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Vasostrict
(vasopressin) Injection
Vasopressin is a polypeptide hormone that causes contraction of vascular and other smooth muscles and antidiuresis. Vasostrict is a sterile, aqueous solution of synthetic arginine vasopressin for intravenous administration. The 1 mL solution contains vasopressin 20 units/mL, chlorobutanol, NF 0.5% as a preservative, and Water for Injection, USP adjusted with acetic acid to pH 3.4 – 3.6.
The chemical name of vasopressin is Cyclo (1-6) L-Cysteinyl-L-Tyrosyl-L-Phenylalanyl-LGlutaminyl-L-Asparaginyl-L-Cysteinyl-L-Prolyl-L-Arginyl-L-Glycinamide. It is a white to off-white amorphous powder, freely soluble in water. The structural formula is:
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One mg is equivalent to 530 units.
Vasostrict® is indicated to increase blood pressure in adults with vasodilatory shock (e.g., postcardiotomy or sepsis) who remain hypotensive despite fluids and catecholamines.
Dilute Vasostrict in normal saline (0.9% sodium chloride) or 5% dextrose in water (D5W) prior to use. Discard unused diluted solution after 18 hours at room temperature or 24 hours under refrigeration.
Table 1 : Preparation of diluted solutions
| Fluid restriction? | Final concentration | Mix | |
| Vasostrict | Diluent | ||
| No | 0.1 units/mL | 2.5 mL (50 units) | 500 mL |
| Yes | 1 unit/mL | 5 mL (100 units) | 100 mL |
Inspect parenteral drug products for particulate matter and discoloration prior to use, whenever solution and container permit.
The goal of treatment is optimization of perfusion to critical organs, but aggressive treatment can compromise perfusion of organs, like the gastrointestinal tract, whose function is difficult to monitor. The following advice is empirical. In general, titrate to the lowest dose compatible with a clinically acceptable response.
For post-cardiotomy shock, start with a dose of 0.03 units/minute. For septic shock, start with a dose of 0.01 units/minute. If the target blood pressure response is not achieved, titrate up by 0.005 units/minute at 10- to 15-minute intervals. The maximum dose for post-cardiotomy shock is 0.1 units/minute and for septic shock 0.07 units/minute. After target blood pressure has been maintained for 8 hours without the use of catecholamines, taper Vasostrict by 0.005 units/minute every hour as tolerated to maintain target blood pressure.
Injection: 20 units per mL; packaged as 1 mL per vial
Vasostrict (vasopressin injection, USP) is supplied in vials as follows:
A carton of 25 multi-dose vials each containing vasopressin 1 mL at 20 units/mL.
Store between 2°C and 8°C (36°F and 46°F). Do not freeze.
Vials may be held up to 12 months upon removal from refrigeration to room temperature storage conditions (20°C to 25°C [68°F to 77°F], USP Controlled Room Temperature), anytime within the labeled shelf life. Once removed from refrigeration, unopened vial should be marked to indicate the revised 12 month expiration date. If the manufacturer's original expiration date is shorter than the revised expiration date, then the shorter date must be used. Do not use Vasostrict beyond the manufacturer's expiration date stamped on the vial.
Discard vial after 48 hours after first puncture.
The storage conditions and expiration periods are summarized in the following table.
| Unopened Refrigerated | Unopened Room Temperature | Opened (After First Puncture) | |
| 1 mL Vial | Until manufacturer expiration date | 12 months or until manufacturer expiration date, whichever is earlier | 48 hours |
Manufactured by: Â Par Pharmaceutical Companies, Inc. , Spring Valley, NY 10977. Revised: March 2015
The following adverse reactions associated with the use of vasopressin were identified in the literature. Because these reactions are reported voluntarily from a population of uncertain size, it is not possible to estimate their frequency reliably or to establish a causal relationship to drug exposure.
Bleeding/lymphatic system disorders: Hemorrhagic shock, decreased platelets, intractable bleeding
Cardiac disorders: Right heart failure, atrial fibrillation, bradycardia, myocardial ischemia
Gastrointestinal disorders: Mesenteric ischemia
Hepatobiliary: Increased bilirubin levels
Renal/urinary disorders: Acute renal insufficiency
Vascular disorders: Distal limb ischemia
Metabolic: Hyponatremia
Skin: Ischemic lesions
Use with catecholamines is expected to result in an additive effect on mean arterial blood pressure and other hemodynamic parameters.
Use with indomethacin may prolong the effect of Vasostrict on cardiac index and systemic vascular resistance [see CLINICAL PHARMACOLOGY].
Use with ganglionic blocking agents may increase the effect of Vasostrict on mean arterial blood pressure [see CLINICAL PHARMACOLOGY].
Use with furosemide increases the effect of Vasostrict on osmolar clearance and urine flow [see CLINICAL PHARMACOLOGY].
Use with drugs suspected of causing SIADH (e.g., SSRIs, tricyclic antidepressants, haloperidol, chlorpropamide, enalapril, methyldopa, pentamidine, vincristine, cyclophosphamide, ifosfamide, felbamate) may increase the pressor effect in addition to the antidiuretic effect of Vasostrict.
Use with drugs suspected of causing diabetes insipidus (e.g., demeclocycline, lithium, foscarnet, clozapine) may decrease the pressor effect in addition to the antidiuretic effect of Vasostrict.
