Hemodynimic effects of systemic and central administration of clonidine in the monkey

1975 ◽  
Vol 228 (4) ◽  
pp. 1276-1279 ◽  
Author(s):  
P Bolme ◽  
RP Forsyth ◽  
T Ishizaki ◽  
KL Melmon
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Systemic Arterial Pressure ◽  
Intraventricular Injection ◽  
Central Administration ◽  
New Information ◽  
Before And After ◽  
Microsphere Method ◽  
Radioactive Microsphere Method

Systemic and regional hemodynamic changes were measured in restrained, conscious rhesus monkeys with indwelling arterial and venous catheters before and after clonidine (5 and 15 mug/kg) was slowly infused intravenously or smaller doses (2 mug/kg) were injected into a lateral cerebral ventricle. Dye-dilution cardiac outputs and the complete distribution of cardiac output were obtained intermittently with the use of the radioactive microsphere method. After the higher intravenous dose and the intraventricular injection, systemic arterial pressure was significantly lowered for 30-45 min. Both of these groups had similar changes in the redistribution of cardiac output and blood flow that outlasted the hypotensive period. Blood flow was maintained or increased in the hepatic and renal arteries at the expense of skin; flow to skeletal muscle and brain also decreased during the first hour. These data support previous studies that indicate that the primary action of clonidine is in the central nervous system and, in addition, add new information about the regional blood flow changes evoked by clonidine.

Hemodynamic basis of oscillations in systemic arterial pressure in conscious rats

1995 ◽  
Vol 269 (1) ◽  
pp. H62-H71 ◽  
Author(s):  
B. J. Janssen ◽  
J. Oosting ◽  
D. W. Slaaf ◽  
P. B. Persson ◽  
H. A. Struijker-Boudier
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Regional Blood Flow ◽  
Systemic Arterial Pressure ◽  
Hemodynamic Pattern ◽  
Cross Correlation Analysis ◽  
Vascular Beds ◽  
Phase Angles

In conscious resting rats, beat-to-beat fluctuations in systemic mean arterial pressure (MAP) were compared with those in cardiac output and those in blood flow in the renal, mesenteric, and hindquarter vascular beds. Spontaneous oscillations (lability) in MAP were observed in frequency bands centered about 1.6 Hz (high: HF), 0.4 Hz (mid: MF), and 0.13 Hz (low: LF). Lability of MAP was confined within the LF (approximately 8 s) band. Lability of cardiac output, on the other hand, showed primary HF oscillations. LF oscillations in regional blood flow were most prominent in the mesenteric and renal vascular beds. In these beds, LF oscillations in blood flow showed negative phase angles with MAP, whereas those between MAP and hindquarter blood flow were positive. Cross correlation analysis indicated that approximately 2 s following a LF change in MAP, LF changes in mesenteric and renal blood flow occurred opposite to those of MAP. Changes in hindquarter flow were negatively correlated with those in MAP about zero time delay. Admittance gains were > or = 1 across all frequencies for all vascular beds, indicating the absence of autoregulation. This hemodynamic pattern suggests that myogenic mechanisms predominantly control mesenteric and renal blood flow in a nonautoregulatory but rather superregulatory manner, while autonomic mechanisms regulate hindquarter blood flow. Thus, in conscious resting rats, spontaneous fluctuations in systemic arterial pressure predominantly exhibit slow (approximately 8 s) oscillations, which do not arise from fluctuations in cardiac output, but originate from regionally specific myogenic oscillatory mechanisms contributing to resistance to flow.

Relationship between vascular reactivity in vitro and blood flows in rats with cirrhosis

1999 ◽  
Vol 97 (3) ◽  
pp. 313-318 ◽  
Author(s):  
Dominique PATERON ◽  
Frédéric OBERTI ◽  
Pascale LEFILLIATRE ◽  
Nary VEAL ◽  
Khalid A. TAZI ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Reactivity ◽  
Regional Blood Flow ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Vascular Responsiveness ◽  
Microsphere Method ◽  
Radioactive Microsphere Method

In cirrhosis there is a hyperdynamic circulation, which occurs mainly in the systemic and splanchnic regions. Using isolated-vessel models, previous studies have shown reduced aortic reactivity to vasoconstrictors in rats with cirrhosis. The aim of the present study was to evaluate and compare the vascular responsiveness to phenylephrine in arterial rings and the blood flows from different regions in rats with cirrhosis and controls. Reactivity was studied in isolated thoracic aortic, superior mesenteric arterial and carotid arterial rings from sham-operated and bile-duct-ligated rats by measuring the cumulative concentration-dependent tension induced by phenylephrine (10-9–10-4 M). Blood flows were measured by the radioactive microsphere method. In rats with cirrhosis, a significant hyporeactivity to phenylephrine was observed in both the aorta and the superior mesenteric artery compared with the corresponding arteries of normal rats. This hyporesponsiveness was corrected by Nω-nitro-l-arginine (0.1 mM). In contrast, carotid artery reactivity and the responses to Nω-nitro-l-arginine were similar in the cirrhotic and control groups. In each case, cardiac output and mesenteric arterial blood flow were significantly higher in cirrhotic than in normal rats. Cerebral blood flows were not significantly different between the two groups. In cirrhotic rats, arterial hyporeactivity may be a consequence of increased regional blood flow and increased production of nitric oxide.

