Venous and arterial responses to norepinephrine in dogs treated with reserpine

1964 ◽  
Vol 206 (2) ◽  
pp. 299-303 ◽  
Author(s):  
Francois M. Abboud ◽  
John W. Eckstein
Keyword(s):  
Small Vessel ◽  
Small Vessels ◽  
Arterial Resistance ◽  
Systemic Vein ◽  
Vasoconstrictor Effect ◽  
Vascular Responsiveness ◽  
Infusion Of Norepinephrine ◽  
Arterial Responses

Experiments were done to see if the effects of norepinephrine upon veins, arteries, and small vessels are augmented in dogs after treatment with reserpine. With intra-arterial injection of increasing doses of norepinephrine into the perfused foreleg there were progressive increments in total, arterial, small vessel, and venous resistances. In animals treated with reserpine the increments in total and small vessel resistances were greatly augmented while increments in segmental arterial resistance were increased only slightly. The venous responses in these treated dogs were not augmented. Similar effects on segmental resistances were noted with infusion of norepinephrine into a systemic vein. The vasoconstrictor effect of tyramine was reduced in treated dogs and was restored after intra-arterial and intravenous norepinephrine. The results indicate that veins do not participate in the increased vascular responsiveness to norepinephrine which occurs in forelegs of dogs after treatment with reserpine.

Effects of vasodilator stimuli on resistance of large and small cerebral vessels

1986 ◽  
Vol 251 (6) ◽  
pp. H1176-H1182 ◽  
Author(s):  
K. Tamaki ◽  
W. Mayhan ◽  
D. Heistad
Keyword(s):  
Cerebral Vessels ◽  
Small Vessel ◽  
Pial Arteries ◽  
Large Arteries ◽  
Small Vessels ◽  
Arterial Resistance ◽  
Vessel Resistance ◽  
Measured Pressure ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

We have examined effects of vasodilator stimuli on segmental resistance in the cerebral circulation. Our hypothesis was that resistance of large arteries, as well as small vessels, contributes to cerebral vascular responses to vasodilator stimuli. We measured cerebral blood flow with microspheres in anesthetized rabbits and measured pressure in pial arteries approximately 100 microns diameter using a servo-null method. These values were used to calculate resistance of large arteries (greater than 100 microns diameter) and small vessels (less than 100 microns diameter). Under control conditions, resistance of large arteries accounted for one-third to one-half of total cerebral vascular resistance. Intracarotid infusion of acetylcholine (1 microgram/min) reduced large arterial resistance by 69% and small vessel resistance by 58%. Adenosine also produced marked reductions in resistance of both large and small cerebral vessels. In contrast, seizures reduced large arterial resistance by 50% and small vessel resistance by 85%. Pial arterial pressure, which depends on the ratio of large and small vessel resistance, increased during infusion of acetylcholine and adenosine, but decreased during seizures. We conclude that both large and small cerebral vessels are responsive to acetylcholine and adenosine, and seizures produce preferential reduction in resistance of small vessels.

scholarly journals Arterial hypertension and unusual ascending aortic dilatation in a neonate with acute kidney injury: mechanistic computer modelling

2018 ◽  
Author(s):  
Sanjay R Kharche
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Ascending Aorta ◽  
Small Vessel ◽  
Aortic Dilatation ◽  
Small Vessels ◽  
Left Ventricle Hypertrophy ◽  
Vessel Resistance ◽  
Underlying Mechanisms ◽  
Ventricle Hypertrophy

