Effects of bromocryptine on hepatic blood volume responses to hepatic nerve stimulation in cats

1986 ◽  
Vol 64 (5) ◽  
pp. 621-624 ◽  
Author(s):  
C. V. Greenway ◽  
F. Burczynski ◽  
I. R. Innes
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Presynaptic Inhibition ◽  
Portal Pressure ◽  
Inhibitory Effect ◽  
Neural Responses ◽  
Norepinephrine Release ◽  
Low Frequencies ◽  
Significant Impairment ◽  
Blood Volumes

Arterial pressures, portal pressures, and hepatic blood volumes were recorded after hepatic denervation in cats anesthetized with pentobarbital. Bromocryptine (50 μg/kg) lowered arterial pressure but did not significantly change portal pressure or hepatic blood volume. However, both portal pressure and hepatic blood volume responses to hepatic nerve stimulation were significantly depressed after bromocryptine especially at low frequencies of stimulation. Responses to intraportal infusions of norepinephrine were significantly impaired only at the highest dose. The inhibitory effect of bromocryptine on the neural responses may, therefore, involve a presynaptic inhibition of norepinephrine release, but the mechanism requires further study. These data provide further suport for the hypothesis that drugs which impair hepatic venous responses to sympathetic stimuli cause significant impairment of postural reflexes and orthostatic hypotension during clinical use.

Effects of hemorrhage and hepatic nerve stimulation on venous compliance and unstressed volume in cat liver

1987 ◽  
Vol 65 (11) ◽  
pp. 2168-2174 ◽  
Author(s):  
C. V. Greenway
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Nerve Stimulation ◽  
Marked Decrease ◽  
Venous Compliance ◽  
Remarkable Feature ◽  
Unstressed Volume ◽  
Passive Response ◽  
The Relationship ◽  
Blood Volumes

Intrahepatic blood volume–pressure relationships were studied using plethysmography to measure hepatic blood volume and a hepatic venous long-circuit to control intrahepatic pressure. In cats anesthetized with pentobarbital or with ketamine–chloralose, hemorrhage (to reduce hepatic blood flow to 60% of control) caused marked reductions in hepatic blood volume and intrahepatic pressure but did not significantly change hepatic blood volume–pressure relationships. We were unable to demonstrate an active reflex venous response to hemorrhage in these preparations, although a large passive response occurred. The volume–pressure relationships in innervated livers were different from those in denervated livers: apparent venous compliance was much greater and apparent unstressed volume was zero or negative. Hepatic nerve stimulation in denervated livers caused a marked decrease in hepatic blood volume at low intrahepatic pressures but failed to alter hepatic blood volumes at high intrahepatic pressures (15 mmHg) (1 mmHg = 133.3 Pa). This resulted in large apparent compliances and apparently negative unstressed volumes, as seen in the innervated livers. Thus blood volume–pressure relationships in innervated livers may not give valid measurements of compliance and unstressed volume. A remarkable feature in all these experiments was the linearity of the relationship between hepatic blood volume and intrahepatic pressure. Exudation of fluid begins at higher intrahepatic pressures in innervated compared with denervated livers.

Hepatic venous resistance site in the dog: localization and validation of intrahepatic pressure measurements

1987 ◽  
Vol 65 (3) ◽  
pp. 352-359 ◽  
Author(s):  
Dallas J. Legare ◽  
W. Wayne Lautt
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vena Cava ◽  
Pressure Rise ◽  
Vascular Occlusion ◽  
Portal Venous Pressure ◽  
Hepatic Veins ◽  
Venous Resistance

Intrahepatic pressure (9.4 ± 0.3 mmHg; 1 mmHg = 133.32 Pa), measured proximal to a hepatic venous resistance site, was insignificantly different from portal venous pressure (9.6 ± 0.4 mmHg). This lobar venous pressure is not wedged hepatic venous pressure as it is measured from side holes in a catheter with a sealed tip. Validation of the lobar venous pressure measurement was done in a variety of ways and using different sizes and configurations of catheters. The site of hepatic venous resistance in the dog is localized to a narrow sphincterlike region about 0.5 cm in length and within 1–2 cm (usually within 1 cm) of the junction of the vena cava and hepatic veins. Sinusoidal and portal venous resistance appears insignificant in the basal state and large increases in liver blood volume (histamine infusion or passive vena caval occlusion) or large decreases in liver blood volume (passive vascular occlusion) do not alter the insignificant pressure gradient between portal and lobar venous pressures. Norepinephrine infusion (1.25 μg∙kg−1∙min−1 intraportal) and hepatic sympathetic nerve stimulation (10 Hz) led to a significantly greater rise in portal venous pressure than in lobar venous pressure, indicating some presinusoidal (and (or) sinusoidal) constriction and this indicates that lobar venous pressure cannot be assumed under all conditions to accurately reflect portal pressure. However, most of the rise in portal venous pressure induced by intraportal infusion of norepinephrine or nerve stimulation and virtually all of the pressure rise induced by histamine could be attributed to the postsinusoidal resistance site. This site was highly localized since 62% of the pressure drop from the portal vein to the inferior vena cava in the basal state occurred over a 0.5-cm length. However, the anatomical position of this site was different in the dog compared with the cat.

