Lack of coupling between adrenal cortical metabolic activity and blood flow in anesthetized dogs

1991 ◽  
Vol 261 (2) ◽  
pp. H410-H415
Author(s):  
N. T. Sakima ◽  
M. J. Breslow ◽  
H. Raff ◽  
R. J. Traystman

To determine whether adrenal O2 consumption and cortical blood flow (CBF) increase during stimulation of cortical secretory activity, exogenous adrenocorticotrophic hormone (ACTH) was infused at 0, 2, and 10 ng.kg-1.min-1 (groups 1, 2, and 3, respectively) into dexamethasone-pretreated, pentobarbital-fentanyl-anesthetized, ventilated dogs. ACTH levels of approximately 20, 100, and 500 pg/ml were obtained in groups 1, 2, and 3, respectively. Cortisol secretion increased after 20 min in groups 2 and 3 (from 0.016 +/- 0.004 to 2.25 +/- 1.36 and from 0.02 +/- 0.01 to 5.32 +/- 1.23 microgram.min-1.g cortex-1, respectively) while adenosine 3',5'-cyclic monophosphate (cAMP) secretion increased after 20 min only in group 3 (from 5.7 +/- 2.8 to 61.3 +/- 18.6 micrograms.min-1.g cortex-1). Whole adrenal gland O2 consumption increased after 20 min in group 3 animals (from 0.89 +/- 0.16 to 1.77 +/- 0.27 ml O2.min-1.100 g tissue-1) but not in the other two groups. CBF measured with radiolabeled microspheres was unaffected by ACTH infusion while O2 extraction increased from a baseline of 5.9 +/- 1.4 to 13.0 +/- 2.4% after 30 min in group 3. These data demonstrate that in anesthetized dogs increases in adrenal cortical secretory activity are associated with increases in O2 consumption, and this increase in O2 consumption is met by increasing O2 extraction, not by increasing cortical blood flow.

1983 ◽  
Vol 244 (1) ◽  
pp. H68-H72
Author(s):  
E. Buchweitz ◽  
H. R. Weiss

Cardiac sympathetic nerve stimulation produces increases in various indices of cardiac work and metabolism. To determine how these increased O2 demands are met, the effects of stimulation of the ansa subclavia on regional arterial and venous O2 saturation, O2 extraction, blood flow, and O2 consumption were determined in the hearts of 16 pentobarbital-anesthetized open-chest dogs. Microspectrophotometric observations of small regional arteries and veins in quick-frozen hearts to determine regional O2 extraction were combined with regional blood flow measurements with radioactive microspheres to determine regional myocardial O2 consumption by the Fick principle. Ansa subclavia stimulation produced significant increases in maximum rate of pressure development, heart rate, and blood pressure. Under control conditions, venous O2 saturation was lower and O2 extraction higher in the subendocardial compared with the subepicardial region of the left ventricle. While sympathetic stimulation did not alter the mean O2 extraction or venous O2 saturation values, there were no longer significant subepicardial vs. subendocardial differences in these parameters. Flow and O2 consumption in these regions increased proportionally during stimulation. The ratio of O2 supply to O2 consumption was not significantly altered by ansa subclavia stimulation, indicating that sympathetic stimulation produced no adverse effect in either region.


1990 ◽  
Vol 259 (3) ◽  
pp. H681-H688 ◽  
Author(s):  
M. J. Breslow ◽  
J. R. Tobin ◽  
T. D. Mandrell ◽  
L. C. Racusen ◽  
H. Raff ◽  
...  

