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Anesth Analg 2001;92:1499-1504
© 2001 International Anesthesia Research Society

CRITICAL CARE AND TRAUMA

The Effects of Endogenous and Exogenous Vasopressin During Experimental Cardiopulmonary Resuscitation

Anette C. Krismer, MD*, Karl H. Lindner, MD*, Volker Wenzel, MD*, Viktoria D. Mayr, MD*, Wolfgang G. Voelckel, MD*, Keith G. Lurie, MD{dagger}, and Hans U. Strohmenger, MD*

*Department of Anesthesiology and Critical Care Medicine, The Leopold-Franzens-University of Innsbruck, Austria; and {dagger}the Cardiac Arrhythmia Center, Cardiovascular Division, Department of Medicine at the University of Minnesota, Minneapolis, Minnesota

Address correspondence to Anette C. Krismer, MD, The Leopold-Franzens-University of Innsbruck, Department of Anesthesiology and Critical Care Medicine, Anichstrasse 35, 6020 Innsbruck, Austria. Address e-mail to anette.krismer{at}uibk.ac.at Address reprint requests to Karl H. Lindner, MD, The Leopold-Franzens-University of Innsbruck, Department of Anesthesiology and Critical Care Medicine, Anichstrasse 35, 6020 Innsbruck, Austria.


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Exogenous vasopressin is a promising vasopressor when blood pressure is critically threatened, but the role of endogenous vasopressin during cardiopulmonary resuscitation (CPR) is unknown. We assessed the role of endogenous versus exogenous vasopressin in a porcine open chest CPR model. Seven minutes before induction of cardiac arrest, seven pigs received 10 µg/kg of a selective vasopressin V1-receptor-antagonist (Blocked Vasopressin group); another 12 pigs in two groups received saline administration only. After 4 min of untreated ventricular fibrillation followed by 3 min of basic life support CPR, six animals received 0.8 U/kg vasopressin (Exogenous Vasopressin group), whereas the blocked vasopressin group (n = 7), and the remaining six animals received saline placebo only (Endogenous Vasopressin group). Defibrillation was attempted after 14 min of CPR. During basic life support CPR, left ventricular myocardial blood flow was significantly (P < 0.05) decreased in the Blocked Vasopressin group compared with the Exogenous Vasopressin group and Endogenous Vasopressin group (42 ± 5 compared with 64 ± 6 and 66 ± 6 mL · min-1 · 100g-1). Left ventricular myocardial blood flow was significantly decreased in the Blocked Vasopressin group versus Exogenous Vasopressin group versus Endogenous Vasopressin group 90 s and 5 min after drug administration, respectively (38 ± 4 and 27 ± 3 vs 145 ± 32 and 110 ± 12 vs 62 ± 4 and 56 ± 6 mL · min-1 · 100g-1, respectively). None of seven Blocked Vasopressin animals, six of six Exogenous Vasopressin pigs, and six of six Endogenous Vasopressin swine had return of spontaneous circulation after 14 min of cardiac arrest including 10 min of CPR (P < 0.05). In conclusion, pigs with blocked endogenous vasopressin had poor coronary perfusion pressure and left ventricular myocardial blood flow during open chest CPR, and could not be successfully resuscitated. All pigs with effective endogenous vasopressin or pigs with effective endogenous vasopressin and additional exogenous vasopressin had good left ventricular myocardial blood flow during experimental CPR, and survived the 1-h postresuscitation phase. We conclude that endogenous vasopressin is an adjunct vasopressor to epinephrine and may serve as a back-up regulator to maintain cardiocirculatory homeostasis.

Implications: The study was designed to assess the role of endogenous versus exogenous vasopressin in a porcine cardiopulmonary resuscitation (CPR) model. Only pigs with effective endogenous vasopressin, or pigs with effective endogenous vasopressin and administration of exogenous vasopressin had good left ventricular myocardial blood flow during experimental CPR, had return of spontaneous circulation after defibrillation and survived the 1-h postresuscitation phase.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
In pharmacologic doses, exogenous vasopressin is a potent vasoconstrictor that uses its effects mainly via V1-receptors (1). During cardiopulmonary resuscitation (CPR), exogenous vasopressin has been shown in both laboratory and clinical investigations to be a promising alternative vasopressor when compared with epinephrine (2–5). In septic patients with vasodilatory shock resistant to norepinephrine, exogenous vasopressin easily increased or stabilized blood pressure, whereas catecholamines could be weaned (6,7).

It has been speculated that exogenous vasopressin is beneficial because of fatigue of endogenous vasopressin stores, especially during prolonged shock states, such as during septicemia (7). During CPR, absolute endogenous vasopressin levels may be too low in relation to the degree of cardiocirculatory collapse. For example, in patients who were successfully resuscitated from cardiac arrest, endogenous vasopressin levels were higher than in those who could not be resuscitated (8,9). Why some patients had significantly different endogenous vasopressin levels, however, could not be determined.

