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PubMed1993

Effects of vasopressin on the response to carotid occlusion in conscious rabbits.

To investigate the interaction between arginine vasopressin and the carotid sinus baroreflex, hemodynamic responses to bilateral carotid occlusion and to controlled reductions in carotid sinus pressure were examined. In the control state and during vasopressin infusion in conscious rabbits, mean arterial pressure, heart rate, mean aortic flow and total peripheral resistance were measured. Vasopressin infusion at 5 or 10 ng/kg/min did not raise arterial pressure, but increased resistance, and decreased heart rate and aortic flow in a dose-dependent manner. The pressure and resistance responses to carotid occlusion or changes in carotid pressure were not altered by vasopressin. The heart rate response was augmented significantly from 23 +/- 5 (mean +/- S.E.) to 40 +/- 8 and 43 +/- 8 beats/min with infusion of 5 and 10 ng/kg/min of vasopressin. Vasopressin did not augment the gain of carotid sinus reflex control of arterial pressure (3.7 +/- 0.5 in control and 3.5 +/- 0.5 during 5 ng/kg/min of vasopressin). With vasopressin infusion at 5 ng/kg/min, following vagal blockade with methylatropine both the arterial pressure and the heart rate responses to carotid pressure changes decreased to 73% and 32% of the response before blockade. The data indicate that vasopressin has little effect on control of arterial pressure by the carotid sinus baroreflex in conscious rabbits when vagal responses are activated.

Animals↗
PubMed1984

Vasopressin impairs or enhances retention of learned submissive behavior in mice depending on the time of application.

The effects of vasopressin on learning and memory were investigated in a paradigm using adaptive capabilities of interacting male mice. Test animals of the DBA/2 strain which were not submissive in a confrontation with a non-aggressive subordinate C57BL/6 mouse on day 1 (baseline), were defeated on day 2 (learning) by an aggressive dominant C57 mouse, and showed learned submissive behavior upon mere contact with a non-aggressive C57 mouse on day 3 (retest). Pretrial injections of lysine-vasopressin (0.01, 0.1 or 1.0 I.U., s.c.) 20 min before defeat on day 2 resulted in less submissive behavior on day 3 compared to controls, with 0.1 I.U. (equal to 370 ng) being the most effective dose. Post-trial injections of vasopressin (0.1 I.U.) immediately after defeat on day 2 significantly improved retention on day 3. Preretention injections of vasopressin (0.1 I.U.) 20 min before testing on day 3 significantly increased learned submissive behavior. The amnesic effect observed after pretrial injections of vasopressin was neither due to state dependency nor to an acquisition deficit, nor to antinociception. It is concluded that processing of the stressful experience of defeat is differently influenced by vasopressin given before or after training, resulting in an impaired or facilitated retention, respectively. Among the hypothetically discussed underlying mechanisms, one suggestion is that exogenous vasopressin interacts with an assumed discriminative stimulus function of endogenously released vasopressin. Another possibility might be that exogenous vasopressin interferes with the defeat-activated opioid peptide system.

Aggression↗
PubMed1990

Effects of peripherally administered arginine-vasopressin on learning, retention and forgetting in mice.

