Evidence for Peripheral Vascular Involvement in Mild Elevation of Blood Pressure in Man

1976 ◽  
Vol 51 (s3) ◽  
pp. 65s-68s
Author(s):  
R. Sivertsson ◽  
R. Sannerstedt ◽  
Y. Lundgren

1. Cardiac output at rest, intra-arterial blood pressure and hand blood flow at maximal vasodilatation were studied in two groups of 18–25-year-old men: forty-four with mild blood pressure elevation were referred from a military enlistment centre, and twenty-nine normotensive volunteers were mainly recruited from the same enlistment centre. 2. The study group was characterized by a significantly higher cardiac index at rest, and a significantly higher blood flow resistance in the hand at maximal vasodilatation than the control group, indicating the presence of structural modifications in the resistance vessels of patients with mild blood pressure elevation. 3. The tendency to increased vascular resistance in the blood vessels of the hand at maximal vasodilatation was more pronounced in patients with a normal cardiac index than in those with a high index. This suggests inclusion in the study group of tense, anxious individuals with an elevated cardiac index but otherwise normal circulation, but does not exclude the possibility that these patients may develop structural changes later on.

2018 ◽  
Vol 1 (108) ◽  
pp. 2-8
Author(s):  
Kęstutis Bunevičius ◽  
Albinas Grunovas ◽  
Jonas Poderys

Background. Occlusion pressure intensity influences the blood flow intensity. Immediately after the cuff pressure is released, reactive hyperaemia occurs. Increased blood flow and nutritive delivery are critical for an anabolic stimulus, such as insulin. The aim of study was to find which occlusion pressure was optimal to increase the highest level of post occlusion reactive hyperaemia. Methods. Participants were randomly assigned into one of the four conditions (n = 12 per group): control group without blood flow restriction, experimental groups with 120; 200 or 300 mmHg occlusion pressure. We used venous occlusion plethysmography and arterial blood pressure measurements. Results. After the onset of 120 and 200 mm Hg pressure occlusion, the blood flow intensity significantly decreased. Occlusion induced hyperaemia increased arterial blood flow intensity 134 ± 11.2% (p < .05) in the group with 120 mmHg, in the group with 200 mmHg it increased 267 ± 10.5% (p < .05), in the group with 300 mmHg it increased 233 ± 10.9% (p < .05). Applied 300 mmHg occlusion from the 12 minute diastolic and systolic arterial blood pressure decreased statistically significantly. Conclusions. Occlusion manoeuvre impacted the vascular vasodilatation, but the peak blood flow registered after occlusion did not relate to applied occlusion pressure. The pressure of 200 mmHg is optimal to impact the high level of vasodilatation. Longer than 12 min 300 mmHg could not be recommended due to the steep decrease of systolic and diastolic blood pressures.


1987 ◽  
Vol 252 (2) ◽  
pp. H291-H300 ◽  
Author(s):  
M. J. Breslow ◽  
C. F. Miller ◽  
S. D. Parker ◽  
A. T. Walman ◽  
R. J. Traystman

A volume-resuscitated porcine endotoxin shock model was used to evaluate the effect on organ blood flow of increasing systemic arterial blood pressure with vasopressors. Administration of 0.05–0.2 mg/kg of Escherichia coli endotoxin (E) reduced mean arterial blood pressure (MAP) to 50 mmHg, decreased systemic vascular resistance to 50% of control, and did not change cardiac output or heart rate. Blood flow to brain, kidney, spleen, and skeletal muscle was reduced during endotoxin shock, but blood flow to left ventricle, small and large intestine, and stomach remained at pre-endotoxin levels throughout the study period. Four groups of animals were used to evaluate the effect of vasopressor therapy. A control group received E and no vasopressor, whereas the other three groups received either norepinephrine, dopamine, or phenylephrine. Vasopressors were administered starting 60 min after E exposure, and the dose of each was titrated to increase MAP to 75 mmHg. Despite the increase in MAP, brain blood flow did not increase in any group. Norepinephrine alone increased blood flow to the left ventricle. Kidney, splanchnic, and skeletal muscle blood flow did not change with vasopressor administration. The dose of norepinephrine required to increase MAP by 20–25 mmHg during E shock was 30 times the dose required for a similar increase in MAP in animals not receiving E. We conclude that hypotension in the fluid resuscitated porcine E shock model is primarily the result of peripheral vasodilatation, that the vascular response to vasoconstrictors in this model is markedly attenuated following E administration, that blood pressure elevation with norepinephrine, dopamine, and phenylephrine neither decreases blood flow to any organ nor increases blood flow to organs with reduced flow, and that norepinephrine, dopamine, and phenylephrine affect regional blood flow similarly in this model.