Changes in regional blood flow and cardiac output after L-glutamate stimulation of A5 cell group

1984 ◽  
Vol 246 (1) ◽  
pp. H44-H51 ◽  
Author(s):  
K. A. Stanek ◽  
J. J. Neil ◽  
W. B. Sawyer ◽  
A. D. Loewy
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Excitatory Amino Acid ◽  
Regional Blood Flow ◽  
Contralateral Side ◽  
Cell Group ◽  
Before And After ◽  
Trunk Musculature ◽  
6 Hydroxydopamine ◽  
Stimulation Of

Changes in regional blood flow and cardiac output were measured by the reference organ method in pentobarbital-anesthetized rats with radioactive microspheres (15 microns) before and after chemical stimulation of the A5 cell group with the excitatory amino acid L-glutamate an agent that excites cell bodies but not fibers of passage. This stimulation caused a decrease in mean arterial pressure, heart rate, cardiac output, and calculated stroke volume. The limb skeletal muscles showed a large increase in blood flow and decrease in vascular resistance, whereas the trunk musculature showed no change in flow or resistance. The blood flow of the entire gastrointestinal tract decreased. Blood flow in the skin decreased with no change in resistance. The cardiac muscle of the ventricles showed a decrease in flow without a change in resistance. The ipsilateral half of the brain showed a decrease in blood flow, while the contralateral side showed no change. The kidneys exhibited no change in blood flow and a decrease in resistance. A5 stimulation in guanethidine-sympathectomized rats caused no change in regional blood flow. In contrast, an increase in cardiac output was observed, and the possible interpretations for this change are discussed. Rats treated with intraventricular injections of 6-hydroxydopamine showed no changes in regional blood flow or cardiac output, indicating that catecholamine neurons are involved in these responses.

Cardiac output distribution before and after endotoxin challenge in the rooster

1981 ◽  
Vol 241 (1) ◽  
pp. R67-R71 ◽  
Author(s):  
G. F. Merrill ◽  
R. E. Russo ◽  
J. M. Halper
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Blood Supply ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Total Blood ◽  
Endotoxin Challenge ◽  
Absolute Flow ◽  
Before And After ◽  
The Brain

Cardiac output and its distribution to selected organs was studied using radiolabeled microspheres in unanesthetized, restrained white Leghorn roosters before and 3 h after an Escherichia coli endotoxin challenge. Cardiac output was not significantly altered in either control or endotoxin-treated animals, nor was there a difference in cardiac output between the two groups. Systemic arterial pressure decreased by 37% in the endotoxin group from 187 +/- 14 to 117 +/- 9 mmHg, thus reflecting a marked reduction in total peripheral resistance. The fraction of cardiac output perfusing the heart, adrenals, and liver (hepatic arterial) was not altered by the challenge. Conversely, the percent of total blood flow received by the kidneys, pancreas, and gut (proventriculus and duodenum) was significantly (P less than 0.05) reduced during endotoxemia. Absolute flow to the brain was also decreased. These findings demonstrate that in the rooster endotoxin-induced systemic arterial hypotension is a sufficient stress to cause a redistribution of blood flow, and that the brain in this species (unlike its counterpart in mammals) probably regulates its blood supply passively during periods of hypotension. Conversely, the reduced blood supply to such organs as the gut, pancreas, and kidney following the endotoxin challenge is similar to changes seen in the more commonly studied mammals during experimental endotoxemia.

Effects of a specific antidiuretic agonist on cardiac output and its distribution in intact and anephric dogs

1988 ◽  
Vol 74 (3) ◽  
pp. 293-299 ◽  
Author(s):  
Jean-Francois Liard
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Regional Blood Flow ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Before And After

1. The specific antidiuretic agonist [4-valine, 8-d-arginine]vasopressin (VDAVP) was administered intravenously to seven conscious dogs at a rate of 10 ng min−1 kg−1. Cardiac output (aortic electromagnetic flowmeter), mean arterial pressure and regional blood flows (radioactive microspheres) were measured before and after 30 min of infusion. 2. Mean arterial pressure fell from 89.9 ± 4.5 (mean ± sem) to 82.3 ± 5.9 mmHg and cardiac output increased from 115.4 ± 8.7 to 163.0 ± 14.4 ml min−1 kg−1. Total peripheral resistance decreased from 41.6 ± 3.7 to 27.8 ± 3.6 units and heart rate increased from 79.2 ± 5.9 to 123.2 ± 5.9 beats/min. Blood flow increased significantly in the myocardium, fat and skeletal muscle vascular bed. 3. In another group of six dogs subjected to a similar protocol 24 h after bilateral nephrectomy, mean arterial pressure fell from 102.2 ± 5.3 to 82.7 ± 3.4 mmHg and cardiac output increased from 125.6 ± 3.0 to 171.2 ± 4.0 ml min−1 kg−1. Total peripheral resistance decreased from 39.3 ± 3.4 to 23.4 ± 1.3 units and heart rate increased from 84 ± 4.9 to 113.3 ± 4.3 beats/min. The increase in cardiac output and the fall in total peripheral resistance did not differ significantly between intact and anephric dogs. Regional blood flow responses differed in some respects in the two groups studied, but there was no evidence that the vasodilatory action of VDAVP depended on the presence of the kidneys. 4. These results indicate that the vasodilatation elicited by the antidiuretic agonist VDAVP in intact dogs is limited to a few vascular beds. Furthermore, this vasodilatation appears to be independent from the renal V2-vasopressin receptors.

Neural control of glucose uptake by skeletal muscle after central administration of NMDA

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Neural Control ◽  
Plasma Insulin ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Glucose Disposal ◽  
Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

Sign in / Sign up

Export Citation Format

Share Document