Prior attempts to study adrenal medullary O2 metabolism during catecholamine secretion have been unsuccessful because venous blood from medulla mixes with venous blood from the much larger cortex. To circumvent this problem, eight adult mongrel dogs were pretreated for 5-6 wk with the adrenocorticolytic agent 1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane (o,p'-DDD). Prednisolone (5 mg/day) and fludrocortisone (0.1 mg.10 kg-1.day-1) were administered orally to prevent adrenocortical insufficiency. Animals were then anesthetized with pentobarbital sodium and subjected to splanchnic nerve stimulation (NS) at 20 and 4 Hz to elicit catecholamine secretion. NS at 20 Hz increased epinephrine secretion from 1.6 +/- 0.7 to 1,780 +/- 762 ng.min-1.g medulla-1 but had no effect on medullary O2 consumption. Medullary blood flow (MQ) increased from 216 +/- 63 to 1,522 +/- 182 ml.min-1.100 g-1, and O2 extraction decreased from 2.7 +/- 0.7 to 0.8 +/- 0.2%. NS at 4 Hz increased epinephrine secretion from 3.1 +/- 1.4 to 76 +/- 17 ng.min-1.g medulla-1 and MQ from 226 +/- 66 to 649 +/- 122 ml.min-1.100 g-1 but had no effect on adrenal O2 consumption or extraction. Cortical blood flow was 342 +/- 98 ml.min-1.100 g-1 at baseline and was unaffected by NS. Gross weight of cortex was reduced by 80% in o,p'-DDD-treated animals, and histological examination of glands from three animals showed only rare islands of glomerulosa cells remaining. These data suggest that increases in MQ during NS do not occur in response to changes in O2 consumption.


1991 ◽  
Vol 260 (1) ◽  
pp. H21-H26
Author(s):  
M. J. Breslow ◽  
J. R. Tobin ◽  
K. L. Kubos ◽  
H. Raff ◽  
R. J. Traystman

The objective of this study was to determine whether three- to fourfold increases in adrenal medullary blood flow (MQ), observed during catecholamine secretion induced by splanchnic nerve stimulation (NS), are necessary for a maximal secretory response. Eight pentobarbital-anesthetized adult male mongrel dogs (25-35 kg) were subjected to two episodes of NS-induced catecholamine secretion. To limit increases in MQ, one NS (20 Hz, 8 V, 1.5 ms) was performed under control conditions, the other was after reduction of adrenal perfusion pressure (PP). PP was 124.8 +/- 6.0 at control and was reduced to 23.0 +/- 1.0 mmHg by inflation of an aortic occluder located 3 in. above the adrenals. NS under control conditions increased ipsilateral MQ (measured using radiolabeled microspheres) from 181 +/- 39 to 1,336 +/- 199 ml.min-1.100 g-1 and adrenal epinephrine secretion from 184 +/- 128 to 11,445 +/- 5,216 ng.min-1.g medulla-1. Contralateral MQ and cortical blood flow were unaffected by NS. Reduction of PP decreased MQ to 32 +/- 6 ml.min-1.100 g-1 and adrenal cortical blood flow from 251 +/- 23 to 25 +/- 6 ml.min-1.100 g-1.PP reduction had no effect on either corticosteroid secretion or unstimulated epinephrine secretion. NS at reduced PP increased ipsilateral MQ to 146 +/- 27 ml.min-1.100 g-1 and epinephrine secretion to 13,935 +/- 5,175 ng.min-1.g medulla-1. These data indicate that epinephrine secretion is not altered when MQ is limited by reduction of PP and suggest that, at normal PP, increases in MQ during catecholamine secretion are not necessary for a maximal secretory response.(ABSTRACT TRUNCATED AT 250 WORDS)


1983 ◽  
Vol 245 (5) ◽  
pp. G697-G702 ◽  
Author(s):  
P. T. Nowicki ◽  
B. S. Stonestreet ◽  
N. B. Hansen ◽  
A. C. Yao ◽  
W. Oh

Regional and total gastrointestinal (GI) blood flow, O2 delivery, and whole-gut O2 extraction and O2 consumption were measured before and 30, 60, and 120 min after feeding in nonanesthetized, awake 2-day-old piglets. Cardiac output and blood flow to kidneys, heart, brain, and liver were also determined. Blood flow was measured using the radiolabeled microsphere technique. In the preprandial condition, total GI blood flow was 106 +/- 9 ml X min-1 X 100 g-1, while O2 extraction was 17.2 +/- 0.9% and O2 consumption was 1.99 +/- 0.19 ml O2 X min-1 X 100 g-1. Thirty minutes after slow gavage feeding with 30 ml/kg artificial pig milk, O2 delivery to the GI tract and O2 extraction rose significantly (P less than 0.05) by 35 +/- 2 and 33 +/- 2%, respectively. The increase in O2 delivery was effected by a significant increase in GI blood flow, which was localized to the mucosal-submucosal layer of the small intestine. O2 uptake by the GI tract increased 72 +/- 4% 30 min after feeding. Cardiac output and blood flow to non-GI organs did not change significantly with feeding, whereas arterial hepatic blood flow decreased significantly 60 and 120 min after feeding. The piglet GI tract thus meets the oxidative demands of digestion and absorption by increasing local blood flow and tissue O2 extraction.