The effects of peripheral injections of (Arg)-vasopressin were investigated on different stages of memory processes using an appetitive visual discrimination task and a one-trial passive avoidance conditioning in mice. The peptide was administered at one of two doses: 50 micrograms/kg or 25 micrograms/kg. The main effects of vasopressin were observed only for the higher dose. Concerning pre-session vasopressin administration in the visual discrimination task, the effect of the peptide seemed to depend on the level of learning reached at the time of treatment. Indeed, we observed a deleterious effect of vasopressin on learning capacities when the peptide was administered before the first learning session, a bimodal effect (either an improvement or an impairment) on performance when the peptide was administered before the second learning session and an important enhancement of retention performance when the peptide was administered before the retention session, performed 24 days after training. When post-session vasopressin administration was assessed, an improvement of performance was observed indicating a facilitatory effect of vasopressin on consolidation processes. When passive avoidance conditioning was used, an enhancement of retention performance was registered only when the peptide was injected before the retention session at the 50 micrograms/kg dose. No facilitation was observed for the 25 micrograms/kg dose whatever the experimental condition was, i.e. post-learning or pre-retention injection. In order to test eventual non-specific effects of vasopressin, the influence of the peptide on locomotor activity was assessed before the two doses. The results show an important reduction of locomotor activity with the 50 micrograms/kg dose, during 4 h following vasopressin injection. No effect was observed with the 25 micrograms/kg dose. The whole results suggest that vasopressin-induced hypoactivity can directly influence the subsequent learning performance when the treatment was performed in pre-session situations. However, when the level of information is sufficient and beyond the direct effect of the drug, a memory effect may be considered with the 50 micrograms/kg dose independently from the locomotor effect, when the treatment was delivered during consolidation period (post-session) or in long-term retrieval situation (pre-session).

Animals↗
PubMed1987

Long-term stimulation of cAMP production in LLC-PK1 pig kidney epithelial cells by salmon calcitonin or a photoactivatable analogue of vasopressin.

A photoreactive analogue of vasopressin, [1-(3-mercapto)propionic acid, 8-(N6-4-azidophenylamidino)lysine]-vasopressin, was compared to salmon calcitonin and [8-arginine]-vasopressin with respect to stimulation of cAMP synthesis in the LLC-PK1 pig kidney epithelial cell line. Without photoactivation, the vasopressin analogue-elicited responses were identical to those induced by vasopressin, in that cAMP synthesis returned to the basal, unstimulated level about 4 h after hormonal treatment. In contrast, the levels of activation of cAMP-dependent protein kinase induced by salmon calcitonin returned to basal approx. 12 h after hormone addition. When activated by ultraviolet irradiation, the vasopressin analogue induced 'permanent' stimulation of adenylate cyclase, whereby cAMP production could be detected even 12.5 h after treatment. Both salmon calcitonin and the photoactivated vasopressin analogue inhibited growth of LLC-PK1 cells, in contrast to vasopressin or the nonactivated analogue. Growth inhibition appeared to be a consequence of the prolonged stimulation of adenylate cyclase. This conclusion was supported by the fact that a LLC-PK1 cell mutant in cAMP-dependent protein kinase was resistant to growth inhibition by salmon calcitonin and activated vasopressin analogue. The results imply that the cAMP-dependent protein kinase is the mediator of the hormone-stimulated growth inhibition.

Animals↗
PubMed2005

Inhibitory effects of different galanin compounds and fragments on osmotically and histamine-induced enhanced vasopressin secretion in rats.

The effects of rat, porcine and human galanin, and the human 1-16 and human 16-30 terminal galanin fragments on vasopressin secretion were studied in rat. The plasma vasopressin level was determined by radioimmunoassay (RIA). There were no changes in the basal vasopressin secretion after galanin administration. A significant increase in vasopressin concentration was detected following 2.5% NaCl or histamine administration. I.c.v. injected rat, porcine or human galanin or the 1-16 N-terminal galanin fragment prevented the plasma vasopressin level enhancement. Following the i.v. administration of rat galanin or the i.c.v. injected 16-30 C-terminal galanin fragment, the vasopressin concentration did not return to the normal level. Administration of the galanin antagonist galantid (M15) i.c.v. before the rat galanin i.c.v. injection prevented the inhibitory effect on the increased plasma vasopressin level following 2.5% NaCl solution or histamine administration. The results indicate that there is no significant difference in the inhibitory effect of rat, porcine or human galanin or the 1-16 galanin fragment on the enhanced plasma vasopressin secretion induced by hyperosmosis or histamine administration. Our findings suggest that galanin, as a peptide modulator, is physiologically involved in the regulation of vasopressin release following different forms of stimulation: an osmotic response or histamine administration.

