Adenosine modulation of hepatic arterial but not portal venous constriction induced by sympathetic nerves, norepinephrine, angiotensin, and vasopressin in the cat

1986 ◽  
Vol 64 (4) ◽  
pp. 449-454 ◽  
Author(s):  
W. Wayne Lautt ◽  
Dallas J. Legare
Keyword(s):  
Smooth Muscle ◽  
Hepatic Artery ◽  
Nerve Stimulation ◽  
Adenosine Receptors ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Basal Tone ◽  
Intrinsic Regulation

Intrinsic regulation of hepatic arterial blood flow depends upon local concentrations of adenosine. The present data show that i.a. infusions of adenosine cause dilation of the hepatic artery and inhibition of arterial vasoconstriction induced by norepinephrine, vasopressin, angiotensin, and hepatic nerve stimulation. Vasoconstriction induced by submaximal nerve stimulation (2 Hz) and norepinephrine infusions (0.25 and 0.5 μg∙kg−1∙min−1, i.p.v.) were equally inhibited by adenosine. Supramaximal nerve stimulation (8 Hz) was inhibited to a lesser extent. The data are consistent with the hypotheses that (a) adenosine causes nonselective inhibition of vasoconstrictor influences on the hepatic artery; and (b) adenosine antagonizes neurally induced vasoconstriction by a purely postsynaptic effect and does not decrease norepinephrine release. In contrast with the hepatic artery, the intrahepatic portal resistance vessels are not affected by even large doses of adenosine; neither responses in basal tone nor antagonism of vasoconstrictor effects of nerve stimulation, norepinephrine, or angiotensin could be demonstrated. The data are consistent with the hypothesis that the smooth muscle of the portal resistance vessels does not contain adenosine receptors, whereas adenosine receptors on the smooth muscle of the hepatic arterial resistance vessels are of major regulatory importance. Whether endogenous levels of adenosine can reach sufficient concentration to modulate endogenous constrictors remains to be determined.

Glucagon inhibition of hepatic arterial responses to hepatic nerve stimulation

1977 ◽  
Vol 233 (6) ◽  
pp. H647-H654 ◽  
Author(s):  
P. D. Richardson ◽  
P. G. Withrington
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Arterial Responses ◽  
Sympathetic Discharge ◽  
Glucagon Concentration

The hepatic arterial vascular bed of the chloaralose-urethan-anesthetized dog was perfused with blood from a cannulated femoral artery. Hepatic arterial blood flow and perfusion pressure were measured. The hepatic periarterial postganglionic sympathetic nerves were stimulated supramaximally at 0.1, 0.5, 1, 2, 5, 10, and 20 Hz; this caused frequency-dependent rises in the calculated hepatic arterial vascular resistance at all frequencies above the threshold of 0.1 or 0.5 Hz. Glucagon was infused intra-arterially in dosese from 0.25 to 10 microgram/min; glucagon antagonized both the vasoconstrictor effects of hepatic nerve stimulation and of intra-arterial injections of norepinephrine. The degree of antagonism of these responses was significantly correlated with the calculated hepatic arterial glucagon concentration. It is possible that glucagon released physiologically in stress and hypoglycemia may protect the hepatic arterial vasculature from the effects of increased sympathetic discharge.

β-Adrenergic receptors in the hepatic arterial bed of the anesthetized cat

1969 ◽  
Vol 47 (5) ◽  
pp. 415-419 ◽  
Author(s):  
C. V. Greenway ◽  
Anne E. Lawson
Keyword(s):  
Adrenergic Receptors ◽  
Electromagnetic Flowmeter ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Infusion ◽  
Arterial Blood ◽  
Basal Tone ◽  
Β Receptor ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

The hepatic arterial blood flow of cats anesthetized with pentobarbital was recorded with an electromagnetic flowmeter. Administration of isoprenaline by close arterial infusion caused a vasodilatation which was blocked after propranolol. Adrenaline caused a variable change but after propranolol it consistently produced vasoconstriction, and after phenoxybenzamine, vasodilatation. One hour after phenoxybenzamine, stimulation of the sympathetic nerves caused a marked vasodilatation which was blocked by propranolol. It is concluded that both α and β adrenergic receptors are present in the hepatic arterial bed. However, β receptor responses may be difficult to elicit if the basal tone of the vascular bed is already reduced by prior procedures.