Background: Neonatal asphyxia caused acute kidney injury and severe hypertension in a newborn patient. An unusually dilatated ascending aorta developed within a few weeks. Dialysis and hypertensive treatment led to partial recovery of the aortic diameters. It was hypothesized that the aortic dilatation may be associated with cardiovascular changes induced by the acute kidney injury. Mathematical modelling was used to better understand the underlying mechanisms of hypertension and aortic dilatation.Methods: Patient observation included systolic blood pressure recording and echocardiographic exams. To explore underlying mechanisms of aortic dilatation and hypertension, a previous whole-body lumped parameter hemodynamics model was adapted to this study. Computer simulations were designed to permit dissection of individual mechanisms. The hypertension inducing effects of altering systemic vascular resistances, stiffnesses, and heart rate on blood flows and pressures were simulated.Results: In agreement with our clinical diagnosis, the mathematical model showed that an increase of systemic small vessel resistance is the prime cause of hypertension. Further, aortic stiffening may also cause hypertension, it was found to be secondary to the potency of systemic small vessel resistance. The cardiac output, as quantified using pressure-volume loop area, reduced significantly due to hypertension. Simultaneous left ventricle hypertrophy and small vessel blocking increased ascending aorta blood flow as well as pressure indicating an enlarged ascending aorta. In contrast, increased arterial stiffness appeared to lower the aortic blood flow and pressures.Conclusions and discussion: Systemic small vessel resistance is an important factor in arterial hypertension, and may also be a key clinical therapeutic target. Left ventricle hypertrophy may also be simultaneously ameliorated when treating systemic small vessels. Treatment of arterial stiffness appears to provide significant benefit but may be secondary to treatment of the systemic small vessels. The quantitative grading of pathophysiological mechanisms provided by the modelling may contribute to treatment recommendations. Further development and individualization of the model will augment its applicability in clinical practice.

Small vessel vasculitis

2020 ◽  
pp. 4573-4579
Author(s):  
Richard A. Watts
Keyword(s):  
Antineutrophil Cytoplasmic Antibody ◽  
Consensus Conference ◽  
Small Vessel ◽  
Small Vessel Vasculitis ◽  
Iga Vasculitis ◽  
Small Vessels ◽  
Chapel Hill ◽  
Familial Association ◽  
Chapel Hill Consensus Conference ◽  
Inflammatory Drugs

Small vessel vasculitis is vasculitis affecting predominately small intraparenchymal arteries, arterioles, capillaries, and venules. There are two main types: antineutrophil cytoplasmic antibody associated and immune complex mediated. The ANCA associated vasculitides are discussed in chapter 19.3 IgA vasculitis (IgAV) was formerly known as Henoch Schönlein purpura. The revised nomenclature reflects the importance of IgA vasculitis in pathogenesis. The Chapel Hill Consensus Conference defined IgA vasculitis as ‘vasculitis with IgA1-dominant immune deposits, affecting small vessels (predominantly capillaries, venules, or arterioles)’. IgA vasculitis often involves skin and gut, and frequently causes arthritis. Glomerulonephritis indistinguishable from IgA nephropathy may occur. Its aetiology is unknown, but it frequently occurs after an infection several days to weeks before. The most frequently isolated organism is beta-haemolytic streptococcus. Drugs such as a penicillin, ampicillin, erythromycin, and non-steroidal anti-inflammatory drugs have been reported as precipitating agents. There is an association with HLA-DRB1*01 in Caucasians and there appears to be a familial association.

Vascular basement membrane alterations and β-amyloid accumulations in an animal model of cerebral small vessel disease

2017 ◽  
Vol 131 (10) ◽  
pp. 1001-1013 ◽  
Author(s):  
Friederike Held ◽  
Alan W.J. Morris ◽  
Daniel Pirici ◽  
Solveig Niklass ◽  
Matthew M.G. Sharp ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Small Vessel Disease ◽  
Collagen Iv ◽  
Cerebral Small Vessel Disease ◽  
Basement Membranes ◽  
Small Vessel ◽  
Small Vessels ◽  
Vessel Disease ◽  
Percentage Area ◽  
Β Amyloid

Non-amyloid cerebral small vessel disease (CSVD) and cerebral amyloid angiopathy (CAA) may be interrelated through the damaged basement membranes (BMs) and extracellular matrix changes of small vessels, resulting in a failure of β-amyloid (Aβ) transport and degradation. We analyzed BM changes and the pattern of deposition of Aβ in the walls of blood vessels in spontaneously hypertensive stroke-prone rats (SHRSP), a non-transgenic CSVD model. In 45 SHRSP and 38 Wistar rats aged 18 to 32 weeks: (i) the percentage area immunostained for vascular collagen IV and laminin was quantified; (ii) the capillary BM thickness as well as endothelial and pericyte pathological changes were analysed using transmission electron microscopy (TEM); and (iii) the presence of vascular Aβ was assessed. Compared with controls, SHRSP exhibited a significantly higher percentage area immunostained with collagen IV in the striatum and thalamus. SHRSP also revealed an age-dependent increase of the capillary BM thickness and of endothelial vacuoles (caveolae) within subcortical regions. Endogenous Aβ deposits in the walls of small blood vessels were observed in the cortex (with the highest incidence found within fronto-parietal areas), striatum, thalamus and hippocampus. Vascular β-amyloid accumulations were frequently detected at sites of small vessel wall damage. Our data demonstrate changes in the expression of collagen IV and of the ultrastructure of BMs in the small vessels of SHRSP. Alterations are accompanied by vascular deposits of endogenous Aβ. Impaired β-amyloid clearance along perivascular and endothelial pathways and failure of extracellular Aβ degradation may be the key mechanisms connecting non-amyloid CSVD and CAA.