Animals↗
PubMed2005

Greater vasopressin-induced vasoconstriction and inferior effects of nitrovasodilators and milrinone in the radial artery than in the internal thoracic artery.

BACKGROUND: Vasopressin may be a potential cause of spasm in both the radial artery and the internal thoracic artery. This study compared the vasopressin-induced contraction and the effects of milrinone, nitroglycerin, and nitroprusside in vasopressin-induced contraction between the human radial artery and the internal thoracic artery to find effective antispastic methods for arterial grafts. METHODS: Concentration-contraction (normalized as force gram produced by each millimeter of the circumference tissue of the artery) curves for vasopressin with or without pretreatment of vasodilators and concentration-relaxation curves for the vasodilators listed were established in the human radial artery (n = 107) and internal thoracic artery (n = 122) segments. RESULTS: Vasopressin induced a greater contraction in the radial artery than in the internal thoracic artery (1.9 +/- 0.2 g/mm vs 0.6 +/- 0.1 g/mm, P < .001) with a higher sensitivity (lower EC(50): -9.28 +/- 0.11 vs -8.91 +/- 0.05 log(10)M, P = .006). Milrinone was less potent than nitroglycerin and nitroprusside with higher EC(50) (P < .05) in both the internal thoracic artery and radial artery. Pretreatment with milrinone and nitroprusside significantly inhibited vasopressin contraction in the internal thoracic artery but had little effect in the radial artery. Pretreatment with nitroglycerin did not significantly inhibit the maximum vasopressin contraction in either the internal thoracic artery or radial artery. CONCLUSION: The radial artery is more prone to develop spasm related to vasopressin than is the internal thoracic artery, and the effect of vasodilators in vasopressin-induced contraction is different in the radial artery from that in the internal thoracic artery. A more significant prophylactic antispastic effect of milrinone and nitroprusside is demonstrated in the internal thoracic artery than in the radial artery. Therefore, more intensive antispastic treatment is necessary in the radial artery than in the internal thoracic artery during coronary artery bypass grafting.

Analysis of Variance↗
PubMed2001

Employing vasopressin during cardiopulmonary resuscitation and vasodilatory shock as a lifesaving vasopressor.

Epinephrine during cardiopulmonary resuscitation (CPR) is being discussed controversially due to its beta-receptor mediated adverse effects such as increased myocardial oxygen consumption, ventricular arrhythmias, ventilation-perfusion defect, postresuscitation myocardial dysfunction, ventricular arrhythmias and cardiac failure. In the CPR laboratory simulating adult pigs with ventricular fibrillation or postcountershock pulseless electrical activity, vasopressin improved vital organ blood flow, cerebral oxygen delivery, resuscitability, and neurological recovery better than did epinephrine. In paediatric preparations with asphyxia, epinephrine was superior to vasopressin, whereas in both paediatric pigs with ventricular fibrillation, and adult porcine models with asphyxia, combinations of vasopressin and epinephrine proved to be highly effective. This may suggest that a different efficiency of vasopressors in paediatric vs. adult preparations; and different effects of dysrhythmic vs. asphyxial cardiac arrest on vasopressor efficiency may be of significant importance. Whether these theories can be extrapolated to humans is unknown at this point in time. In patients with out-of-hospital ventricular fibrillation, a larger proportion of patients treated with vasopressin survived 24 h compared with patients treated with epinephrine; during in-hospital CPR, comparable short-term survival was found in groups treated with either vasopressin or epinephrine. Currently, a large trial of out-of-hospital cardiac arrest patients being treated with vasopressin vs. epinephrine is ongoing in Germany, Austria and Switzerland. The new CPR guidelines of both the American Heart Association, and European Resuscitation Council recommend 40 U vasopressin intravenously, and 1 mg epinephrine intravenously as equally effective for the treatment of adult patients in ventricular fibrillation; however, no recommendation for vasopressin was made to date for adult patients with asystole and pulseless electrical activity, and paediatrics due to lack of clinical data. When adrenergic vasopressors were unable to maintain arterial blood pressure in patients with vasodilatory shock, continuous infusions of vasopressin ( approximately 0.04 to approximately 0.1 U/min) stabilised cardiocirculatory parameters, and even ensured weaning from catecholamines.

