Effects of an Intravenous Infusion of Noradrenaline on the Plasma Concentration of Free and Sulfoconjugated Catecholamines in Anesthetized Dogs

Pharmacology ◽  
1986 ◽  
Vol 32 (2) ◽  
pp. 90-100 ◽  
Author(s):  
J.L. Cuche ◽  
G. Jondeau ◽  
G. Ruget ◽  
F. Selz ◽  
J.C. Piga ◽  
...  
1958 ◽  
Vol 193 (2) ◽  
pp. 375-378 ◽  
Author(s):  
Richard T. Jones ◽  
William D. Blake

Several parameters related to the dynamics of distribution and renal excretion of epinephrine were studied in anesthetized dogs before and during oral administration of thyroid extract. These parameters include: a) plasma concentration and renal excretion of epinephrine during constant infusion of l-epinephrine bitartrate, b) the rate of disappearance from plasma and volume of distribution of epinephrine, and c) the resting excretion of endogenous epinephrine before and during thyroid feeding. Except for an increase in the percentage of infused epinephrine excreted in the urine, there were essentially no changes in these parameters after feeding thyroid.


1984 ◽  
Vol 247 (5) ◽  
pp. R905-R910 ◽  
Author(s):  
G. J. Taborsky ◽  
J. B. Halter ◽  
D. Baum ◽  
J. D. Best ◽  
D. Porte

Since pentobarbital anesthesia is known to attenuate certain autonomic reflexes, we tested whether pentobarbital would suppress both basal and stimulated levels of plasma catecholamines and whether a large stimulus might counterbalance this suspected suppression. In untrained dogs, sampled by venipuncture, pentobarbital (30 mg/kg iv) decreased the plasma concentration of epinephrine (E) from 146 +/- 9 to 38 +/- 8 (SE) pg/ml (n = 46) and norepinephrine (NE) from 276 +/- 13 to 91 +/- 10 pg/ml (both P less than 0.0005), suggesting that barbiturate anesthesia suppresses sympathetic outflow in these mildly stressed animals. Pentobarbital also had a marked suppressive effect on the lower baseline catecholamines (E, 84 +/- 14 pg/ml; NE, 118 +/- 10 pg/ml; n = 6) of trained, chronically catheterized dogs, suggesting that it was capable of suppressing resting sympathetic outflow as well. To determine whether pentobarbital anesthesia also suppressed reflex activation of the sympathetic nervous system, the plasma catecholamine response to the neuroglucopenic agent, 2-deoxy-D-glucose (2-DG), was measured in conscious and in pentobarbital-anesthetized dogs. In conscious dogs, the administration of 2-DG (100 mg/kg iv) doubled the base-line plasma concentration of E and NE 30 min after the 2-DG injection. In contrast, the administration of 2-DG (100 mg/kg iv) to pentobarbital-anesthetized dogs produced no significant increase of either plasma catecholamine, suggesting marked suppression of this sympathetic reflex.(ABSTRACT TRUNCATED AT 250 WORDS)


1978 ◽  
Vol 234 (1) ◽  
pp. R66-R71 ◽  
Author(s):  
D. J. Ramsay ◽  
L. C. Keil ◽  
M. C. Sharpe ◽  
J. Shinsako

The effects of intravenous infusion of Asp1. Ile5-angiotensin II on blood pressure, plasma vasopressin, ACTH and 11-hydroxycorticosteroid levels and on plasma renin activity were studied in five trained, conscious dogs. The dogs were prepared with bilateral carotid loops. Infusion of angiotensin II at rates of 5, 10, and 20 ng/kg.min raised its plasma concentration from 23 +/- 7 to 48 +/- 8, 125 +/- 8, and 187 +/- 21 pg/ml, respectively. The lowest rate of infusion was mildly pressor, the two higher rates more so. All rates of infusion promptly increased vasopressin levels and depressed renin levels. The two higher rates also stimulated ACTH, although with a latency of 30-45 min. Since the rates of infusion of angiotensin II employed produced plasma levels within the physiological range, it is suggested that peripherally generated angiotensin II may play an important role in the regulation of vasopressin, and ACTH secretion.


1995 ◽  
Vol 83 (1) ◽  
pp. 127-133. ◽  
Author(s):  
Kazuhiko Saitoh ◽  
Yoshihiro Hirabayashi ◽  
Reiju Shimizu ◽  
Hirokazu Fukuda

Background Bupivacaine-induced cardiovascular depression is known to be difficult to treat, and the efficacy of epinephrine for treatment of bupivacaine-induced cardiovascular depression is in doubt. We compared the efficacy of amrinone with that of epinephrine for the treatment of bupivacaine-induced cardiovascular depression in anesthetized dogs. Methods In dogs receiving 1.5-2% sevoflurane anesthesia, 0.5% bupivacaine was infused at a rate of 0.5 mg.kg-1.min-1 intravenously until mean arterial blood pressure decreased to 40 mmHg or less. In the amrinone group (n = 9), amrinone (4 mg.kg-1, intravenously) was given immediately after cardiovascular depression, followed by intravenous infusion at a rate of 0.1 mg.kg-1.min-1. In the epinephrine group (n = 9), epinephrine (0.01 mg.kg-1, intravenously) was given as a bolus, and the same dose was given again as required. Results All nine dogs that received amrinone survived. Of the nine dogs that received epinephrine, five survived; fatal cardiovascular depression developed in the four remaining animals (P < 0.05). Only one animal in the amrinone group showed tachyrhythmia with wide QRS complexes during resuscitation, whereas all nine animals in the epinephrine group showed tachyrhythmia with wide QRS complexes during resuscitation. Conclusions Amrinone is superior to epinephrine for the treatment of bupivacaine-induced cardiovascular depression in sevoflurane-anesthetized dogs.


1960 ◽  
Vol 15 (6) ◽  
pp. 1113-1116 ◽  
Author(s):  
Joseph S. Redding ◽  
G. Carl Voigt ◽  
Peter Safar

Lightly anesthetized dogs were subjected to obstructive asphyxia (simulating laryngospasm). When spontaneous breathing efforts ceased, the lungs were flooded with sea water for 30 seconds, according to a standardized experiment described previously. Five dogs were treated with intermittent positive pressure artificial respiration with 100% oxygen (IPPB/O2) for 3 hours. Five additional dogs were treated identically except for the addition of an intravenous infusion of dog plasma 50 ml/kg body weight, 10 minutes after the start of artificial respiration. All the dogs treated only with IPPB/O2 for 3 hours were more completely reoxygenated than were those ventilated with IPPB/air for 10 minutes in the earlier experiment. However, death with pulmonary edema followed the cessation of IPPB/O2 as well as IPPB/air. When the hemoconcentration and hypovolemia, caused by flooding of the lungs with sea water, were corrected by plasma infusion in addition to IPPB/O2, four of the five dogs survived. Submitted on May 19, 1960


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