Abstract
Newborn rats were treated with guanethidine sulfate for the first 3 weeks of life in order to produce a partial permanent peripheral sympathectomy. The rats were allowed to grow to 250-300 grams on a normal sodium diet. Using diethyl ether anesthesia, arterial and venous cannulas were placed and the animals allowed to awaken in restraining cages. The rats were divided into four groups: awake (n = 6), halothane 1.3 vol % (n = 8), enflurane 2.2 vol % (n = 8), and ketamine 125 mg/kg, ip (n = 8). The protocol consisted of a one-hour control awake period, one hour of stable anesthesia (one group received no anesthesia), and one-half-hour iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity was measured at the end of each time period. Thirty untreated normal rats were similarly divided into four groups and served as the control. The degree of peripheral sympathectomy was assessed through cardiac norepinephrine concentrations, plasma catecholamines, and response to 50% hemorrhage. Guanethidine treatment resulted in a 78% decrease in cardiac norepinephrine from 189 ± 15 ng/g in the untreated animals compared with 42.4 ± 5 ng/g in the treated animals. The 5-fold increase seen in plasma norepinephrine to acute decapitation was completely absent in the treated animals. Hemorrhage of 50% of blood volume resulted in a 75% mortality rate in the treated animals, while there were no deaths 30 min after hemorrhage in the normal animals. Blood pressure for the 30 treated animals during the awake period was 114 ± 2 mmHg, which was significantly less than 124 ± 1 mmHg in the untreated animals (P < 0.05). Likewise, plasma renin activity of 1.58 ± 0.25 ng.ml -1.h -1 in the treated group was significantly less than 2.59 ± 0.21 ng.ml -1.h -1 in the untreated rats (P < 0.05). With the induction and maintenance of stable anesthesia, blood pressure decreased to 82 ± 2 mmHg with halothane, 92 ± 4 mmHg with enflurane, and 104 ± 4 mmHg with ketamine in the treated animals. Plasma renin activity did not increase in either treated or untreated animals. Similar degrees of blood pressure decreases were seen in untreated animals. With the infusion of saralasin, a further decrease of approximately 20 mmHg in blood pressure was seen, in both the treated and untreated rats anesthetized with halothane. However, in treated rats anesthetized with enflurane or ketamine, no depressor response to saralasin was seen, which is in marked contrast to the response seen in untreated animals. The plasma renin response in the treated animals also was blunted. Using this animal model, these experiments suggest that partial peripheral sympathectomy does not result in deleterious effects when rats are anesthetized with halothane, enflurane, or ketamine anesthesia.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 32-37 |
| Number of pages | 6 |
| Journal | Anesthesiology |
| Volume | 58 |
| Issue number | 1 |
| State | Published - 1983 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Anesthesiology and Pain Medicine
Cite this
Blood pressure control during anesthesia : Importance of the peripheral sympathetic nervous system and renin. / Miller, Edward; Beckman, J. J.; Woodside, J. R.; Althaus, M. S.; Peach, M. J.
In: Anesthesiology, Vol. 58, No. 1, 1983, p. 32-37.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Blood pressure control during anesthesia
T2 - Importance of the peripheral sympathetic nervous system and renin
AU - Miller, Edward
AU - Beckman, J. J.
AU - Woodside, J. R.
AU - Althaus, M. S.
AU - Peach, M. J.
