Redistribution of Regional Blood Flow after Administration of Saralasin in Salt-Depleted Dogs

1978 ◽  
Vol 55 (s4) ◽  
pp. 243s-246s
Author(s):  
Chang-Seng Liang ◽  
Haralambos Gavras ◽  
H. R. Brunner
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Regional Blood Flow ◽  
Partial Agonist ◽  
Left Ventricular ◽  
Control Group ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Salt Depletion ◽  
Aortic Blood Pressure

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.

Carotid chemoreceptor reflex parasympathetic coronary vasodilation in the dog

1985 ◽  
Vol 249 (6) ◽  
pp. H1167-H1175 ◽  
Author(s):  
B. R. Ito ◽  
E. O. Feigl
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Carotid Body ◽  
Cardiac Metabolism ◽  
Transient Increase ◽  
Coronary Vasodilation ◽  
Arterial Blood ◽  
Body Regions ◽  
Aortic Blood ◽  
Aortic Blood Pressure

The hypothesis that carotid body chemoreceptor activation with hypoxic-hypercapnic blood elicits reflex coronary vasodilation was investigated. Circumflex or anterior descending coronary artery blood flow was measured in alpha-chloralose-anesthetized, closed-chest dogs. To minimize changes in cardiac metabolism, the heart was paced at a constant rate after atrioventricular heart block, propranolol (1 mg/kg) was given to prevent beta-receptor-mediated alterations in cardiac contractility, and aortic blood pressure was stabilized by means of a blood reservoir. The carotid body regions were vascularly isolated and perfused at constant pressure with arterial blood or hypoxic-hypercapnic blood. Under these conditions, carotid body chemoreceptor stimulation with hypoxic or hypoxic-hypercapnic blood for 90 s produced atrial bradycardia and a transient increase in coronary blood flow of 36–53% above prestimulation values. The augmented coronary flow was accompanied by a transient increase in coronary sinus O2 tension of 4.6–5.7 mmHg. Aortic blood pressure varied less than 10 mmHg. Intracarotid injections of nicotine (0.1 microgram/kg) or cyanide (150 micrograms) produced similar results. The coronary response to chemoreceptor stimulation with hypoxic blood or drugs was abolished when the reflex arc was interrupted with atropine (0.5 mg/kg). It is concluded that transient reflex parasympathetic coronary vasodilation is elicited by hypoxic or hypoxic-hypercapnic stimulation of carotid body chemoreceptors.

scholarly journals EFFECT OF DIFFERENT OCCLUSION PRESSURE ON PECULIARITIES OF MUSCLE BLOOD FLOW

2018 ◽  
Vol 1 (108) ◽  
pp. 2-8
Author(s):  
Kęstutis Bunevičius ◽  
Albinas Grunovas ◽  
Jonas Poderys
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Arterial Blood Flow ◽  
Control Group ◽  
Reactive Hyperaemia ◽  
Occlusion Pressure ◽  
Arterial Blood ◽  
Flow Intensity ◽  
Blood Flow Intensity

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.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Cardiovascular actions of beta-phenylethylamine

1979 ◽  
Vol 236 (4) ◽  
pp. H592-H595
Author(s):  
C. S. Liang ◽  
D. Sprecher
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Left Ventricular ◽  
Peripheral Vascular Resistance ◽  
Adrenergic Nerve ◽  
Peripheral Vascular ◽  
Vascular Effects ◽  
Aortic Blood ◽  
Total Peripheral Vascular Resistance ◽  
Aortic Blood Pressure

beta-Phenylethylamine increased mean aortic blood pressure, total peripheral vascular resistance, left ventricular dP/dt, and (dP/dt)/P in chloralose-anesthetized dogs. Pretreatment with phentolamine reduced the increases in aortic blood pressure and total peripheral vascular resistance produced by beta-phenylethylamine, whereas, the effects of beta-phenylethylamine on left ventricular dP/dt and (dP/dt)/P were abolished by propranolol. beta-Phenylethylamine pretreatment, but increased both after phentolamine pretreatment. Furthermore, both the cardiac and vascular effects of beta-phenylethylamine were abolished by desipramine. These results indicate that beta-phenylethylamine exerts both positive inotropic and vasoconstrictory effects, probably by releasing endogenous norepinephrine from the adrenergic nerve endings.

