The effects of intraportl infusions of glucagon on the hepatic arterial and portal venous vascular beds of the dog: Inhibition of hepatic arterial vasoconstrictor responses to noradrenaline

Unlike many peripheral vascular beds, the sympathetic nervous system exerts little control on cerebral blood flow. The contractile response of isolated rabbit middle cerebral artery (MCA) segments to electrical field stimulation of its intramural nerves is less than in a similar-sized artery from the ear. This study was undertaken to characterize and compare the perivascular neuromuscular relationships and innervation density of similar-sized arteries varying in diameter from these two different regional arterial beds to see if there were structural correlates for these functional differences.

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Adrenergic Stimulation of Regional Plasminogen Activator Release in Rabbits

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646315 ◽

1992 ◽

Vol 68 (05) ◽

pp. 545-549 ◽

Cited By ~ 5

Author(s):

W L Chandler ◽

S C Loo ◽

D Mornin

Keyword(s):

Lower Extremity ◽

Plasminogen Activator ◽

Beta Blocker ◽

Time Course ◽

Vascular System ◽

Adrenergic Stimulation ◽

Epinephrine Administration ◽

Adrenergic Antagonist ◽

Vascular Beds ◽

Stimulation Of

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.

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Vascular Endothelial Growth Factor (VEGF165) and Its Influence on Angiogenesis Versus Arteriogenesis in Different Vascular Beds

Journal of Endovascular Therapy ◽

10.1583/1545-1550(2002)009<0842:vegfva>2.0.co;2 ◽

2002 ◽

Vol 9 (6) ◽

pp. 842-854 ◽

Cited By ~ 2

Author(s):

Sigrid Nikol ◽

Jaroslav Pelisek ◽

Markus G. Engelmann ◽

Masumi Shimizu ◽

Alexandra Fuchs ◽

...

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Vascular Endothelial ◽

Vascular Beds ◽

Endothelial Growth Factor

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Maternal Anti-HPA-1a Antibodies Increase Endothelial Cell Apoptosis and Permeability

Journal of Vascular Research ◽

10.1159/000515703 ◽

2021 ◽

pp. 1-9

Author(s):

Rima Dardik ◽

Ophira Salomon

Keyword(s):

Endothelial Cells ◽

Endothelial Cell ◽

Intracranial Hemorrhage ◽

Cell Apoptosis ◽

Endothelial Damage ◽

Αvβ3 Integrin ◽

Endothelial Cell Apoptosis ◽

Vascular Beds ◽

Alloimmune Thrombocytopenia

Intracranial hemorrhage (ICH) associated with fetal/neonatal alloimmune thrombocytopenia (FNAIT) is attributed mainly to endothelial damage caused by binding of maternal anti-HPA-1a antibodies to the αvβ3 integrin on endothelial cells (ECs). We examined the effect of anti-HPA-1a antibodies on EC function using 2 EC lines from different vascular beds, HMVEC of dermal origin and hCMEC/D3 of cerebral origin. Anti-HPA-1a sera significantly increased apoptosis in both HMVEC and hCMEC/D3 cells and permeability in hCMEC/D3 cells only. This increase in both apoptosis and permeability was significantly inhibited by a monoclonal anti-β3 antibody (SZ21) binding to the HPA-1a epitope. Our results indicate that (1) maternal anti-HPA-1a antibodies impair EC function by increasing apoptosis and permeability and (2) ECs from different vascular beds vary in their susceptibility to pathological effects elicited by maternal anti-HPA-1a antibodies on EC permeability. Examination of maternal anti-HPA-1a antibodies for their effect on EC permeability may predict potential ICH associated with FNAIT.

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Endothelial Dysfunction in Shock States

Physiology ◽

10.1152/physiologyonline.1993.8.4.145 ◽

1993 ◽

Vol 8 (4) ◽

pp. 145-148 ◽

Cited By ~ 2

Author(s):

AGB Kovach ◽

AM Lefer

Keyword(s):

Nitric Oxide ◽

Endothelial Dysfunction ◽

Tissue Injury ◽

Circulatory Shock ◽

Relaxing Factor ◽

Vascular Beds ◽

Endothelium Derived Relaxing Factor

Circulatory shock results in dysfunction of the endothelium in various vascular beds. This dysfunction is characterized by marked impairment in the vasculature's ability to relax to endothelium-dependent vasodilators. This loss of endothelium-derived relaxing factor, or nitric oxide, leads to profound tissue injury.