Adenosine modulation of vasoconstrictor responses to stimulation of sympathetic nerves and norepinephrine infusion in the superior mesenteric artery of the cat

1988 ◽  
Vol 66 (7) ◽  
pp. 937-941 ◽  
Author(s):  
W. Wayne Lautt ◽  
Leslie K. Lockhart ◽  
Dallas J. Legare
Keyword(s):  
Superior Mesenteric Artery ◽  
Nerve Stimulation ◽  
Adenosine Receptors ◽  
Mesenteric Artery ◽  
Sympathetic Nerves ◽  
Sympathetic Nerve Stimulation ◽  
Vascular Bed ◽  
Norepinephrine Infusion ◽  
Resistance Vessels ◽  
Stimulation Of

Vasoconstriction induced by sympathetic nerve stimulation and by norepinephrine infusion in the superior mesenteric artery of cats anesthetized with pentobarbital was inhibited by adenosine infusions in a dose-related way. The responses to nerve stimulation were not inhibited to a greater extent than the responses to norepinephrine, thus suggesting no presynaptic modulation of sympathetic nerves supplying the resistance vessels of the feline intestinal vascular bed. Blockade of adenosine receptors using 8-phenyltheophylline did not alter the degree of constriction induced by nerve stimulation or norepinephrine infusion, indicating that in the fasted cat, endogenous adenosine co-released or released subsequent to constriction does not affect the peak vasoconstriction reached. Isoproterenol caused similar degrees of vasodilation as adenosine but did not show significant antagonism of the pooled responses to nerve stimulation or norepinephrine infusion; there was no tendency for the degree of dilation induced by isoproterenol to correlate with the inhibition of constrictor responses. Thus, the effect of adenosine on nerve- and norepinephrine-induced constriction is not secondary to nonspecific vasodilation.

scholarly journals Combined resection of the hepatic artery without reconstruction in pancreaticoduodenectomy: a case report of pancreatic cancer with an aberrant hepatic artery

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Tadao Kuribara ◽  
Tatsuo Ichikawa ◽  
Kiyoshi Osa ◽  
Takeshi Inoue ◽  
Satoshi Ono ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Hepatic Artery ◽  
Locally Advanced ◽  
Pancreatic Head ◽  
Arterial Embolization ◽  
Arterial Blood Flow ◽  
Temporary Increase ◽  
Combined Resection ◽  
Arterial Blood ◽  
Arterial Resection

Abstract Background Pancreaticoduodenectomy (PD) is rarely performed for pancreatic cancer with hepatic arterial invasion owing to its poor prognosis and high surgical risks. Although there has been a recent increase in the reports of PD combined with hepatic arterial resection due to improvements in disease prognosis and operative safety, PD with major arterial resection and reconstruction is still considered a challenging treatment. Case presentation A 61-year-old man with back pain was diagnosed with pancreatic head and body cancer. Although distant metastasis was not confirmed, the tumor had extensively invaded the hepatic artery; therefore, we diagnosed the patient with locally advanced unresectable pancreatic cancer. After gemcitabine plus nab-paclitaxel (GnP) therapy, the tumor considerably decreased in size from 35 to 20 mm. Magnetic resonance imaging revealed a gap between the tumor and the hepatic artery. Tumor marker levels returned to their normal range, and we decided to perform conversion surgery. In this case, an artery of liver segment 2 (A2) had branched from the left gastric artery; therefore, we decided to preserve A2 and perform PD combined with hepatic arterial resection without reconstruction. After four cycles of GnP therapy, we performed hepatic arterial embolization to prevent postoperative ischemic complications prior to surgery. Immediately after embolization, collateral arterial blood flow to the liver was observed. Operation was performed 19 days after embolization. Although there was a temporary increase in liver enzyme levels and an ischemic region was found near the surface of segment 8 of the liver after surgery, no liver abscess developed. The postoperative course was uneventful, and S-1 was administered for a year as adjuvant chemotherapy. The patient is currently alive without any ischemic liver events and cholangitis and has not experienced recurrence in the past 4 years since the surgery. Conclusions In PD for pancreatic cancer with hepatic arterial invasion, if a part of the hepatic artery is aberrant and can be preserved, combined resection of the common and proper hepatic artery without reconstruction might be feasible for both curability and safety.

Responses of isolated perfused arteries to catecholamines and nerve stimulation

1965 ◽  
Vol 209 (2) ◽  
pp. 376-382 ◽  
Author(s):  
Larry A. Rogers ◽  
Richard A. Atkinson ◽  
John P. Long
Keyword(s):  
Nerve Stimulation ◽  
Mesenteric Artery ◽  
Muscle Tone ◽  
Low Frequency ◽  
Sympathetic Nerves ◽  
Gas Mixture ◽  
Constant Flow ◽  
Pressor Responses ◽  
Resistance Vessels ◽  
Small Resistance