Animals↗
PubMed2003

Intra-arterial vasopressin in the human forearm: pharmacodynamics and the role of nitric oxide.

BACKGROUND AND OBJECTIVES: Diverse vascular effects have been ascribed to vasopressin, including the potential to cause vasodilation, vasoconstriction, and nitric oxide release. The objective of this study was to establish the pharmacodynamics, reproducibility, and nitric oxide dependence of the vasomotor actions of vasopressin in the forearm resistance vessels. METHODS: Blood flow in both forearms of 12 healthy men was measured with venous occlusion plethysmography. Continuous and discontinuous doses of 1 to 300 pmol/min vasopressin were administered by the intrabrachial route. For assessment of the contribution of nitric oxide, vasopressin was coadministered with a "nitric oxide clamp," a balanced coinfusion of 4 micromol/min L-N(G)-monomethylarginine (a nitric oxide synthase inhibitor) and 0.3 to 0.8 nmol/min sodium nitroprusside (an exogenous nitric oxide donor) to block endogenous nitric oxide production and restore normal basal blood flow, respectively. RESULTS: Vasopressin produced a dose-dependent biphasic change in blood flow with a maximum reduction in percentage change in blood flow ratio of infused and control arms of 22% +/- 5% at 3 pmol/min (P <.01) and an increase of 80% +/- 30% at 300 pmol/min (P <.01). There were no significant differences in repeated responses obtained either within or between days. Repeated discontinuous dosing did not change the magnitude of the maximum vasoconstriction or vasodilation, but prolonged continuous infusion produced maximal vasodilation at 12 minutes that subsequently resulted in substantial tachyphylaxis (P =.04). Although there was no augmentation of vasoconstriction, the nitric oxide clamp abolished vasopressin-induced vasodilation (P <.05). CONCLUSIONS: Intra-arterial vasopressin causes a reproducible dose-dependent biphasic change in forearm blood flow. Vasomotor responses are time-dependent with a modest delay to peak vasodilation and tachyphylaxis with prolonged sustained infusion. Nitric oxide release is a major contributor to vasopressin-induced vasodilation but does not directly oppose low-dose vasopressin-induced vasoconstriction.

Adult↗
PubMed1997

Endothelin contributes to the hemodynamic effects of vasopressin in spontaneous hypertension.

Changes in blood pressure, cardiac output, and total peripheral conductance evoked by intravenous infusions of [Arg8]-vasopressin (vasopressin) were recorded before and after pretreatment with bosentan, a non-selective endothelin antagonist, in conscious unrestrained spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). The presser effects of vasopressin were exaggerated in SHR compared to WKY. Pretreatment with bosentan failed to change hemodynamic responses of WKY to vasopressin, but it blunted the increases in blood pressure and the decreases in conductance evoked by vasopressin in SHR. In contrast, bosentan failed to change cardiac output responses of SHR to vasopressin. Except at the highest dose of vasopressin, bosentan abolished the exaggerated pressor responsiveness of the SHR to vasopressin. The results suggest that endothelin contributes to the exaggerated pressor responsiveness of SHR to vasopressin, and that this effect is exerted at the level of the resistance vessels and not on factors that regulate cardiac output.

Animals↗
PubMed1999

Vasopressin increases vascular endothelial growth factor secretion from human vascular smooth muscle cells.