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Non-coronary Interventions: An Introduction to Peripheral Arterial Interventions

Interventional Cardiology Review ◽

10.15420/icr.2016:8:2 ◽

2016 ◽

Vol 11 (2) ◽

pp. 128

Author(s):

Brock Cookman ◽

Suhail Allaqaband ◽

Tonga Nfor ◽

◽

...

Keyword(s):

Strong Relationship ◽

Ageing Population ◽

Peripheral Vascular ◽

Endovascular Interventions ◽

Cardiovascular Morbidity And Mortality ◽

Vascular Beds ◽

Peripheral Arterial ◽

Peripheral Artery Diseases ◽

Broad Understanding

With an ageing population, the burden of peripheral artery diseases (PADs) is increasing. The treatment of these diseases has largely been performed by interventional radiologists, vascular surgeons and interventional cardiologists. Due to the strong relationship between PAD and overall cardiovascular morbidity and mortality, cardiologists need to play a greater role in the management of PAD. The physician who cares for the patient with peripheral vascular disease should have a broad understanding of atherosclerotic disease involving all vascular beds. Endovascular interventions play a major role in relieving symptoms and reducing morbidity related to PAD, but long-term optimal medical treatment is an essential determinant of prognosis. This paper reviews current endovascular/percutaneous interventions for PAD.

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EXTRAHEPATIC AND EXTRARENAL RENIN INACTIVATION IN THE DOG

Journal of Endocrinology ◽

10.1677/joe.0.0600217 ◽

1974 ◽

Vol 60 (2) ◽

pp. 217-222

Author(s):

R. FAGARD ◽

E. FOSSION ◽

M. CAMPFORTS ◽

A. AMERY

Keyword(s):

Blood Vessels ◽

Pulmonary Circulation ◽

Plasma Renin ◽

Glass Container ◽

Plasma Renin Concentration ◽

Vascular Beds ◽

Extrarenal Renin

SUMMARY It was demonstrated previously that renin disappears quickly from the circulation after nephrectomy in the hepatectomized dog. In the present study the plasma renin concentration (PRC) was measured in the efferent and afferent blood vessels of several vascular beds (pulmonary circulation, splanchnic region, spleen, both inferior limbs and pelvis, head) in the anhepatic and in the anhepatic and anephric dog in order to investigate extrarenal and extrahepatic renin inactivation. However, no significant arteriovenous differences in PRC could be traced. The blood of these dogs kept in vitro at 37 °C in a glass container showed no decline in PRC within 3 h of removal. Therefore no specific extrahepatic and extrarenal renin-inactivating mechanism was found which could explain the rapid disappearance of renin from the blood in vivo in the anhepatic and anephric dog.

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Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01229.2005 ◽

2006 ◽

Vol 291 (1) ◽

pp. H441-H450 ◽

Cited By ~ 22

Author(s):

Timofei V. Kondratiev ◽

Kristina Flemming ◽

Eivind S. P. Myhre ◽

Mikhail A. Sovershaev ◽

Torkjel Tveita

Keyword(s):

Blood Volume ◽

Tissue Oxygenation ◽

Limiting Factor ◽

Myocardial Tissue ◽

Circulating Blood Volume ◽

Profound Hypothermia ◽

Group 3 ◽

Vascular Beds ◽

Group 2 ◽

Group 1

It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2supply and/or malfunctioning O2extraction occur during rewarming from deep/profound hypothermia of different duration. Three groups of rats ( n = 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15°C, kept at 15°C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by >50% in response to cooling. O2consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h ( group 2) but recovered to only 60% in those rewarmed after 5 h ( group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15°C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2extraction function well during deep/profound hypothermia, and, despite low CO, O2supply was not a limiting factor for survival in the present experiments.

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