Abstract
Urethane-anesthetized rats were used to study the mechanism of cocaine-induced death. Continuous recording of the changes in five physiological parameters, including respiratory rate (RR), electroencephalogram (EEG), blood pressure (BP), electrocardiogram (ECG), and body temperature (BT), were conducted after intraperitoneal (IP) administration of a single dose of cocaine HCl (70 mg/kg). In the control group (normothermic with core body temperature 37.7±0.1°C spontaneously breathing), the death rate was 88% (15/17), and the average time to respiratory arrest was 12.99±1.40 min (mean±SEM). The first set experiments investigated the contribution of hypothermia to cocaine-induced death. The hypothermic group (core body temperature 33.9±0.3°C and spontaneously breathing) had a death rate of 81.5% (22/27), and an average time to respiratory arrest of 16.70±1.24 min, which was significantly (p<0.05) prolonged. A substantial decrease in respiratory rate was seen in normothermic group, while all the other measured parameters remained relatively stable until respiratory arrest. Sequential arterial blood gas data in this group showed a decrease in PaO2 from 116.0±5.7 mmHg to 57.7±4.6 mmHg, and increase in PaCO2 from 27.7±2.2 mmHg to 42.7±3.0 mmHg, and a decrease in pH from 7.467±0.039 to 7.357±0.003. To confirm that respiratory depression was an important mechanism of cocaine-induced death in this model, ten normothermic rats underwent mechanical ventilation, and all survived cocaine exposure. This study points to the important role of respiratory depression as a cause of cocaine-induced death.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 625-633 |
| Number of pages | 9 |
| Journal | Pharmacology, Biochemistry and Behavior |
| Volume | 39 |
| Issue number | 3 |
| DOIs | |
| State | Published - 1991 |
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Keywords
- Cocaine
- Hypothermia
- Mechanism of death
- Rat
- Respiratory depression
- Seizures
- Urethane
ASJC Scopus subject areas
- Biochemistry
- Behavioral Neuroscience
- Pharmacology
Cite this
Cocaine-induced respiratory depression in urethane-anesthetized rats : A possible mechanism of cocaine-induced death. / Tseng, Chui Chung; Derlet, Robert W.; Stark, Larry G.; Albertson, Timothy E.
In: Pharmacology, Biochemistry and Behavior, Vol. 39, No. 3, 1991, p. 625-633.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cocaine-induced respiratory depression in urethane-anesthetized rats
T2 - A possible mechanism of cocaine-induced death
AU - Tseng, Chui Chung
AU - Derlet, Robert W.
AU - Stark, Larry G.
AU - Albertson, Timothy E
PY - 1991
Y1 - 1991
N2 - Urethane-anesthetized rats were used to study the mechanism of cocaine-induced death. Continuous recording of the changes in five physiological parameters, including respiratory rate (RR), electroencephalogram (EEG), blood pressure (BP), electrocardiogram (ECG), and body temperature (BT), were conducted after intraperitoneal (IP) administration of a single dose of cocaine HCl (70 mg/kg). In the control group (normothermic with core body temperature 37.7±0.1°C spontaneously breathing), the death rate was 88% (15/17), and the average time to respiratory arrest was 12.99±1.40 min (mean±SEM). The first set experiments investigated the contribution of hypothermia to cocaine-induced death. The hypothermic group (core body temperature 33.9±0.3°C and spontaneously breathing) had a death rate of 81.5% (22/27), and an average time to respiratory arrest of 16.70±1.24 min, which was significantly (p<0.05) prolonged. A substantial decrease in respiratory rate was seen in normothermic group, while all the other measured parameters remained relatively stable until respiratory arrest. Sequential arterial blood gas data in this group showed a decrease in PaO2 from 116.0±5.7 mmHg to 57.7±4.6 mmHg, and increase in PaCO2 from 27.7±2.2 mmHg to 42.7±3.0 mmHg, and a decrease in pH from 7.467±0.039 to 7.357±0.003. To confirm that respiratory depression was an important mechanism of cocaine-induced death in this model, ten normothermic rats underwent mechanical ventilation, and all survived cocaine exposure. This study points to the important role of respiratory depression as a cause of cocaine-induced death.
AB - Urethane-anesthetized rats were used to study the mechanism of cocaine-induced death. Continuous recording of the changes in five physiological parameters, including respiratory rate (RR), electroencephalogram (EEG), blood pressure (BP), electrocardiogram (ECG), and body temperature (BT), were conducted after intraperitoneal (IP) administration of a single dose of cocaine HCl (70 mg/kg). In the control group (normothermic with core body temperature 37.7±0.1°C spontaneously breathing), the death rate was 88% (15/17), and the average time to respiratory arrest was 12.99±1.40 min (mean±SEM). The first set experiments investigated the contribution of hypothermia to cocaine-induced death. The hypothermic group (core body temperature 33.9±0.3°C and spontaneously breathing) had a death rate of 81.5% (22/27), and an average time to respiratory arrest of 16.70±1.24 min, which was significantly (p<0.05) prolonged. A substantial decrease in respiratory rate was seen in normothermic group, while all the other measured parameters remained relatively stable until respiratory arrest. Sequential arterial blood gas data in this group showed a decrease in PaO2 from 116.0±5.7 mmHg to 57.7±4.6 mmHg, and increase in PaCO2 from 27.7±2.2 mmHg to 42.7±3.0 mmHg, and a decrease in pH from 7.467±0.039 to 7.357±0.003. To confirm that respiratory depression was an important mechanism of cocaine-induced death in this model, ten normothermic rats underwent mechanical ventilation, and all survived cocaine exposure. This study points to the important role of respiratory depression as a cause of cocaine-induced death.
KW - Cocaine
KW - Hypothermia
KW - Mechanism of death
KW - Rat
KW - Respiratory depression
KW - Seizures
KW - Urethane
UR - http://www.scopus.com/inward/record.url?scp=0026094332&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026094332&partnerID=8YFLogxK
U2 - 10.1016/0091-3057(91)90138-R
DO - 10.1016/0091-3057(91)90138-R
M3 - Article
C2 - 1784591
AN - SCOPUS:0026094332
VL - 39
SP - 625
EP - 633
JO - Pharmacology Biochemistry and Behavior
JF - Pharmacology Biochemistry and Behavior
SN - 0091-3057
IS - 3
ER -