Vascular endothelial growth factor (VEGF) is a potent and specific mitogen of vascular endothelial cells which promotes neovascularization in vitro. To determine whether vasopressin induces VEGF secretion in human vascular smooth muscle cells, we performed enzyme-linked immunosorbent assays. Vasopressin potently induced a time-dependent and concentration-dependent (maximal, 10(-7) M) increase in VEGF secretion by human vascular smooth muscle cells that was maximal after 24 h. Furthermore, vasopressin also concentration-dependently caused mitogenic effect, as reflected by total protein content of cells per culture well. These vasopressin-induced VEGF secretion increase and mitogenic effect of these cells were potently inhibited by vasopressin V1A receptor antagonists, confirming this is a vasopressin V1A receptor-mediated event. These results indicate that vasopressin increases VEGF secretion in human vascular smooth muscle cells, the magnitude of VEGF secretion being temporally related to the mitogenic effect of vascular smooth muscle cells and the potency of the growth-promoting stimulus. Vasopressin-induced VEGF secretion by proliferating vascular smooth muscle cells could act as a paracrine hormone to powerfully influence the permeability and growth of the overlying vascular endothelium, vasopressin play a more fundamental role in the regulation of vascular function than has previously been recognized.

Antidiuretic Hormone Receptor Antagonists↗
PubMed1999

Eicosapentaenoic acid inhibits vasopressin-activated Ca2+ influx and cell proliferation in rat aortic smooth muscle cell lines.

The purpose of this study was to clarify how eicosapentaenoic acid (EPA), an omega-3 polyunsaturated fatty acid, modulates the vascular action of vasopressin in rat aortic smooth muscle cell lines. The effects of EPA on Ca2+ mobilization and DNA synthesis elicited by vasopressin were investigated and compared to those of Ca2+ channel blocking agents, by means of Ca2+ measurements and the incorporation of [3H]thymidine. Patch-clamp techniques were also employed. Vasopressin (100 nM) elicited an initial peak of intracellular Ca2+ ([Ca2+]i), followed by a sustained phase due to Ca2+ entry. Nifedipine or nicardipine (1 microM), a potent L-type Ca2+ channel blocker, partly inhibited the sustained phase, but La3+ completely abolished it. EPA (10 microM) also inhibited it even in the presence of nicardipine. Under voltage-clamp conditions with CsCl-internal solution, depolarizing pulses positive to -30 mV from a holding potential of -40 mV elicited a slow inward current. The inward current was blocked by La3+, nicardipine, and nifedipine (1 microM), suggesting that the inward current mainly consisted of the voltage-dependent L-type Ca2+ channel (ICa.L). EPA (1-30 microM) also inhibited ICa.L in a concentration-dependent manner. The inhibitory effect of EPA was observed at concentrations higher than 1 microM, and its half-maximal inhibitory concentration (IC50) was 7.6 microM. Vasopressin induced a long-lasting inward current at a holding potential of -40 mV. The vasopressin-induced current was considered as a non-selective cation current (Icat) with a reversal potential of approximately +0 mV. Both nifedipine and nicardipine (10 microM) failed to inhibit it significantly, but La3+ completely abolished Icat. EPA also inhibited vasopressin-induced Icat in a concentration-dependent manner; its IC50 value was 5.9 microM. Vasopressin (100 nM) stimulated [3H]thymidine incorporation. Exclusion of extracellular Ca2+ with EGTA or La3+ markedly inhibited it. EPA (3-30 microM) also inhibited the incorporation induced by vasopressin, while nifedipine and nicardipine (1 microM) only partly inhibited it. These results suggested that EPA, unlike nifedipine and nicardipine, inhibited vasopressin-induced Ca2+-entry and proliferation in rat vascular smooth muscle cells, where the inhibitory effects of EPA on Icat as well as ICa.L might be involved. Thus, EPA would exert hypotensive and antiatherosclerotic effects.

Animals↗
PubMed1998

Phenotypic and state-dependent expression of the electrical and morphological properties of oxytocin and vasopressin neurones.