Included as part of the PRECAUTIONS section.
Use in patients with impaired cardiac response may worsen cardiac output.
No formal carcinogenicity or fertility studies with vasopressin have been conducted in animals. Vasopressin was found to be negative in the in vitro bacterial mutagenicity (Ames) test and the in vitro Chinese hamster ovary (CHO) cell chromosome aberration test. In mice, vasopressin has been reported to have an effect on function and fertilizing ability of spermatozoa.
Pregnancy Category C
There are no adequate or well-controlled studies of Vasostrict in pregnant women. It is not known whether vasopressin can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Animal reproduction studies have not been conducted with vasopressin [see CLINICAL PHARMACOLOGY].
Because of increased clearance of vasopressin in the second and third trimester, the dose of Vasostrict may need to be up-titrated to doses exceeding 0.1 units/minute in post-cardiotomy shock and 0.07 units/minute in septic shock.
Vasostrict may produce tonic uterine contractions that could threaten the continuation of pregnancy.
It is not known whether vasopressin is present in human milk. However, oral absorption by a nursing infant is unlikely because vasopressin is rapidly destroyed in the gastrointestinal tract. Consider advising a lactating woman to pump and discard breast milk for 1.5 hours after receiving vasopressin to minimize potential exposure to the breastfed infant.
Safety and effectiveness of Vasostrict in pediatric patients with vasodilatory shock have not been established.
Clinical studies of vasopressin did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS, and CLINICAL PHARMACOLOGY].
Overdosage with Vasostrict can be expected to manifest as consequences of vasoconstriction of various vascular beds (peripheral, mesenteric, and coronary) and as hyponatremia. In addition, overdosage may lead less commonly to ventricular tachyarrhythmias (including Torsade de Pointes), rhabdomyolysis, and non-specific gastrointestinal symptoms.
Direct effects will resolve within minutes of withdrawal of treatment.
Vasostrict is contraindicated in patients with known allergy or hypersensitivity to 8-L-arginine vasopressin or chlorobutanol.
The vasoconstrictive effects of vasopressin are mediated by vascular V1 receptors. Vascular V1 receptors are directly coupled to phopholipase C, resulting in release of calcium, leading to vasoconstriction. In addition, vasopressin stimulates antidiuresis via stimulation of V2 receptors which are coupled to adenyl cyclase.
At therapeutic doses exogenous vasopressin elicits a vasoconstrictive effect in most vascular beds including the splanchnic, renal and cutaneous circulation. In addition, vasopressin at pressor doses triggers contractions of smooth muscles in the gastrointestinal tract mediated by muscularV1-receptors and release of prolactin and ACTH via V3 receptors. At lower concentrations typical for the antidiuretic hormone vasopressin inhibits water diuresis via renal V2 receptors. In patients with vasodilatory shock vasopressin in therapeutic doses increases systemic vascular resistance and mean arterial blood pressure and reduces the dose requirements for norepinephrine. Vasopressin tends to decrease heart rate and cardiac output. The pressor effect is proportional to the infusion rate of exogenous vasopressin. Onset of the pressor effect of vasopressin is rapid, and the peak effect occurs within 15 minutes. After stopping the infusion the pressor effect fades within 20 minutes. There is no evidence for tachyphylaxis or tolerance to the pressor effect of vasopressin in patients.
At infusion rates used in vasodilatory shock (0.01-0.1 units/minute) the clearance of vasopressin is 9 to 25 mL/min/kg in patients with vasodilatory shock. The apparent t½ of vasopressin at these levels is ≤ 10 minutes. Vasopressin is predominantly metabolized and only about 6% of the dose is excreted unchanged in urine. Animal experiments suggest that the metabolism of vasopressin is primarily by liver and kidney. Serine protease, carboxipeptidase and disulfide oxido-reductase cleave vasopressin at sites relevant for the pharmacological activity of the hormone. Thus, the generated metabolites are not expected to retain important pharmacological activity.
Indomethacin more than doubles the time to offset for vasopressin's effect on peripheral vascular resistance and cardiac output in healthy subjects [see DRUG INTERACTIONS]. The ganglionic blocking agent tetra-ethylammonium increases the pressor effect of vasopressin by 20% in healthy subjects [see DRUG INTERACTIONS].
Furosemide increases osmolar clearance 4-fold and urine flow 9-fold when co-administered with exogenous vasopressin in healthy subjects [see DRUG INTERACTIONS]. Halothane, morphine, fentanyl, alfentanyl and sufentanyl do not impact exposure to endogenous vasopressin.
Pregnancy: Because of a spillover into blood of placental vasopressinase the clearance of exogenous and endogenous vasopressin increases gradually over the course of a pregnancy. During the first trimester of pregnancy the clearance is only slightly increased. However, by the third trimester the clearance of vasopressin is increased about 4-fold and at term up to 5-fold. After delivery the clearance of vasopressin returns to pre-conception baseline within two weeks.
Increases in systolic and mean blood pressure following administration of vasopressin were observed in 7 studies in septic shock and 8 in post-cardiotomy vasodilatory shock.
No information provided. Please refer to the WARNINGS AND PRECAUTIONS section.