1997 ◽  
Vol 17 (6) ◽  
pp. 686-694 ◽  
Author(s):  
Elvire Vaucher ◽  
Josiane Borredon ◽  
Gilles Bonvento ◽  
Jacques Seylaz ◽  
Pierre Lacombe

We earlier reported that electrical stimulation of the rat nucleus basalis of Meynert (NBM) induces large cerebral blood flow increases, particularly in frontal cortical areas but also in some subcortical regions. The present study was designed to address the issue of blood flow control exerted by NBM projections. To this aim, we have determined whether these flow increases were associated with proportionate changes in metabolic activity as evaluated by cerebral glucose utilization (CGU) strictly under the same experimental conditions in the conscious rat. An electrode was chronically implanted in a reactive site of the NBM as determined by laser-Doppler flowmetry (LDF) of the cortical circulation. One to two weeks later, while the cortical blood flow was monitored by LDF, we measured CGU using the [14C]2-deoxyglucose autoradiographic technique during unilateral electrical stimulation of the NBM, and analyzed the local flow-metabolism relationship. The large increases in cortical blood flow induced by NBM stimulation, exceeding 300% in various frontal areas, were associated with at most 24% increases in CGU (as compared with the control group) in one frontal area. By contrast, strong increases in CGU exceeding 150% were observed in subcortical regions ipsilateral to the stimulation, especially in extrapyramidal structures, associated with proportionate CBF changes. Thus, none of the blood flow changes observed in the cortex can be ascribed to an increased metabolic activity, whereas CBF and CGU were coupled in many subcortical areas. This result indicates that different mechanisms, which do not necessarily involve any metabolic factor, contribute to the regulation of the cerebral circulation at the cortical and subcortical level. Because the distribution of the uncoupling is coincident with that of cholinergic NBM projections directly reaching cortical microvessels, these data strongly support the hypothesis that NBM neurons are capable of exerting a neurogenic control of the cortical microcirculation.


1984 ◽  
Vol 246 (3) ◽  
pp. H374-H379
Author(s):  
K. Talafih ◽  
G. J. Grover ◽  
H. R. Weiss

The purpose of this study was to determine if thyroxine-induced hypertrophic hearts can maintain an adequate O2 supply-consumption balance both at rest and under hypoxic stress. New Zealand White rabbits were given 0.5 mg/kg L-thyroxine (T4) for 3 or 16 days, and a third group served as a control. Chests were opened under anesthesia, and myocardial blood flow was determined using microspheres. In half of these animals, microspectrophotometric determinations were made on left ventricular arterial and venous O2 saturation, and by combining this data with blood flows, O2 consumption was determined. The other animals were then subjected to hypoxia (8% O2 in N2), and flows and O2 consumption were again determined. T4 increased arterial pressure and heart rate in normoxic animals and also increased myocardial blood flow 65 and 210% for 3- and 16-day T4 groups, respectively, with no regional differences. O2 extraction was also increased in T4 animals. O2 consumption increased 134 and 280% in 3- and 16-day T4 groups. Only normoxic saline controls had a regional O2 consumption difference with subendocardial O2 consumption higher than subepicardial values. When compared with their respective normoxic groups, blood flow increased 49 and 101% for the hypoxic 3- and 16-day T4 groups. Hypoxia had no effect on saline control blood flow. Hypoxia decreased O2 extraction 29 and 41%, respectively, in the 3- and 16-day T4 groups and was unchanged in saline controls.(ABSTRACT TRUNCATED AT 250 WORDS)


1996 ◽  
Vol 270 (5) ◽  
pp. F833-F838 ◽  
Author(s):  
D. S. Majid ◽  
L. G. Navar