1978 ◽  
Vol 55 (s4) ◽  
pp. 243s-246s
Author(s):  
Chang-Seng Liang ◽  
Haralambos Gavras ◽  
H. R. Brunner

1. Salt depletion was produced in five dogs by a low salt diet and daily administration of frusemide for 5 days; a control group of five dogs was placed on the same diet, to which 2·5 g of sodium chloride was added. 2. Saralasin infusion (0·5 μg min−1 kg−1) reduced mean aortic blood pressure and total peripheral vascular resistance and increased cardiac output in salt-depleted dogs, but did not affect the heart rate and left ventricular dP/dt. 3. Saralasin infusion increased mean aortic blood pressure slightly in normal dogs; other systemic haemodynamic parameters did not change significantly. 4. Saralasin decreased hepatic arterial flow in both normal and salt-depleted dogs, but increased blood flow to left ventricle and kidneys only in salt-depleted dogs. 5. These results suggest that saralasin exerts a partial agonist effect in normal dogs to increase arterial blood pressure, but causes a depressor response during salt depletion because it reverses the vasoconstrictor effect of angiotensin II, particularly on the renal and coronary circulations.


2021 ◽  
Vol 71 (3) ◽  
pp. 1033-36
Author(s):  
Fatima Iqbal ◽  
Manzoor Ahmed Faridi ◽  
Aisha Saeed ◽  
Inamullah Shah

Objective: To compare the result of the combination of hyperbaric bupivacaine plus fentanyl with hyperbaric bupivacaine alone in patients undergoing caesarean section in spinal anaesthesia. Study Design: Comparative, cross-sectional study. Place and Duration of Study: Department of Anesthesia, Fauji Foundation Hospital, Rawalpindi Pakistan, from Dec 2017 to Jun 2018. Methodology: After consulting the institutional ethical review committees a total of 60 females between ages 18-40 years were enrolled for caesarean section delivery. They were divided into two groups. The study group (n=30) received a subarachnoid injection of 0.5% hyperbaric bupivacaine (10mg) 2ml with 25ug of fentanyl 0.5ml and control group (n=30) was injected 0.5% hyperbaric bupivacaine 12.5mg (2.5 ml) only. Pain experienced during the procedure was assessed by using 10-point visual analogue scoring method. The mean duration of analgesia, mean arterial blood pressure and heart rate after surgery were compared between two groups. Results: The mean duration of analgesia was 206.5/min ± 6.4 in the study group and it was 163.6min ± 7.2 in the control group (p=0.001). Mean arterial BP after surgery was 92.3mmHg ± 3.8 in the study group and 88.7mmHg ± 4.1 in the control group (p=0.001). The mean heart rate recorded after surgery was 75.2/min ± 5.2 in the study group and it was 70.4/min ± 6.1 in the control group (p=0.001). Conclusions: The mean duration of analgesia was significantly longer in the study group when compared with the control group with better mean arterial blood pressure and heart rate response after Caesarean section.


2012 ◽  
Vol 39 (4) ◽  
pp. 752-758 ◽  
Author(s):  
CHARLES GASPAROVIC ◽  
CLIFFORD QUALLS ◽  
ERNEST R. GREENE ◽  
WILMER L. SIBBITT ◽  
CARLOS A. ROLDAN

Objective.In previous studies cerebral blood flow (CBF) was found to be altered in patients with systemic lupus erythematosus (SLE) compared to controls. We investigated the relationships between CBF and clinical data from subjects with SLE with the aim of determining the pathologic factors underlying altered CBF in SLE.Methods.A total of 42 SLE subjects and 19 age- and sex-matched healthy control subjects were studied. Dynamic susceptibility contrast (DSC) magnetic resonance imaging (MRI) was used to measure CBF. Patients and controls underwent complete clinical and laboratory evaluations in close proximity with their MRI studies.Results.A higher CBF was present in the SLE group and was independently associated in statistical models with higher systolic blood pressure (SBP; p < 0.01). The intensity of the relationships (slope of curve) between CBF and mean arterial blood pressure, diastolic blood pressure, or blood levels of tissue plasminogen activator in the SLE group was significantly blunted relative to the control group.Conclusion.These findings are consistent with an underlying cerebral hyperperfusion in SLE induced by elevated but nonhypertensive levels of SBP. The factors underlying this relationship may be functional and/or structural (atherosclerotic, thrombotic, thromboembolic, or vasculitic) cerebrovascular disease.


2012 ◽  
Vol 27 (4) ◽  
pp. 318-324 ◽  
Author(s):  
Marcos De Simone Melo ◽  
Matheus Rodrigues Bonfim ◽  
Elisabeth Dreyer ◽  
Betina Silvia Beozzo Bassanezi ◽  
Artur Udelsmann

PURPOSE: To evaluate the hemodynamic changes following SMOFlipid emulsion therapy with after bupivacaine intoxication in swines. METHODS: Large White pigs were anesthetized with thiopental, tracheal intubation was performed and mechanical ventilation was instituted. Hemodynamic variables were recorded with invasive pressure monitoring and pulmonary artery catheterization (Swan-Ganz catheter). After a 30-minute resting period, 5 mg.kg-1 of bupivacaine by intravenous injection was administered and new hemodynamic measures were performed 1 minute later; the animals were than randomly divided into two groups and received 4 ml.kg-1 of saline solution or 4 ml.kg-1 of SMOFlipid emulsion 20%. Hemodynamic changes were then re-evaluated at 5, 10, 15, 20 and 30 minutes. RESULTS: Bupivacaine intoxication caused fall in arterial blood pressure, cardiac index, ventricular systolic work index mainly and no important changes in vascular resistances. SMOFlipid emulsion therapy was able to improve blood pressure mainly by increasing vascular resistance since the cardiac index had no significant improvement in our study. Hemodynamic results of the use of lipid emulsion in bupivacaine intoxication were better than the control group. CONCLUSION: The SMOFlipid emulsion is a option for reversing hypotension in cases of intoxication by bupivacaine.


