title: The hemodynamic effects of treatment with interleukin-2 and lymphokine-activated killer cells.
abstract: OBJECTIVE
  To determine the hemodynamic alterations occurring during therapy with the maximally tolerated doses of interleukin-2 and lymphokine-activated killer cells.
  
  
  METHODS
  Case series.
  
  
  METHODS
  Referal-based inpatient oncology service at a university medical center.
  
  
  METHODS
  A sequential sample of 13 patients with metastatic colon carcinoma, malignant melanoma, or hypernephroma who were receiving treatment with interleukin-2 and lymphokine-activated killer cells in the maximally tolerated doses.
  
  
  RESULTS
  Pretreatment variables of mean arterial pressure, systemic vascular resistance, heart rate, pulmonary capillary wedge pressure, and cardiac index were compared with the same variables measured either immediately before the eighth dose of interleukin-2 or immediately before the initiation of pressor support with dopamine hydrochloride. When these values were compared with the pretreatment values, patients showed a significant decrease in mean arterial pressure (92 mm Hg compared with 75 mm Hg; P less than 0.0001), and systemic vascular resistance (15.1 compared with 8.5 mm Hg/L . min; P less than 0.0001), but an increase in heart rate (73 compared with 110 beats/min; P less than 0.0001) and cardiac index (3.1 compared with 4.7 L/min . m2 body surface area; P less than 0.0001). No significant change was noted in pulmonary capillary wedge pressure. Low systemic vascular resistance persisted throughout interleukin-2 therapy. Although blood pressure normalized in 24 hours, the systemic vascular resistance remained below baseline levels 6 days after interluekin therapy had been stopped.
  
  
  METHODS
  Blood pressure was successfully supported at greater than 90 mm Hg with dopamine hydrochloride or phenylephrine hydrochloride, or both.
  
  
  CONCLUSIONS
  Therapy with high doses of interleukin-2 induces hemodynamic changes consistent with a high-output and low-resistance state similar to changes noted during the early phase of septic shock.
authors.affiliation: Loyola University Stritch School of Medicine, Maywood, Illinois.
authors.forename: E R
authors.initials: ER
authors.lastname: Gaynor
authors.forename: L
authors.initials: L
authors.lastname: Vitek
authors.forename: L
authors.initials: L
authors.lastname: Sticklin
authors.forename: S P
authors.initials: SP
authors.lastname: Creekmore
authors.forename: M E
authors.initials: ME
authors.lastname: Ferraro
authors.forename: J X
authors.initials: JX
authors.lastname: Thomas
authors.forename: S G
authors.initials: SG
authors.lastname: Fisher
authors.forename: R I
authors.initials: RI
authors.lastname: Fisher
mesh_terms: D006439:Hemodynamics; D006801:Humans; D007022:Hypotension / Q000188:drug therapy / Q000209:etiology; D007376:Interleukin-2 / Q000009:adverse effects* / Q000627:therapeutic use; D007694:Killer Cells, Natural / Q000276:immunology*; D008991:Monitoring, Physiologic; D009369:Neoplasms / Q000628:therapy; D012772:Shock, Septic / Q000503:physiopathology; D013610:Tachycardia / Q000188:drug therapy / Q000209:etiology; D014655:Vascular Resistance
chemical_list: D007376:Interleukin-2