, S. Maier, R. Ladurner, A. Kleinsasser, V. Wenzel, M. W. Dunser, H. Ulmer, and W. R. Hasibeder Arginine vasopressin reduces intestinal oxygen supply and mucosal tissue oxygen tension Am J Physiol Heart Circ Physiol, July 1, 2005; 289(1): H168 - H173. [Abstract] [Full Text] [PDF]

				M. A. Scheurer, S. M. Bradley, and A. M. Atz Vasopressin to attenuate pulmonary hypertension and improve systemic blood pressure after correction of obstructed total anomalous pulmonary venous return J. Thorac. Cardiovasc. Surg., February 1, 2005; 129(2): 464 - 466. [Full Text] [PDF]

				P. C. Dyke II and J. D. Tobias Vasopressin: Applications in Clinical Practice J Intensive Care Med, July 1, 2004; 19(4): 220 - 228. [Abstract] [PDF]

				N. A. Nussmeier, C. B. Probert, D. Hirsch, J. R. Cooper Jr., I. D. Gregoric, T. J. Myers, and O. H. Frazier Anesthetic Management for Implantation of the Jarvik 2000TM Left Ventricular Assist System Anesth. Analg., October 1, 2003; 97(4): 964 - 971. [Abstract] [Full Text] [PDF]

				J. A. Guzman, A. E. Rosado, and J. A. Kruse Vasopressin vs. norepinephrine in endotoxic shock: systemic, renal, and splanchnic hemodynamic and oxygen transport effects J Appl Physiol, August 1, 2003; 95(2): 803 - 809. [Abstract] [Full Text] [PDF]

				D. L.S. Morales, M. J. Garrido, J. D. Madigan, D. N. Helman, J. Faber, M. R. Williams, D. W. Landry, and M. C. Oz A double-blind randomized trial: prophylactic vasopressin reduces hypotension after cardiopulmonary bypass Ann. Thorac. Surg., March 1, 2003; 75(3): 926 - 930. [Abstract] [Full Text] [PDF]

				W. J. Gomes, M. R. Erlichman, M. L. Batista-Filho, M. Knobel, D. R. Almeida, A. C. Carvalho, R. Catani, and E. Buffolo Vasoplegic syndrome after off-pump coronary artery bypass surgery Eur. J. Cardiothorac. Surg., February 1, 2003; 23(2): 165 - 169. [Abstract] [Full Text] [PDF]

				T. N. Albright, M. A. Zimmerman, and C. H. Selzman Vasopressin in the Cardiac Surgery Intensive Care Unit Am. J. Crit. Care., July 1, 2002; 11(4): 326 - 330. [Abstract] [Full Text] [PDF]

				K. Meersschaert, L. Brun, M. Gourdin, S. Mouren, M. Bertrand, B. Riou, and P. Coriat Terlipressin-Ephedrine Versus Ephedrine to Treat Hypotension at the Induction of Anesthesia in Patients Chronically Treated with Angiotensin Converting-Enzyme Inhibitors: A Prospective, Randomized, Double-Blinded, Crossover Study Anesth. Analg., April 1, 2002; 94(4): 835 - 840. [Abstract] [Full Text] [PDF]

				K. A. Thielmeier, J. R. Pank, R. D. Dowling, and L. A. Gray JR Anesthetic and Perioperative Considerations in Patients Undergoing Placement of Totally Implantable Replacement Hearts Seminars in Cardiothoracic and Vascular Anesthesia, November 1, 2001; 5(4): 335 - 344. [Abstract] [PDF]

				C. L. Holmes, B. M. Patel, J. A. Russell, and K. R. Walley Physiology of Vasopressin Relevant to Management of Septic Shock Chest, September 1, 2001; 120(3): 989 - 1002. [Abstract] [Full Text] [PDF]

				M. W. Dunser, A. J. Mayr, H. Ulmer, N. Ritsch, H. Knotzer, W. Pajk, G. Luckner, N. J. Mutz, and W. R. Hasibeder The Effects of Vasopressin on Systemic Hemodynamics in Catecholamine-Resistant Septic and Postcardiotomy Shock: A Retrospective Analysis Anesth. Analg., July 1, 2001; 93(1): 7 - 13. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): David N. Helman Mathew R. Williams Yoshifumi Naka Mehmet C. Oz Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Morales, D. L.S. Articles by Oz, M. C. Search for Related Content PubMed PubMed Citation Articles by Morales, D. L.S. Articles by Oz, M. C.