1963 ◽  
Vol 205 (6) ◽  
pp. 1275-1278 ◽  
Author(s):  
W. G. Kubicek ◽  
A. P. Thal

The objectives of this investigation were: 1) To study the effect of diverting renal vein blood flow into the portal vein system upon renal function and hypertension produced by Goldblatt clamps. 2) To study the effects of passing the adrenal vein blood directly into the liver via the portal vein upon arterial blood pressure and upon Goldblatt hypertension. Renal vein blood was diverted into the portal vein by either a reverse Eck fistula or a direct renal to portal vein anastomosis. Clearance rates of p-aminohippurate and creatinine were used to measure renal blood flow and glomerular filtration rate. Goldblatt clamps on the renal arteries of four control dogs resulted in an average blood pressure elevation of 45/28 mm Hg. After a reverse Eck fistula in four dogs, average renal blood flow values indicated a fall of approximately 27% with no change in arterial blood pressure. Subsequent application of Goldblatt clamps resulted in an elevation in arterial blood pressure similar to the control animals. In two dogs, a direct renal to portal vein anastomosis yielded similar results. Diverting adrenal vein blood directly into the liver produced a small rise in the control arterial blood pressure and an apparent increase in the Goldblatt hypertension in two dogs.


2007 ◽  
Vol 293 (6) ◽  
pp. G1281-G1287 ◽  
Author(s):  
Joel Petersson ◽  
Olof Schreiber ◽  
Andreas Steege ◽  
Andreas Patzak ◽  
Anna Hellsten ◽  
...  

The role of NO in inflammatory bowel disease is controversial. Studies indicate that endothelial nitric oxide synthase (eNOS) might be involved in protecting the mucosa against colonic inflammation. The aim of this study was to investigate the involvement of nitric oxide (NO) in regulating colonic mucosal blood flow in two different colitis models in rats. In anesthetized control and colitic rats, the distal colon was exteriorized and the mucosa visualized. Blood flow (laser-Doppler flowmetry) and arterial blood pressure were continuously monitored throughout the experiments, and vascular resistance was calculated. Trinitrobenzene sulfonic acid (TNBS) or dextran sulfate sodium (DSS) was used to induce colitis. All groups were given the NOS inhibitor Nω-nitro-l-arginine (l-NNA) or the inducible NOS (iNOS) inhibitor l- N6-(1-iminoethyl)-lysine (l-NIL). iNOS, eNOS, and neuronal NOS (nNOS) mRNA in colonic samples were investigated with real-time RT-PCR. Before NOS inhibition, colonic mucosal blood flow, expressed as perfusion units, was higher in both colitis models compared with the controls. The blood flow was reduced in the TNBS- and DSS-treated rats during l-NNA administration but was not altered in the control group. Vascular resistance increased more in the TNBS- and DSS-treated rats than in the control rats, indicating a higher level of vasodilating NO in the colitis models. l-NIL did not alter blood pressure or blood flow in any of the groups. iNOS and eNOS mRNA increased in both colitis models, whereas nNOS remained at the control level. TNBS- and DSS-induced colitis results in increased colonic mucosal blood flow, most probably due to increased eNOS activity.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Badlishah Sham Nurul-Iman ◽  
Yusof Kamisah ◽  
Kamsiah Jaarin ◽  
Hj Mohd Saad Qodriyah

This study was performed to explore the effects of virgin coconut oil (VCO) in male rats that were fed with repeatedly heated palm oil on blood pressure, plasma nitric oxide level, and vascular reactivity. Thirty-two male Sprague-Dawley rats were divided into four groups: (i) control (basal diet), (ii) VCO (1.42 mL/kg, oral), (iii) five-times-heated palm oil (15%) (5HPO), and (iv) five-times-heated palm oil (15%) and VCO (1.42 mL/kg, oral) (5HPO + VCO). Blood pressure was significantly increased in the group that was given the 5HPO diet compared to the control group. Blood pressure in the 5HPO + VCO group was significantly lower than the 5HPO group. Plasma nitric oxide (NO) level in the 5HPO group was significantly lower compared to the control group, whereas in the 5HPO + VCO group, the plasma NO level was significantly higher compared to the 5HPO group. Aortic rings from the 5HPO group exhibited attenuated relaxation in response to acetylcholine and sodium nitroprusside as well as increased vasoconstriction to phenylephrine compared to the control group. Aortic rings from the 5HPO + VCO group showed only attenuated vasoconstriction to phenylephrine compared to the 5HPO group. In conclusion, VCO prevents blood pressure elevation and improves endothelial functions in rats fed with repeatedly heated palm oil.


Sign in / Sign up

Export Citation Format

Share Document