Loss of hepatic venous responsiveness after endotoxin in anesthetized cats

1984 ◽  
Vol 246 (5) ◽  
pp. H658-H663 ◽  
Author(s):  
K. L. Seaman ◽  
C. V. Greenway
Keyword(s):  
Cardiac Output ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Nerve Stimulation ◽  
Bolus Injection ◽  
Portal Pressure ◽  
Intravenous Bolus ◽  
Salmonella Enteriditis ◽  
Slow Intravenous Infusion

Endotoxin (from Salmonella enteriditis ) was administered either as an intravenous bolus injection after administration of indomethacin to prevent the acute anaphylactoid response or as a slow intravenous infusion to cats anesthetized with pentobarbital. Within 30 min, hepatic blood volume measured by plethysmography increased by 30%. However, unlike the outflow block seen in dogs after endotoxin, this increase in blood volume was associated with a fall in portal and hepatic lobar venous pressures. Responses to hepatic nerve stimulation (1-8 Hz), to intravenous infusions of norepinephrine (0.2-1.0 microgram X kg-1 X min-1), and to infusions into the hepatic artery of norepinephrine (0.1-0.5 microgram X kg-1 X min-1) and angiotensin II (0.1-0.5 microgram X kg-1 X min-1) were compared before and 150 min after endotoxin administration. Both portal pressure and hepatic blood volume responses to these stimuli were markedly depressed by 150 min after endotoxin. We conclude that in cats endotoxin causes a markedly depressed responsiveness of hepatic venous smooth muscle to agonists and a modest pooling of blood in the liver probably due to impairment of preexisting sympathetic tone. Although these hepatic venous effects were observed at a time when cardiac output was not markedly depressed, it is suggested that they may play a significant role in the later development of reduced cardiac output and shock.

Evaluation of topical phenol as a means of producing autonomic denervation of the liver

1984 ◽  
Vol 62 (7) ◽  
pp. 849-853 ◽  
Author(s):  
W. Wayne Lautt ◽  
Anne M. Carroll
Keyword(s):  
Blood Pressure ◽  
Topical Application ◽  
Nerve Stimulation ◽  
Sympathetic Neurons ◽  
Portal Pressure ◽  
Nerve Degeneration ◽  
Hepatic Glycogen ◽  
Glucose Levels ◽  
Afferent Nerves ◽  
Chronic Denervation

Topical application of 90% phenol around the bile duct, portal vein, and hepatic artery, as well as along each of the three hepatic ligaments was tested for effectiveness of rapid and chronic denervation in cats. Because phenol produces nonselective nerve degeneration, it was assumed that proof of functional sympathectomy was adequate proof of disruption of parasympathetic and afferent nerves as well. Functional sympathetic neurons were evaluated by measuring physiological responses to direct electrical stimulation of the anterior hepatic plexus. Acute or rapid denervation was assessed by the degree of rise in portal blood pressure produced by nerve stimulation. Complete denervation appeared within 20 min and was still present by 80 min postapplication. Chronic denervation was tested by applying the phenol and recovering the cats for 6–14 days. An equal number (n = 6) of sham-denervated cats were compared. Phenol denervation did not alter basal glucose, insulin or glucagon levels, hematocrit, blood pressure, or hepatic glycogen levels. These variables are a good index of stress and metabolic status. Nerve stimulation in the chronic sham group raised portal pressure, arterial pressure, and blood glucose levels, whereas the chronic-denervated group showed no responses. The health of the two groups appeared normal with the sole difference being that the painted itssues were mildly discolored and more adhesions appeared in the phenol-denervated set. Thus phenol is a useful tool for producing hepatic denervation. It is less traumatic, faster, and more certain than surgical denervation. In addition, the hepatic lymphatics can be preserved using the topical application of phenol.