An isolated preparation of the dog's mesenteric artery with branching small resistance vessels and sympathetic nerves attached has been devised. The branching arterial segments were perfused by a constant-flow technique; the pressor responses to intra-arterially injected catecholamine and to nerve stimulation were recorded. The preparation gave reproducible pressor responses to injected catecholamine and to nerve stimulation for periods of several hours. Decreasing the temperature or increasing the pH (by decreasing CO2 in the gas mixture) of the vessel bath increased arterial smooth muscle tone and potentiated the pressor responses to injected catecholamine and to nerve stimulation. Increasing the temperature of the bath decreased the tone and reactivity of this preparation. Low-frequency continuous nerve stimulation potentiated the responses of this preparation to intra-arterially injected catecholamines.

scholarly journals Endovascular retrieval of a dislocated pushable coil in the common hepatic artery using a cerebral stent retriever

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Mohammed Shamseldin ◽  
Albrecht Stier ◽  
Norbert Hosten ◽  
Ralf Puls
Keyword(s):  
Case Report ◽  
Hepatic Artery ◽  
Common Hepatic Artery ◽  
Stent Retriever ◽  
Arterial Blood Flow ◽  
Slowing Down ◽  
Arterial Blood ◽  
First Case ◽  
Stent Retrievers ◽  
The Common

Abstract Background This is case of removing a dislocated pushable coil from the common hepatic artery (CHA) as a possible complication of using pushable coils in the embolization of an upper gastrointestinal bleeding (UGIB) from the gastroduodenal artery (GDA) by using a pRESET stent retriever (Phenox, Bochum, Germany) which is utilized mainly for treatment of endovascular stroke. Case presentation An 88-year-old female patient was referred to our hospital to get an emergency embolization of the GDA causing an UGIB with a relevant drop of the hemoglobin level. During the routine embolization of the GDA using pushable coils, a complete dislocation of the last coil into the CHA took place leading to a relevant slowing down of the arterial blood flow to the liver. A decision was thereby made to remove the dislocated coil to avoid further possible complications which was successfully achieved. Conclusions Various stent retrievers have been proven to be effective in removing dislocated coils during intracerebral coiling of different pathologies. This case report is to our knowledge the first case report proving the high efficacy and safety of using yet another stent retriever, namely a pRESET stent retriever in removing a fully dislocated coil in the abdominal vessels, namely in this case the CHA.

scholarly journals Sympathetic nerve stimulation induces local endothelial Ca2+ signals to oppose vasoconstriction of mouse mesenteric arteries

2012 ◽  
Vol 302 (3) ◽  
pp. H594-H602 ◽  
Author(s):  
Lydia W. M. Nausch ◽  
Adrian D. Bonev ◽  
Thomas J. Heppner ◽  
Yvonne Tallini ◽  
Michael I. Kotlikoff ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Adrenergic Receptor ◽  
Ryanodine Receptors ◽  
Electrical Field Stimulation ◽  
Sympathetic Nerves ◽  
Mesenteric Arteries ◽  
Sympathetic Nerve Stimulation ◽  
Voltage Dependent

It is generally accepted that the endothelium regulates vascular tone independent of the activity of the sympathetic nervous system. Here, we tested the hypothesis that the activation of sympathetic nerves engages the endothelium to oppose vasoconstriction. Local inositol 1,4,5-trisphosphate (IP3)-mediated Ca2+ signals (“pulsars”) in or near endothelial projections to vascular smooth muscle (VSM) were measured in an en face mouse mesenteric artery preparation. Electrical field stimulation of sympathetic nerves induced an increase in endothelial cell (EC) Ca2+ pulsars, recruiting new pulsar sites without affecting activity at existing sites. This increase in Ca2+ pulsars was blocked by bath application of the α-adrenergic receptor antagonist prazosin or by TTX but was unaffected by directly picospritzing the α-adrenergic receptor agonist phenylephrine onto the vascular endothelium, indicating that nerve-derived norepinephrine acted through α-adrenergic receptors on smooth muscle cells. Moreover, EC Ca2+ signaling was not blocked by inhibitors of purinergic receptors, ryanodine receptors, or voltage-dependent Ca2+ channels, suggesting a role for IP3, rather than Ca2+, in VSM-to-endothelium communication. Block of intermediate-conductance Ca2+-sensitive K+ channels, which have been shown to colocalize with IP3 receptors in endothelial projections to VSM, enhanced nerve-evoked constriction. Collectively, our results support the concept of a transcellular negative feedback module whereby sympathetic nerve stimulation elevates EC Ca2+ signals to oppose vasoconstriction.

scholarly journals Hepatic Artery Pseudoaneurysm Rupture with Acute Portal Vein Occlusion Treated with Coronary Stent Graft and Trans-splenic Portal Vein Stenting