Neither in the cardiac arrest nor in the critical care setting are the effects of endogenous versus exogenous vasopressin well understood. This study therefore aimed to assess the effects of endogenous versus exogenous vasopressin on cardiocirculatory variables, epinephrine levels, left ventricular myocardial blood flow, and return of spontaneous circulation in an established porcine CPR model. Our hypothesis was that there would be no differences in study end points among groups.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
This project was approved by the Animal Investigational Committee of our institution, and the animals were managed in accordance with the guidelines of the American Physiological Society and according to Utstein-style guidelines (10) on 19 healthy domestic pigs weighing 20–30 kg. Anesthesia management, surgical instrumentation, and measurements were performed as previously described (11). Aortic pressure was measured with a saline-filled catheter using a pressure transducer (Model 1290A; Hewlett-Packard, Böblingen, Germany), which was calibrated to atmospheric pressure at the level of the right atrium. Pressure tracings were recorded continuously before cardiac arrest, and during the period of open-chest CPR, with a data acquisition system (Dewetron Port 2000; Graz, Austria). Coronary perfusion pressure was defined as the time-coincident difference between aortic and right atrial diastolic pressure. After the thorax had been opened by median sternotomy, a 5F catheter was introduced via the left auricle into the left atrium to inject radiolabeled microspheres for measurement of myocardial blood flow. Blood flow during CPR was measured with radioactively labeled microspheres (Cerium141, Niobium95, and Ruthenium105; DuPont, Boston, MA) according to the technique described by Heymann et al. (12) Arterial blood samples for plasma catecholamines were measured according to the technique described by Dirks et al (13).

Fifteen minutes before cardiac arrest, 5000 U IV heparin was administered to prevent intracardiac clot formation, the FIO2 was increased to 1.0, a single dose of 0.3 mg IV buprenorphine and 8 mg pancuronium was given, and hemodynamic variables and epinephrine levels were measured. Nineteen animals were randomly assigned into three groups 7 min before induction of cardiac arrest to different protocols to simulate blocked endogenous vasopressin, effective endogenous vasopressin, and exogenous vasopressin, respectively (Table 1). The Antagonist group (n = 7) received 10 µg/kg of the selective vasopressin V1-receptor-antagonist [ß-Mercapto-ß,ß-Cyclopenta-methylenepropionyl, O-Me-Tyr, Arg]-vasopressin, whereas the Exogenous Vasopressin group (n = 6), and the Endogenous Vasopressin animals (n = 6) received saline placebo only (investigators were blinded to the drugs). A 50-Hz alternating current was then applied via two subcutaneous needle electrodes to induce ventricular fibrillation. Cardiopulmonary arrest was defined as the point at which the aortic pulse pressure decreased profoundly to hydrostatic pressure; ventilation was stopped at that point. After 4 min of ventricular fibrillation, open-chest CPR was performed manually, and mechanical ventilation was resumed using the identical ventilation variables as before cardiac arrest. The chest compression rate was 80/min, with the thumb of the right hand placed on the left ventricle while the fingers encircled the right ventricle. After 3 min of CPR, the Exogenous Vasopressin group received 0.8 U/kg arginine vasopressin (Pitressin; Parke-Davis, Berlin, Germany) diluted to 10 mL normal saline, by injection into the right atrium. At the same time, the Blocked Vasopressin pigs and the Endogenous Vasopressin animals were given 10 mL of saline placebo by the same route (investigators were blinded to the drugs).


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  		Table 1. Experimental Protocol and Return of Spontaneous Circulation
 
Hemodynamic variables, left ventricular myocardial blood flow, and epinephrine plasma levels were measured after 90 s of CPR, as well as 90 s and 5 min after drug administration. After 14 min of cardiac arrest, including 10 min of CPR, up to 3 internal countershocks were administered with energy of 2, 2, and 4 Joules/kg, respectively. Return of spontaneous circulation was defined as an unassisted pulse with a systolic arterial pressure of >=80 mm Hg, and pulse pressure of >=40 mm Hg, lasting for 5 min. After finishing the experimental protocol, the animals were killed and autopsied to check correct positioning of the catheters and damage to the rib cage and internal organs and to harvest the internal organs.