Inhibitory control of proximal colonic motility by the sympathetic nervous system

1987 ◽  
Vol 253 (4) ◽  
pp. G531-G539 ◽  
Author(s):  
R. A. Gillis ◽  
J. Dias Souza ◽  
K. A. Hicks ◽  
A. W. Mangel ◽  
F. D. Pagani ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Nerve Stimulation ◽  
Adrenergic Receptors ◽  
Vagal Stimulation ◽  
Colonic Motility ◽  
Inhibitory Effect ◽  
Proximal Colon ◽  
Pelvic Nerve ◽  
Sympathetic Nervous

The purpose of this study is to determine whether or not the sympathetic nervous system provides a tonic inhibitory input to the colon in chloralose-anesthetized cats. Proximal and midcolonic motility were monitored using extraluminal force transducers. An intravenous bolus injection of 5 mg of phentolamine in 14 animals elicited a pronounced increase in proximal colon contractility. The minute motility index changed from 0 +/- 0 to 26 +/- 4 after phentolamine administration. Midcolonic motility also increased in response to phentolamine. Specific blockade of alpha 2-receptors, but not alpha 1-receptors, caused the same response seen with phentolamine. alpha-Adrenergic blockade increased colon contractility after spinal cord transection but not after ganglionic blockade. Blockade of alpha-adrenergic receptors was also performed before vagal and pelvic nerve stimulation and in both cases increased colonic motility. Vagal stimulation alone had no effect on colonic contractility, while pelvic nerve stimulation increased motility at the midcolon. alpha-Receptor blockade did not alter the ineffectiveness of vagal stimulation but did unmask excitatory effects of pelvic nerve stimulation on the proximal colon. All excitatory colonic responses were prevented by blocking muscarinic cholinergic receptors. These data indicate that tonic sympathetic nervous system activity exerts an inhibitory effect on colonic motility. The inhibitory effect is mediated through alpha 2-adrenergic receptors. Based on these findings, we suggest that alterations in sympathetic nervous system activity may be extremely important for the regulation of circular muscle contractions in the colon.

Adrenergic and nonadrenergic cotransmitters inhibit insulin secretion during sympathetic stimulation in dogs

1992 ◽  
Vol 263 (1) ◽  
pp. E72-E78
Author(s):  
J. Lorrain ◽  
I. Angel ◽  
N. Duval ◽  
M. T. Eon ◽  
A. Oblin ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Blocking Agent ◽  
Norepinephrine Release ◽  
Sympathetic Nerve Stimulation ◽  
K Channels ◽  
Adrenoceptor Antagonist

Vascular and biochemical responses to pancreatic sympathetic nerve stimulation were investigated in the blood-perfused pancreas of anesthetized dogs. During sympathetic nerve stimulation, pancreatic perfusion pressure and norepinephrine release increased, whereas insulin secretion decreased. The latter effect did not occur after pretreatment with the alpha 2-adrenoceptor antagonist idazoxan. However, after beta-adrenoceptor blockade with propranolol, neither single administration of idazoxan nor the alpha 1-adrenoceptor antagonist prazosin or glibenclamide, a blocker of ATP-modulated K+ channels, affected the decrease in insulin secretion induced by sympathetic nerve stimulation. In contrast, the combination of glibenclamide with idazoxan markedly antagonised the decrease in insulin release evoked by the latter procedure. After depletion of catecholamines with syrosingopine, the stimulation-induced inhibition of insulin secretion remained unchanged even though no increases in pancreas perfusion pressure or norepinephrine release were observed. In this preparation, glibenclamide inhibited the decrease in insulin release by 50%. In animals pretreated with the neuronal blocking agent bretylium, all of the responses to sympathetic nerve stimulation were abolished. These results indicate that the inhibitory effects exerted by the sympathetic nervous system on insulin secretion are mediated not only by the classical neurotransmitter norepinephrine acting on alpha 2-adrenoceptors but also by a nonadrenergic cotransmitter that can maintain transmission under conditions of catecholamine deficiency. The postulated nonadrenergic cotransmitter(s) acts, at least partly, via the opening of ATP-modulated K+ channels blockable by glibenclamide, and its release can be prevented by the neuronal blocking agent bretylium.

scholarly journals Effect of angiotensin II on renal nerve stimulation-induced norepinephrine release in dogs

1987 ◽  
Vol 43 ◽  
pp. 96
Author(s):  
Toshiyuki Matsuoka ◽  
Yoshiharu Hayashi ◽  
Mizue Suzuki-Kusaba ◽  
Susumu Satoh
Keyword(s):  
Angiotensin Ii ◽  
Nerve Stimulation ◽  
Norepinephrine Release ◽  
Renal Nerve ◽  
Renal Nerve Stimulation
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