Visualization of mouse spinal cord intramedullary arteries using phase- and attenuation-contrast tomographic imaging

2016 ◽  
Vol 23 (4) ◽  
pp. 966-974 ◽  
Author(s):  
Yong Cao ◽  
Xianzhen Yin ◽  
Jiwen Zhang ◽  
Tianding Wu ◽  
Dongzhe Li ◽  
...  
Keyword(s):  
Spinal Cord ◽  
High Resolution ◽  
Synchrotron Radiation ◽  
Three Dimensional ◽  
Small Vessel ◽  
Imaging Method ◽  
Central Sulcus ◽  
Contrast Imaging ◽  
Mouse Spinal Cord ◽  
Small Vessels

Many spinal cord circulatory disorders present the substantial involvement of small vessel lesions. The central sulcus arteries supply nutrition to a large part of the spinal cord, and, if not detected early, lesions in the spinal cord will cause irreversible damage to the function of this organ. Thus, early detection of these small vessel lesions could potentially facilitate the effective diagnosis and treatment of these diseases. However, the detection of such small vessels is beyond the capability of current imaging techniques. In this study, an imaging method is proposed and the potential of phase-contrast imaging (PCI)- and attenuation-contrast imaging (ACI)-based synchrotron radiation for high-resolution tomography of intramedullary arteries in mouse spinal cord is validated. The three-dimensional vessel morphology, particularly that of the central sulcus arteries (CSA), detected with these two imaging models was quantitatively analyzed and compared. It was determined that both PCI- and ACI-based synchrotron radiation can be used to visualize the physiological arrangement of the entire intramedullary artery network in the mouse spinal cord in both two dimensions and three dimensions at a high-resolution scale. Additionally, the two-dimensional and three-dimensional vessel morphometric parameter measurements obtained with PCI are similar to the ACI data. Furthermore, PCI allows efficient and direct discrimination of the same branch level of the CSA without contrast agent injection and is expected to provide reliable biological information regarding the intramedullary artery. Compared with ACI, PCI might be a novel imaging method that offers a powerful imaging platform for evaluating pathological changes in small vessels and may also allow better clarification of their role in neurovascular disorders.

Venous and arterial responses to stimulation of beta adrenergic receptors

1965 ◽  
Vol 209 (2) ◽  
pp. 383-389 ◽  
Author(s):  
Francois M. Abboud ◽  
John W. Eckstein ◽  
Ben G. Zimmerman
Keyword(s):  
Blood Flow ◽  
Adrenergic Receptors ◽  
Total Blood ◽  
Small Vessels ◽  
Beta Receptors ◽  
Blood Pressures ◽  
Arterial Responses ◽  
Total Blood Flow ◽  
Arteries And Veins ◽  
Stimulation Of

The effects of intra-arterial injections of isoproterenol on small vessels, arteries, and veins were studied in the paw and muscle of the foreleg of dog. Total blood flow to the foreleg was held constant. Blood pressures were measured in large and small arteries and veins. In some experiments venous outflow from paw and muscle was measured. The small vessel segment was the site of major dilatation. Venodilator responses were small, but they were enhanced when isoproterenol was injected in the presence of venous constriction induced by intra-arterial infusions of norepinephrine. Dichloroisoproterenol and nethalide blocked the dilator responses to isoproterenol in all segments but they did not block the dilator responses to acetylcholine or glyceryl trinitrate. Isoproterenol did not change the distribution of blood flow within the foreleg; responses in muscle and paw were not significantly different. The results indicate that stimulation of beta receptors with isoproterenol causes much more dilatation in small vessels than in veins in the foreleg and that small vessels of both paw and muscle dilate equally.

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