Oxytocin and vasopressin secreting neurones of the hypothalamic supraoptic nucleus share many membrane characteristics and a roughly similar morphology. However, these two neurone types differ in the relative expression of some intrinsic and synaptic currents, and in the extent of their respective dendritic arbors. Spike depolarizing afterpotentials are present in both types, but more frequently give rise to prolonged burst discharges in vasopressin neurones. Oxytocin, but not vasopressin neurones, are characterized by a depolarization-activated, sustained outward rectifier which turns on near spike threshold, and which can produce prolonged spike frequency adaptation. When this sustained current is deactivated by small hyperpolarizing pulses, a rebound depolarization sufficient to evoke short spike trains follows the offset of these pulses. Both oxytocin and vasopressin neurones exhibit a transient outward rectification underlain by an Ia-type current. This transient rectifier delays spiking to depolarizing stimuli from a relatively hyperpolarized baseline, and is more prominent in vasopressin neurones. As a result, oxytocin neurones may be more reactive to depolarizing inputs. Both cell types receive glutamatergic, excitatory synaptic inputs and both possess R,S- alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor subtypes. The AMPA receptor channel on both cell types is characterized by a relatively high calcium permeability and voltage-dependent rectification, characteristic of a diminished presence of the GluR2 AMPA subunit. However, AMPA-mediated synaptic transients are larger, and decay faster, in oxytocin compared with vasopressin neurones, suggesting a potential difference for synaptic integration. The characteristics of NMDA-mediated synaptic transients are similar in oxytocin and vasopressin neurones, but some data suggest NMDA receptors may be less involved in the glutamatergic activation of oxytocin neurones. In both cell types, synaptic release of glutamate often coactivates AMPA and NMDA receptors. The dendritic morphology of oxytocin and vasopressin neurones in female rats differs from one another and exhibits considerable plasticity as a function of endocrine state. In virgin rats, oxytocin neurones have more dendritic branches and a greater total dendritic length compared with lactation, when the arbor is much less extensive. A complementary change occurs in vasopressin dendrites, which are more extensive during lactation. This reorganization suggests that oxytocin neurones may be more electronically compact during lactation. In addition, such dramatic shifts in overall dendritic length imply that significant gains and losses in either the total number of synapses, or in synaptic density, are incurred by both cell types as a function of reproductive state.

Action Potentials↗
PubMed1997

Central vasopressin is required for the complete development of deoxycorticosterone-salt hypertension in rats with hereditary diabetes insipidus.

It has been shown that vasopressin receptors are upregulated in the brain and that the central vasopressin pathway is involved in the development of deoxycorticosterone acetate (DOCA)-salt hypertension. However, it is unclear whether central vasopressin, in itself, is essential for this type of hypertension. To clarify this issue, the effect of centrally administered vasopressin on the development of DOCA-salt hypertension was studied in homozygous Brattleboro rats which genetically lack vasopressin. In homozygous Brattleboro rats, treatment with intracerebroventricular infusion of vasopressin (1 ng/h) alone or DOCA-salt (weekly subcutaneous injection of 30 mg/kg deoxycorticosterone acetate and 0.3% NaCl to drink) alone had no effect on systolic blood pressure (SBP). On the other hand, hypertension was partially restored in homozygous Brattleboro rats treated with intracerebroventricular infusion of vasopressin and DOCA-salt (SBP: 175 +/- 4 mmHg), although the magnitude of elevation of SBP was one-third of that in Long Evans rats treated with DOCA-salt (278 +/- 15 mmHg). These hypertensive homozygous Brattleboro rats showed an increase in fluid intake and urinary sodium excretion, as observed in DOCA-salt hypertensive Long Evans rats. These results suggest that central vasopressin is required for the complete development of DOCA-salt hypertension and the mechanism is, in part, due to enhanced sodium intake through the additive effect of central vasopressin and DOCA-salt.

Animals↗
PubMed1999

Bradykinin modulates arginine vasopressin-induced calcium influx in vascular myocytes.