Comparability of baseline data was tested using Student’s t-test for continuous variables. One-way analysis of variance was used to determine statistical significance between groups; these were corrected with the Bonferroni method for multiple comparisons. Survival rates were analyzed using Fisher’s exact test. A two-tailed P < 0.05 was considered statistically significant.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Before initiation of the experiment, there were no differences in weight and hemodynamic variables among groups (Table 2). Five minutes after administration of the V1-antagonist or saline placebo, mean arterial pressure decreased by approximately 20% in the Blocked Vasopressin group and was significantly (P < 0.05) lower when compared with the Exogenous Vasopressin and the Endogenous Vasopressin groups (Table 2). During CPR, mean arterial pressure was significantly lower in the Blocked Vasopressin group compared with the Exogenous Vasopressin and Endogenous Vasopressin animals. Administration of exogenous vasopressin during CPR was followed by a significant increase in coronary perfusion pressure when compared with the other two groups.


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  		Table 2. Hemodynamic Variables at Prearrest, and During Cardiopulmonary Resuscitation
 
After drug administration, myocardial blood flow was significantly lower in the Blocked Vasopressin group when compared with the Exogenous Vasopressin and Endogenous Vasopressin animals. The effect was most pronounced on endocardial blood flow, where perfusion was reduced by more than 50% in the Blocked Vasopressin group. Ninety seconds and five minutes after drug administration, left ventricular myocardial blood flow increased significantly in the Exogenous Vasopressin group when compared with the other two groups. Administration of the V1-antagonist was associated with an increase in plasma epinephrine levels before and after induction of cardiac arrest when compared with the Exogenous Vasopressin and Endogenous Vasopressin groups. Injection of exogenous vasopressin was followed by a decrease in epinephrine levels when compared with the Blocked Vasopressin and Endogenous Vasopressin animals.

After 14 min of cardiac arrest, none of the seven Blocked Vasopressin animals, six of six Exogenous Vasopressin animals, and six of six Endogenous Vasopressin animals had return of spontaneous circulation, and survived the 1-h postresuscitation phase (P < 0.05).


   Discussion
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
To determine the role of endogenous and exogenous vasopressin interacting with V1-receptors in critical illness such as during cardiac arrest, three different study arms are necessary: one group with blocked V1-receptors (and therefore a blunted response to endogenously released vasopressin); another cohort of swine with only saline administration during CPR to determine the effects of endogenous vasopressin; and a group of animals given exogenous vasopressin during CPR to study the effects of both exogenous and endogenous vasopressin. In this report, we administered a validated V1-antagonist (14,15), placebo and vasopressin according to the aforementioned study strategy. Thus, we suggest that the present experiment is a useful tool to investigate the role of both endogenous and exogenous vasopressin and their effects on V1-receptors during CPR with a minimum of confounding variables.

The V1-antagonist led to a significant decrease in blood pressure even before induction of cardiac arrest and a concomitant increase in plasma epinephrine levels when compared with the Exogenous Vasopressin and Endogenous Vasopressin groups. Although vasopressin is not the first-line blood pressure regulating mediator, this may indicate that vasopressin is needed as an additional back-up vasopressor during normal cardiocirculatory conditions. This was impressively shown in several studies in critical care unit patients with peripheral catecholamine-resistant vasodilation, when exogenous vasopressin increased left ventricular myocardial blood flow and enabled weaning of catecholamines (6,7). Possibly, the back-up vasopressor vasopressin of the back-up vasopressor epinephrine may be therefore particularly valuable in stress situations, as in our pigs, which underwent a sternotomy for instrumentation before initiation of the experimental CPR protocol. Although a surgical procedure indicates considerable stress, cardiac arrest reflects the most severe possible stress for an organism, resulting in a massive discharge of endogenous epinephrine in an attempt to restore normal cardiocirculatory conditions to survive (16). Beyond the dramatic increase in circulating epinephrine, it is not known how global ischemia affects target organ receptor number and function. In an animal study, increased plasma catecholamine concentrations after CPR did not lead to a decrease in the total density of ß-adrenoreceptors but to an increase in high-affinity ß-adrenoreceptors in right atrial cells in a laboratory model (17). As before induction of cardiac arrest, there was a trend to higher epinephrine plasma levels during CPR in the blocked vasopressin animals than in the Exogenous Vasopressin and Endogenous Vasopressin groups; this may indicate that the neuroendocrinologic system of these animals tried to compensate for the lack of effective endogenous vasopressin with a massive discharge of endogenous epinephrine. In agreement with the results of a previous CPR investigation, exogenous vasopressin administration was followed by a decrease in endogenous plasma epinephrine levels (11). This may indicate that baroreceptors in the arterial vasculature registered increased organ perfusion after exogenous vasopressin and subsequently down-regulated endogenous epinephrine secretion. These results were partially confirmed in a small in-hospital CPR study when exogenous vasopressin caused an increase in coronary perfusion pressure and a decrease in plasma epinephrine levels in four of ten patients being resuscitated after prolonged unsuccessful advanced cardiac life support (18).