2019 ◽  
Vol 03 (01) ◽  
pp. 062-064
Author(s):  
Stephen Allison ◽  
Arthie Jeyakumar ◽  
Guy Johnson ◽  
Matthew Kogut
Keyword(s):  
Portal Vein ◽  
Hepatic Artery ◽  
Stent Graft ◽  
Coronary Stent ◽  
Arterial Blood Flow ◽  
Artery Pseudoaneurysm ◽  
Portal Vein Occlusion ◽  
Bleeding Vessel ◽  
Vein Occlusion ◽  
Arterial Blood

AbstractDelayed massive hemorrhage following pancreaticoduodenectomy is a potentially fatal condition. These patients are often not surgical candidates, and endovascular therapy is the primary option of treatment, usually trans-arterial embolization. However, the bleeding vessel can occasionally be treated with a stent graft rather than embolization. This decreases the risk of hepatic necrosis by preserving hepatic arterial blood flow, particularly in patients with compromised portal veins. The authors present a brief case report of delayed pseudoaneurysm rupture from a replaced proper hepatic artery after pancreaticoduodenectomy with resultant portal vein occlusion, caused by hematoma mass effect. The hepatic artery was treated with a coronary stent. During the same session, trans-splenic portal vein stenting was done.

scholarly journals Computational Modeling of the Liver Arterial Blood Flow for Microsphere Therapy: Effect of Boundary Conditions

2020 ◽  
Vol 7 (3) ◽  
pp. 64
Author(s):  
Amirtahà Taebi ◽  
Rex M. Pillai ◽  
Bahman S. Roudsari ◽  
Catherine T. Vu ◽  
Emilie Roncali
Keyword(s):  
Blood Flow ◽  
Boundary Conditions ◽  
Hepatic Artery ◽  
Transarterial Embolization ◽  
Arterial Blood Flow ◽  
Patient Specific ◽  
Computational Domain ◽  
Arterial Tree ◽  
Arterial Blood ◽  
Therapy Effect

Transarterial embolization is a minimally invasive treatment for advanced liver cancer using microspheres loaded with a chemotherapeutic drug or radioactive yttrium-90 (90Y) that are injected into the hepatic arterial tree through a catheter. For personalized treatment, the microsphere distribution in the liver should be optimized through the injection volume and location. Computational fluid dynamics (CFD) simulations of the blood flow in the hepatic artery can help estimate this distribution if carefully parameterized. An important aspect is the choice of the boundary conditions imposed at the inlet and outlets of the computational domain. In this study, the effect of boundary conditions on the hepatic arterial tree hemodynamics was investigated. The outlet boundary conditions were modeled with three-element Windkessel circuits, representative of the downstream vasculature resistance. Results demonstrated that the downstream vasculature resistance affected the hepatic artery hemodynamics such as the velocity field, the pressure field and the blood flow streamline trajectories. Moreover, the number of microspheres received by the tumor significantly changed (more than 10% of the total injected microspheres) with downstream resistance variations. These findings suggest that patient-specific boundary conditions should be used in order to achieve a more accurate drug distribution estimation with CFD in transarterial embolization treatment planning.

Participation of adrenoceptors in liver blood flow regulation in anesthetized dogs

1987 ◽  
Vol 253 (5) ◽  
pp. H1053-H1058
Author(s):  
N. Terada ◽  
S. Koyama ◽  
J. Horiuchi ◽  
T. Takeuchi
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Vascular Resistance ◽  
Adrenergic Receptors ◽  
Liver Blood Flow ◽  
Arterial Blood Flow ◽  
Tissue Blood Flow ◽  
Intact Group ◽  
Arterial Blood

We evaluated involvement of adrenergic receptors in the responses of the hepatic vasculature to reduction either of portal venous flow or hepatic arterial inflow. Portal vein occlusion caused an increase in hepatic arterial blood flow (HAF) and decreases in hepatic arterial pressure (HAP) and hepatic arterial vascular resistance (HAR) in the intact group. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the portal vein produced a greater decrease in HAP as compared with that in the intact group. No significant changes in HAF, HAR, or hepatic tissue blood flow (HTF) occurred after the treatment. These results indicate that the compensatory response of the hepatic arterial vasculature to altered portal blood flow (PVF) is regulated independently of the intrahepatic adrenergic receptors. Hepatic arterial occlusion caused a significant decrease in portal venous pressure, PVF, and HTF. Portal venous vascular resistance (PVR) was reduced slightly, but not significantly. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the hepatic artery produced an opposite effect: to increase PVF and significantly decrease PVR. These results indicate that intrahepatic alpha-adrenoceptors participate in the regulation of portal vascular tone to maintain portal vein pressure at a steady level, when inflow from the hepatic artery is reduced.

Sign in / Sign up

Export Citation Format

Share Document