UNLABELLED: We investigated direct, endothelium-independent effects of bradykinin on arginine vasopressin-induced calcium influx in vascular smooth muscle cells. We studied cultured rat vascular smooth muscle cells by using the whole-cell voltage-clamp and calcium fluorescence imaging methods. Exposing cultured vascular smooth muscle cells (A7r5 cell line) to arginine vasopressin (100 nM) produced a transient increase in [Ca2+]i, followed by a sustained increase in [Ca2+]i. This was readily reversible (n=28). At a holding potential of -40 to -60 mV, arginine vasopressin induced a sustained inward current correlated with a sustained increase in [Ca2+]i. Bradykinin (30 nM to 30 microM) had no effect on arginine vasopressin-induced [Ca2+]i transients. However, during the sustained phase of increased [Ca2+]i, bradykinin reversibly attenuated relative fluorescence and inward current in the presence of arginine vasopressin (n=14). This was concentration dependent and inhibited by [D-Phe7]-bradykinin (30 microM), a kinin receptor antagonist. Also, sustained arginine vasopressin-mediated increases in [Ca2+]i and inward current were attenuated by Ca2+-free or La3+-supplemented perfusate but not by nifedipine (n=5). CONCLUSIONS: (1) Bradykinin can attenuate arginine vasopressin-induced and sustained Ca2+ influx and sustained inward current through a novel endothelium-independent process. (2) The direct effect of bradykinin on arginine vasopressin-induced increases in [Ca2+]i sustained Ca2+ influx in vascular smooth muscle cells is concentration dependent and kinin-receptor mediated. (3) Arginine vasopressin-induced sustained [Ca2+]i elevation correlates with the activation of a dihydropyridine-insensitive, Ca2+-conducting inward current.

Animals↗
PubMed2001

Hemodynamic effects of tracheal administration of vasopressin in dogs.

BACKGROUND: Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) has been shown to be more effective than optimal doses of epinephrine. Earlier studies had been performed on a porcine model, but pigs produce lysine vasopressin hormone, while humans and dogs do not. This study was designed to compare the effects of tracheal vasopressin with those of NaCl 0.9% (placebo) on haemodynamic variables in a dog model. METHODS: Five dogs were allocated to receive either vasopressin 1.2 U/kg or placebo (10 ml of NaCl 0.9%) via the tracheal route after being anesthetized and ventilated. Haemodynamic variables were determined and arterial blood gases were measured. RESULTS: All animals of the vasopressin group demonstrated a significant increase of the systolic (from 135+/-7 to 165+/-6 mmHg, P<0.05), diastolic (from 85+/-10 to 110+/-10 mmHg, P<0.05) and mean blood pressure (from 98.5+/-3 to 142.2+/-5, P<0.05). Blood pressure rose rapidly and lasted for more than an hour (plateau effect). Heart rate decreased significantly following vasopressin (from 54+/-9 to 40+/-5 beats per min, P<0.05) but not in the placebo group. These changes were not demonstrated with placebo injection. CONCLUSION: Tracheal administration of vasopressin was followed by significantly higher diastolic, systolic and mean blood pressures in the vasopressin group compared with the placebo group. Blood gases remained unchanged in both groups. Vasopressin administered via the trachea may be an acceptable alternative for vasopressor administration during CPR, when intravenous access is delayed or not available, however, further investigation is necessary.

Animals↗
PubMed2002

Resuscitation from cardiac arrest with adrenaline/epinephrine or vasopressin: effects on intestinal mucosal tonometer pCO(2) during the postresuscitation period in rats.

