Pregnancy alters the hemodynamic responses to cocaine in the rat

H. O. Morishima, T. B. Cooper, T. Hara, Edward Miller

Research output: Contribution to journalArticle

Abstract

To test our hypotheses that the hemodynamic response to cocaine may be altered during pregnancy, cocaine (0.33 mg/kg/min) was infused intravenously to chronically catheterized pregnant and nonpregnant female rats. Cardiac output and regional blood flow were measured, and cocaine concentrations in plasma and tissues, as well as plasma cholinesterase activity were determined. Results were compared between pregnant and nonpregnant groups. Cocaine produced a significant decrease in heart rate, accompanied by a fall in cardiac output, and decreased cerebral, myocardial, and placental blood flow in pregnant rats. The plasma cocaine concentration in pregnant animals was lower than that of nonpregnant ones, but tissue concentrations were similar in both groups. These results indicate that pregnancy enhances cardiovascular responses to subtoxic doses of cocaine. There was little placental transfer of cocaine with a fetal to maternal plasma concentration ratio of 0.28.

Original languageEnglish (US)
Pages (from-to)69-79
Number of pages11
JournalDevelopmental Pharmacology and Therapeutics
Volume19
Issue number2-3
StatePublished - 1992
Externally publishedYes

Fingerprint

Cocaine
Hemodynamics
Pregnancy
Cardiac Output
Cholinesterases
Regional Blood Flow
Heart Rate
Mothers

Keywords

  • Cocaine
  • Hemodynamic response
  • Pregnant rat
  • Tissue distribution

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Pharmacology (medical)

Cite this

Pregnancy alters the hemodynamic responses to cocaine in the rat. / Morishima, H. O.; Cooper, T. B.; Hara, T.; Miller, Edward.

In: Developmental Pharmacology and Therapeutics, Vol. 19, No. 2-3, 1992, p. 69-79.

Research output: Contribution to journalArticle

Morishima, H. O. ; Cooper, T. B. ; Hara, T. ; Miller, Edward. / Pregnancy alters the hemodynamic responses to cocaine in the rat. In: Developmental Pharmacology and Therapeutics. 1992 ; Vol. 19, No. 2-3. pp. 69-79.
@article{8a6fb9e0d461476985136485978852c6,
title = "Pregnancy alters the hemodynamic responses to cocaine in the rat",
abstract = "To test our hypotheses that the hemodynamic response to cocaine may be altered during pregnancy, cocaine (0.33 mg/kg/min) was infused intravenously to chronically catheterized pregnant and nonpregnant female rats. Cardiac output and regional blood flow were measured, and cocaine concentrations in plasma and tissues, as well as plasma cholinesterase activity were determined. Results were compared between pregnant and nonpregnant groups. Cocaine produced a significant decrease in heart rate, accompanied by a fall in cardiac output, and decreased cerebral, myocardial, and placental blood flow in pregnant rats. The plasma cocaine concentration in pregnant animals was lower than that of nonpregnant ones, but tissue concentrations were similar in both groups. These results indicate that pregnancy enhances cardiovascular responses to subtoxic doses of cocaine. There was little placental transfer of cocaine with a fetal to maternal plasma concentration ratio of 0.28.",
keywords = "Cocaine, Hemodynamic response, Pregnant rat, Tissue distribution",
author = "Morishima, {H. O.} and Cooper, {T. B.} and T. Hara and Edward Miller",
year = "1992",
language = "English (US)",
volume = "19",
pages = "69--79",
journal = "Developmental Pharmacology and Therapeutics",
issn = "0379-8305",
publisher = "S. Karger AG",
number = "2-3",

}

TY - JOUR

T1 - Pregnancy alters the hemodynamic responses to cocaine in the rat

AU - Morishima, H. O.

AU - Cooper, T. B.

AU - Hara, T.

AU - Miller, Edward

PY - 1992

Y1 - 1992

N2 - To test our hypotheses that the hemodynamic response to cocaine may be altered during pregnancy, cocaine (0.33 mg/kg/min) was infused intravenously to chronically catheterized pregnant and nonpregnant female rats. Cardiac output and regional blood flow were measured, and cocaine concentrations in plasma and tissues, as well as plasma cholinesterase activity were determined. Results were compared between pregnant and nonpregnant groups. Cocaine produced a significant decrease in heart rate, accompanied by a fall in cardiac output, and decreased cerebral, myocardial, and placental blood flow in pregnant rats. The plasma cocaine concentration in pregnant animals was lower than that of nonpregnant ones, but tissue concentrations were similar in both groups. These results indicate that pregnancy enhances cardiovascular responses to subtoxic doses of cocaine. There was little placental transfer of cocaine with a fetal to maternal plasma concentration ratio of 0.28.

AB - To test our hypotheses that the hemodynamic response to cocaine may be altered during pregnancy, cocaine (0.33 mg/kg/min) was infused intravenously to chronically catheterized pregnant and nonpregnant female rats. Cardiac output and regional blood flow were measured, and cocaine concentrations in plasma and tissues, as well as plasma cholinesterase activity were determined. Results were compared between pregnant and nonpregnant groups. Cocaine produced a significant decrease in heart rate, accompanied by a fall in cardiac output, and decreased cerebral, myocardial, and placental blood flow in pregnant rats. The plasma cocaine concentration in pregnant animals was lower than that of nonpregnant ones, but tissue concentrations were similar in both groups. These results indicate that pregnancy enhances cardiovascular responses to subtoxic doses of cocaine. There was little placental transfer of cocaine with a fetal to maternal plasma concentration ratio of 0.28.

KW - Cocaine

KW - Hemodynamic response

KW - Pregnant rat

KW - Tissue distribution

UR - http://www.scopus.com/inward/record.url?scp=0026997566&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026997566&partnerID=8YFLogxK

M3 - Article

C2 - 1340439

AN - SCOPUS:0026997566

VL - 19

SP - 69

EP - 79

JO - Developmental Pharmacology and Therapeutics

JF - Developmental Pharmacology and Therapeutics

SN - 0379-8305

IS - 2-3

ER -