Although it is well recognized that whole kidney and cortical blood flow exhibit efficient autoregulation in response to alterations in renal arterial pressure (RAP), the autoregulatory behavior of medullary blood flow (MBF) has remained uncertain. We have evaluated MBF responses to stepwise reductions in RAP for both short-term (2 min, n = 6) and longer periods (15 min, n = 7) using single-fiber laser-Doppler flowmetry with needle probes inserted into the mid-medullary region in denervated kidneys of 13 anesthetized dogs. The changes in cortical blood flow (CBF) were assessed with either a surface probe or a needle probe inserted into the cortex. Control total renal blood flow (RBF), assessed by electromagnetic flow probe in these dogs, was 5.2 +/- 0.3 ml.min-1.g-1, and glomerular filtration rate was 0.97 +/- 0.05 ml.min-1.g-1 (n = 7). RBF, MBF, and CBF all exhibited efficient autoregulatory behavior during changes in RAP from 150 to 75 mmHg. The slopes of RAP vs. RBF, CBF, as well as MBF, were not significantly different from zero within this range of RAP. Below RAP of 75 mmHg, all indexes of blood flow showed linear decreases with reductions in pressure. The data indicate that blood flow in the renal medulla of dogs exhibits efficient autoregulatory behavior, similar to that in the cortex.


1988 ◽  
Vol 65 (5) ◽  
pp. 2069-2074 ◽  
Author(s):  
R. L. Stork ◽  
D. L. Bredle ◽  
C. K. Chapler ◽  
S. M. Cain

Polycythemia increases blood viscosity so that systemic O2 delivery (QO2) decreases and its regional distribution changes. We examined whether hypoxia, by promoting local vasodilation, further modified these effects in resting skeletal muscle and gut in anesthetized dogs after hematocrit had been raised to 65%. One group (CON, n = 7) served as normoxic controls while another (HH, n = 6) was ventilated with 9% O2--91% N2 for 30 min between periods of normoxia. Polycythemia decreased cardiac output so that QO2 to both regions decreased approximately 50% in both groups. In compensation, O2 extraction fraction increased to 65% in muscle and to 50% in gut. When QO2 was reduced further during hypoxia, blood flow increased in muscle but not in gut. Unlike previously published normocythemic studies, there was no initial hypoxic vasoconstriction in muscle. Metabolic vasodilation during hypoxia was enhanced in muscle when blood O2 reserves were first lowered by increased extraction with polycythemia alone. The increase in resting muscle blood flow during hypoxia with no change in cardiac output may have decreased O2 availability to other more vital tissues. In that sense and under these experimental conditions, polycythemia caused a maladaptive response during hypoxic hypoxia.


1988 ◽  
Vol 254 (1) ◽  
pp. E45-E51 ◽  
Author(s):  
A. A. van Lambalgen ◽  
H. C. Runge ◽  
G. C. van den Bos ◽  
L. G. Thijs

High serum lactate may not reflect the severity of endotoxin shock: the lactate load could even be formed immediately after the endotoxin challenge. During the first 30 min after endotoxin injection (Escherichia coli; 1.5 mg/kg iv) into anesthetized dogs (4 mg.kg-1.h-1 etomidate, n = 19) we studied arterial lactate concentration; contributions of portal and splanchnic (n = 6), renal and pulmonary (n = 7), and femoral (n = 6) vascular beds to the early lactate rise; and regional O2 extraction and blood flow (microspheres). In control dogs (n = 5, no endotoxin), we found no significant hemodynamic and biochemical changes. Endotoxin caused an immediate decrease in blood pressure, cardiac output, and organ perfusion, followed by recovery after approximately 5 min to approximately 75% of preshock values at t = 30 min (except for renal blood flow, which remained low). Arterial lactate concentration started to increase almost immediately after endotoxin and increased rapidly until t = 15 min (to 300%) and then leveled off, but in spite of the hemodynamic recovery it remained elevated. A major part of the early increase in lactate concentration can be explained by splanchnic lactate production. The total splanchnic bed released more lactate than the portal bed, indicating that the liver produces lactate. We conclude that the lactate concentration later in canine endotoxin shock depends on events that occur during early shock in which the liver may play a crucial role.


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