BACKGROUND: The use of vasopressin instead of adrenaline/epinephrine during resuscitation improves vital organ perfusion, but the effects on mesenteric perfusion following successful resuscitation are not fully evaluated. The present study was designed to compare the effects of vasopressin and adrenaline/epinephrine, given to rats during resuscitation from ventricular fibrillation, on to mesenteric ischaemia, as determined by intestinal mucosal tonometer pCO(2) during the postresuscitation period. METHODS AND RESULTS: Male Sprague-Dawley rats (n=28) were allocated randomly to receive vasopressin (0.8 U/kg) or adrenaline/epinephrine (90 microg/kg) after 5 min of ventricular fibrillation. Precordial chest compression was initiated 4 min after the start of ventricular fibrillation, continued for 4 min, and followed by defibrillation. Seven of 14 (vasopressin) and 12 of 14 (adrenaline/epinephrine) rats were successfully defibrillated (P=0.10, Fisher's exact test) and observed for 60 min. Intestinal mucosal tonometer pCO(2) measurements before cardiac arrest and 15, 30, and 60 min following return of spontaneous circulation were 47+/-3, 73+/-8, 63+/-7, and 56+/-6 mmHg in the vasopressin group and 48+/-5, 78+/-7, 67+/-6, and 62+/-6 mmHg in the adrenaline/epinephrine group (P<0.05 at 60 min between vasopressin and adrenaline/epinephrine). Right atrial hemoglobin oxygen saturations at these time points were 73+/-5, 51+/-12, 58+/-11, and 63+/-5% in the vasopressin group and 76+/-7, 44+/-10, 52+/-10 and 54+/-8% in the adrenaline/epinephrine group (P<0.05 at 60 min between vasopressin and adrenaline/epinephrine). CONCLUSIONS: We conclude that in this rat model the administration of vasopressin instead of adrenaline/epinephrine for CPR tends to be associated with lower resuscitation success, but less mesenteric ischaemia during the postresuscitation period in successfully resuscitated rats.

Adrenergic Agonists↗
PubMed2002

Vasopressin with delayed combination of nitroglycerin increases survival rate in asphyxia rat model.

Recently, vasopressin has been reported as a more effective drug than epinephrine (adrenaline) for cardiopulmonary resuscitation (CPR). However, vasopressin decreases myocardial blood flow (MBF) because of its strong vasoconstriction, to maintain better coronary perfusion pressure (CPP) compared with epinephrine. Nitroglycerin is well known to be able to maintain MBF and increase survival rate. In a VF model, vasopressin combined with nitroglycerin maintained CPP; however, low survival rates were observed compared with vasopressin alone. We investigated the effectiveness of the delayed use of nitroglycerin combined with vasopressin in a severe asphyxia model. Fourteen Sprague-Dawley male rats were divided into two groups: vasopressin 0.8 U/kg alone (V-Gr.), and nitroglycerin 0.3 microg/kg 45 s after the administration of 0.8 U/kg vasopressin (VN-Gr.). Six min after asphyxia induced by obstructing the tracheal tube, CPR was performed in two ways. Three animals resuscitated in the V-Gr. (42%) and six/seven (84%) in the VN-Gr. (P<0.05). In the 6 min of asphyxia rat model, vasopressin combined with delayed nitroglycerin is more effective than vasopressin alone.

Animals↗
PubMed2002

Central infusion of vasopressin in male rats accelerates extinction of conditioned taste avoidance induced by LiCl.

In shock avoidance tasks, extinction is prolonged when vasopressin is infused into the lateral ventricle after an acquisition session. Experiments were performed to determine whether a dose of vasopressin that does not induce conditioned taste avoidance (CTA) could prolong extinction of a LiCl-induced CTA when it is infused into the lateral ventricle of Sprague-Dawley male rats after acquisition. The first experiment was designed to determine whether infusion of vasopressin into the lateral ventricle would induce a CTA. Consumption of a sucrose solution was paired with infusion of vasopressin or saline, and even after two pairings, none of the vasopressin-treated rats showed decreases in sucrose consumption. Therefore, in the second experiment, this same dose of vasopressin was infused into the lateral ventricle 50 min after consumption of a sucrose solution was paired with an injection of LiCl. Vasopressin increased the rate of extinction of the LiCl-induced CTA. These results are the opposite of what has been found after peripheral administration of vasopressin before acquisition and/or extinction of a LiCl-induced CTA. Possible reasons for the difference in the direction of the effect on extinction include differential effects of vasopressin depending on the route of administration, the timing of injection, and the presence of aversive effects produced by the neuropeptide.

Animals↗