PY - 1983
Y1 - 1983
N2 - Newborn rats were treated with guanethidine sulfate for the first 3 weeks of life in order to produce a partial permanent peripheral sympathectomy. The rats were allowed to grow to 250-300 grams on a normal sodium diet. Using diethyl ether anesthesia, arterial and venous cannulas were placed and the animals allowed to awaken in restraining cages. The rats were divided into four groups: awake (n = 6), halothane 1.3 vol % (n = 8), enflurane 2.2 vol % (n = 8), and ketamine 125 mg/kg, ip (n = 8). The protocol consisted of a one-hour control awake period, one hour of stable anesthesia (one group received no anesthesia), and one-half-hour iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity was measured at the end of each time period. Thirty untreated normal rats were similarly divided into four groups and served as the control. The degree of peripheral sympathectomy was assessed through cardiac norepinephrine concentrations, plasma catecholamines, and response to 50% hemorrhage. Guanethidine treatment resulted in a 78% decrease in cardiac norepinephrine from 189 ± 15 ng/g in the untreated animals compared with 42.4 ± 5 ng/g in the treated animals. The 5-fold increase seen in plasma norepinephrine to acute decapitation was completely absent in the treated animals. Hemorrhage of 50% of blood volume resulted in a 75% mortality rate in the treated animals, while there were no deaths 30 min after hemorrhage in the normal animals. Blood pressure for the 30 treated animals during the awake period was 114 ± 2 mmHg, which was significantly less than 124 ± 1 mmHg in the untreated animals (P < 0.05). Likewise, plasma renin activity of 1.58 ± 0.25 ng.ml -1.h -1 in the treated group was significantly less than 2.59 ± 0.21 ng.ml -1.h -1 in the untreated rats (P < 0.05). With the induction and maintenance of stable anesthesia, blood pressure decreased to 82 ± 2 mmHg with halothane, 92 ± 4 mmHg with enflurane, and 104 ± 4 mmHg with ketamine in the treated animals. Plasma renin activity did not increase in either treated or untreated animals. Similar degrees of blood pressure decreases were seen in untreated animals. With the infusion of saralasin, a further decrease of approximately 20 mmHg in blood pressure was seen, in both the treated and untreated rats anesthetized with halothane. However, in treated rats anesthetized with enflurane or ketamine, no depressor response to saralasin was seen, which is in marked contrast to the response seen in untreated animals. The plasma renin response in the treated animals also was blunted. Using this animal model, these experiments suggest that partial peripheral sympathectomy does not result in deleterious effects when rats are anesthetized with halothane, enflurane, or ketamine anesthesia.
AB - Newborn rats were treated with guanethidine sulfate for the first 3 weeks of life in order to produce a partial permanent peripheral sympathectomy. The rats were allowed to grow to 250-300 grams on a normal sodium diet. Using diethyl ether anesthesia, arterial and venous cannulas were placed and the animals allowed to awaken in restraining cages. The rats were divided into four groups: awake (n = 6), halothane 1.3 vol % (n = 8), enflurane 2.2 vol % (n = 8), and ketamine 125 mg/kg, ip (n = 8). The protocol consisted of a one-hour control awake period, one hour of stable anesthesia (one group received no anesthesia), and one-half-hour iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity was measured at the end of each time period. Thirty untreated normal rats were similarly divided into four groups and served as the control. The degree of peripheral sympathectomy was assessed through cardiac norepinephrine concentrations, plasma catecholamines, and response to 50% hemorrhage. Guanethidine treatment resulted in a 78% decrease in cardiac norepinephrine from 189 ± 15 ng/g in the untreated animals compared with 42.4 ± 5 ng/g in the treated animals. The 5-fold increase seen in plasma norepinephrine to acute decapitation was completely absent in the treated animals. Hemorrhage of 50% of blood volume resulted in a 75% mortality rate in the treated animals, while there were no deaths 30 min after hemorrhage in the normal animals. Blood pressure for the 30 treated animals during the awake period was 114 ± 2 mmHg, which was significantly less than 124 ± 1 mmHg in the untreated animals (P < 0.05). Likewise, plasma renin activity of 1.58 ± 0.25 ng.ml -1.h -1 in the treated group was significantly less than 2.59 ± 0.21 ng.ml -1.h -1 in the untreated rats (P < 0.05). With the induction and maintenance of stable anesthesia, blood pressure decreased to 82 ± 2 mmHg with halothane, 92 ± 4 mmHg with enflurane, and 104 ± 4 mmHg with ketamine in the treated animals. Plasma renin activity did not increase in either treated or untreated animals. Similar degrees of blood pressure decreases were seen in untreated animals. With the infusion of saralasin, a further decrease of approximately 20 mmHg in blood pressure was seen, in both the treated and untreated rats anesthetized with halothane. However, in treated rats anesthetized with enflurane or ketamine, no depressor response to saralasin was seen, which is in marked contrast to the response seen in untreated animals. The plasma renin response in the treated animals also was blunted. Using this animal model, these experiments suggest that partial peripheral sympathectomy does not result in deleterious effects when rats are anesthetized with halothane, enflurane, or ketamine anesthesia.
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M3 - Article
VL - 58
SP - 32
EP - 37
JO - Anesthesiology
JF - Anesthesiology
SN - 0003-3022
IS - 1
ER -