Increased epinephrine levels are associated with a considerable increase in myocardial oxygen consumption, resulting in a severe mismatch of cardiac oxygen delivery and myocardial oxygen consumption (19). Although speculative, use of exogenous vasopressin during CPR may therefore have a positive effect on resuscitation success primarily by improving left ventricular myocardial blood flow via a strong peripheral vasoconstriction and, secondly, by reducing epinephrine plasma levels. During unsuccessful prolonged advanced cardiac life support, vasopressin resulted in dramatic increases in blood pressure with subsequent return of spontaneous circulation. This may suggest that that vasopressin filled a void that epinephrine was not able to cover to improve left ventricular myocardial blood flow to a level that ensures successful defibrillation, indicating a possible life-saving role of vasopressin during CPR. A coronary perfusion pressure between 20 mm Hg and 30 mm Hg during CPR is one of the best predictors of return of spontaneous circulation in both animals and humans (20). The blocked vasopressin animals reached this level only very briefly, whereas coronary perfusion pressure in the endogenous vasopressin animals was at this level for the entire experiment, and remained at approximately 40 to 50 mm Hg after exogenous vasopressin, with corresponding values for left ventricular myocardial blood flow. It is therefore not surprising that all exogenous vasopressin and endogenous vasopressin animals in our study could be successfully defibrillated and survived the 60-minute postresuscitation phase, whereas all the pigs treated with the V1-antagonist died. Obviously, the combination of exogenous and endogenous vasopressin in terms of increasing left ventricular myocardial blood flow was extremely efficient in our model, but there were are also interesting differences between the Blocked Vasopressin and the Endogenous Vasopressin groups.

Although there was no significant difference in coronary perfusion pressure between Blocked Vasopressin versus the Endogenous Vasopressin groups, there was a significantly increased left ventricular myocardial blood flow in the Endogenous Vasopressin group. The effect was most marked on endocardial blood flow. This may underlie the important observation that six of six Endogenous Vasopressin, but none of seven Blocked Vasopressin animals, had return of spontaneous circulation. This is actually surprising because open-chest CPR yields good coronary perfusion pressure and should render successful return of spontaneous circulation more likely by itself. This may indicate that endogenous vasopressin plays an important—or possibly, as in our study—a life-saving role in the stress response of an organism to cardiac arrest and subsequent CPR. This observation is striking because epinephrine is the endogenous stress hormone that has been considered the primary drug to reverse profound decreases in left ventricular myocardial blood flow during shock states (16). This investigation therefore gives weight to the assumption that endogenous vasopressin is an adjunct vasopressor to epinephrine and may serve as a back-up regulator to maintain cardiocirculatory homeostasis. This effect may have been underestimated so far because of the design of most studies, which only used exogenous vasopressin, and did not consider the role of endogenous vasopressin, which warrants further investigation.

A limitation of this study is that there are different vasopressin receptors in pigs (lysine vasopressin) and humans (arginine vasopressin), which may result in a different hemodynamic response to exogenously administered arginine vasopressin. In addition, this study lacks dose-response data. Also, use of potent anesthetics may have impaired cardiovascular function and the response of the autonomic nervous system. Furthermore, we used young, healthy pigs that were free from atherosclerotic disease. Open-chest CPR was chosen because it provides excellent blood flow and therefore comparable conditions rendering a better control of confounding variables. Furthermore, we are unable to determine whether vasopressin receptors had been completely blocked because we did not measure vasopressin levels during CPR; therefore a certain, small percentage of vasopressin activity may have been present. Because we were unable to measure left ventricular myocardial blood flow using radioactive microspheres in the postresuscitation phase as a result of limitations posed by government regulations in Austria, we cannot comment on the effects of drugs given during CPR on organ perfusion after successful defibrillation. Finally, it should be mentioned that we did not measure vasopressin plasma levels in our swine; we are therefore unable to comment on levels on the duration and extent of endogenous vasopressin discharge.

In conclusion, pigs with blocked endogenous vasopressin had poor coronary perfusion pressure and left ventricular myocardial blood flow during open-chest CPR and could not be resuscitated successfully, whereas all pigs with effective endogenous vasopressin or pigs with effective endogenous vasopressin and administration of exogenous vasopressin had good left ventricular myocardial blood flow during experimental CPR and survived the 60-minute postresuscitation phase.


   Acknowledgments
 
Supported, in part, by the Austrian Science Foundation grant 14169-MED, Vienna, Austria; the Founder’s Grant of the Society of Critical Care Medicine, Anaheim, California; and a Dean’s grant for Medical School graduates of the Leopold-Franzens-University of Innsbruck, Austria.


   Footnotes
 
To be submitted, in part, to the 73rdScientific Sessions of the American Heart Association Medicine, New Orleans, LA, November 2000.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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Accepted for publication February 14, 2001.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2001 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press