Effects of oxygen on regional hemodynamics in hemorrhagic shock

1996 ◽  
Vol 271 (1) ◽  
pp. H203-H211 ◽  
Author(s):  
H. Bitterman ◽  
V. Brod ◽  
G. Weisz ◽  
D. Kushnir ◽  
N. Bitterman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Biceps Femoris ◽  
Total Blood ◽  
Biceps Femoris Muscle ◽  
Arterial Blood ◽  
Femoris Muscle

This study investigated mechanisms of the hemodynamic effects of oxygen in hemorrhagic shock induced by bleeding 30% of the total blood volume in anesthetized rats. An ultrasonic flowmeter was used to monitor regional blood flow. Changes in tissue perfusion were assessed by the laser-Doppler technique. The inhalation of 100% oxygen induced a significant increase in mean arterial blood pressure (MABP) and vascular resistance in the hindquarters, with a concomitant decrease in blood flow in the distal aorta and biceps femoris muscle. In contrast, oxygen did not change vascular resistance in the superior mesenteric artery (SMA) and renal beds and induced a significant increase in blood flow to the renal artery, SMA, and small bowel in hemorrhaged rats. L-Arginine (100 mg/kg iv) but not D-arginine or the vehicle (0.9% NaCl) completely abolished the effects of oxygen on blood pressure and reversed its effects on blood flow and resistance in the hindquarters and biceps femoris muscle. Administration of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (50 mg/kg iv) significantly increased MABP and the resistance in the three vascular beds. Pretreatment of hemorrhaged rats with a superoxide dismutase mimic, the NO-stable radical 2,2,6,6-tetramethylpiperidine-N-oxyl (5 mg/kg iv), resulted in significantly diminished effects of oxygen on hindquarter hemodynamics. These results demonstrate a differential effect of oxygen, which increases vascular resistance in the hindquarters without a significant effect in the splanchnic and renal beds, thus favoring an increase in splanchnic and renal perfusion. It is suggested that inactivation of NO by reactive oxygen species may underlie the effects of oxygen on hindquarter vascular tone during shock.

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
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Index ◽  
Structural Changes ◽  
Vascular Involvement ◽  
Control Group ◽  
Study Group ◽  
Blood Pressure Elevation ◽  
Pressure Elevation ◽  
Arterial Blood

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.

scholarly journals Effects of prolonged reduction in blood flow on submandibular secretory function in anesthetized sheep

2003 ◽  
Vol 95 (2) ◽  
pp. 751-757 ◽  
Author(s):  
A. S. Thakor ◽  
C. N. Brown ◽  
A. V. Edwards
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Salivary Flow ◽  
Secretory Function ◽  
Frequency Dependent ◽  
Aortic Blood ◽  
Aortic Blood Pressure ◽  
Protein Output ◽  
Stimulation Of

Submandibular vascular and secretory responses to parasympathetic chorda-lingual (C-L) stimulation were investigated in anesthetized sheep before, during, and after an intracarotid (ic) infusion of endothelin-1 (ET-1). Stimulation of the peripheral end of the C-L nerve at 4 and 8 Hz produced a frequency-dependent reduction in submandibular vascular resistance (SVR) associated with a frequency-dependent increase in submandibular blood flow, salivary flow, and Na+, K+, and protein output from the gland. During stimulation at 4 Hz, ic ET-1 significantly increased SVR ( P < 0.01), without significantly affecting either the aortic blood pressure or heart rate. Submandibular blood flow (SBF) was reduced by 48 ± 4% and the flow of saliva by 50 ± 1%. The effect on blood and salivary flow persisted for at least 30 min after the infusion of ET-1. The reduction in SBF was associated with a diminution in the output of Na+,K+, and protein in the saliva ( P < 0.01). These effects persisted for 30 min after the infusion of ET-1 had been discontinued and were linearly related to the flow of plasma throughout.

Effect of increased preload on the synthesized aortic blood pressure waveform

2010 ◽  
Vol 109 (2) ◽  
pp. 484-490 ◽  
Author(s):  
Kevin S. Heffernan ◽  
James E. Sharman ◽  
Eun Sun Yoon ◽  
Eui Jin Kim ◽  
Su Jin Jung ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Augmentation Index ◽  
Arterial Compliance ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Aortic Blood Flow ◽  
Aortic Blood ◽  
Reservoir Function ◽  
Aortic Blood Pressure ◽  
Aortic Reservoir Function

In the present study, we examined the influence of preload augmentation via passive leg elevation (PLE) on synthesized aortic blood pressure, aortic augmentation index (AIx), and aortic capacitance (a reflection of aortic reservoir function). Central and peripheral hemodynamics were measured via tonometry with a generalized transfer function in 14 young, healthy men (age = 24 yr). Aortic blood flow was calculated from the left ventricular outflow tract (LVOT) velocity-time integral (VTI) using standard two-dimensional echocardiographic-Doppler techniques. Measures were made in the supine position at rest (Pre), during PLE, and during recovery (Post). There was a significant increase in LVOT-VTI, synthesized aortic systolic blood pressure (BP) and AIx from Pre to PLE, with values returning to baseline Post ( P < 0.05). There was a reduction in aortic capacitance from Pre to PLE, with values returning to baseline Post ( P < 0.05). There was no change in heart rate, systemic arterial compliance, aortic elastance, aortic wave travel timing, or vascular resistance ( P > 0.05). Change in AIx from Pre to PLE was associated with change in LVOT-VTI ( r = 0.66, P < 0.05) and inversely associated with change in aortic capacitance ( r = −0.73, P < 0.05). These data suggest that in a setting of isolated augmented preload with minimal changes in other potential confounders, the morphology of the synthesized aortic BP waveform and AIx may be related to changes in aortic reservoir function.

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