Effect of insulin on regional vascular resistances in conscious rats

1996 ◽  
Vol 270 (2) ◽  
pp. R450-R455
Author(s):  
E. Qadir ◽  
J. P. Porter
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Low Dose ◽  
Chronic Administration ◽  
High Dose ◽  
Ganglionic Blockade ◽  
Conscious Rats ◽  
Before And After ◽  
Vascular Beds ◽  
Renal Vascular

In the rat, but not in humans and other mammals, chronic administration of insulin produces hypertension. The present aim was to determine the effect of acute insulin infusion on regional vascular resistances and to determine the neurogenic contribution to the response. Conscious rats were infused with insulin (2 or 6 mU/min) before and after ganglionic blockade with chlorisondamine (5 mg/kg). The low dose of insulin produced an increase in arterial pressure and hindquarter vascular resistance; the high dose produced a gradual decrease in arterial pressure and renal resistance. After ganglionic blockade, the hindquarter vasoconstriction produced by the low dose was abolished. The high dose of insulin produced both hindquarter and renal vasodilation. Thus the low dose of insulin had a selective neurogenic vasoconstrictor effect in rat skeletal muscle vascular beds. With higher doses, direct vasodilatory effects in both skeletal muscle and renal vascular beds appeared. This greater sensitivity of the sympathoexcitatory effects of insulin in rats may explain the ability of chronic insulin infusions to increase blood pressure in this species.

Regional hemodynamics during postexercise hypotension. I. Splanchnic and renal circulations

2004 ◽  
Vol 97 (6) ◽  
pp. 2065-2070 ◽  
Author(s):  
Mollie P. Pricher ◽  
Lacy A. Holowatz ◽  
Jay T. Williams ◽  
Jennifer M. Lockwood ◽  
John R. Halliwill
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Peak Oxygen Uptake ◽  
Renal Vasculature ◽  
Vascular Conductance ◽  
Regional Hemodynamics ◽  
Postexercise Hypotension ◽  
Vascular Beds ◽  
Renal Vascular

Moderate exercise elicits a relative postexercise hypotension that is caused by an increase in systemic vascular conductance. Previous studies have shown that skeletal muscle vascular conductance is increased postexercise. It is unclear whether these hemodynamic changes are limited to skeletal muscle vascular beds. The aim of this study was to determine whether the splanchnic and/or renal vascular beds also contribute to the rise in systemic vascular conductance during postexercise hypotension. A companion study aims to determine whether the cutaneous vascular bed is involved in postexercise hypotension (Wilkins BW, Minson CT, and Halliwill JR. J Appl Physiol 97: 2071–2076, 2004). Heart rate, arterial pressure, cardiac output, leg blood flow, splanchnic blood flow, and renal blood flow were measured in 13 men and 3 women before and through 120 min after a 60-min bout of exercise at 60% of peak oxygen uptake. Vascular conductances of leg, splanchnic, and renal vascular beds were calculated. One hour postexercise, mean arterial pressure was reduced (79.1 ± 1.7 vs. 83.4 ± 1.8 mmHg; P < 0.05), systemic vascular conductance was increased by ∼10%, leg vascular conductance was increased by ∼65%, whereas splanchnic (16.0 ± 1.8 vs. 18.5 ± 2.4 ml·min−1·mmHg−1; P = 0.13) and renal (20.4 ± 3.3 vs. 17.6 ± 2.6 ml·min−1·mmHg−1; P = 0.14) vascular conductances were unchanged compared with preexercise. This suggests there is neither vasoconstriction nor vasodilation in the splanchnic and renal vasculature during postexercise hypotension. Thus the splanchnic and renal vascular beds neither directly contribute to nor attenuate postexercise hypotension.

Benefit/Risk Profile of Combined Antiplatelet Therapy with Ticlopidine and Aspirin

1991 ◽  
Vol 65 (05) ◽  
pp. 504-510 ◽  
Author(s):  
Raffaele De Caterina ◽  
Rosa Sicari ◽  
Walter Bernini ◽  
Guido Lazzerini ◽  
Giuliana Buti Strata ◽  
...  
Keyword(s):  
Platelet Function ◽  
Low Dose ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Stable Coronary Artery Disease ◽  
High Dose ◽  
Single Drug ◽  
Before And After ◽  
Serum Thromboxane ◽  
Artery Disease

SummaryTiclopidine (T) and aspirin (ASA) are two antiplatelet drugs both capable of prolonging bleeding time (BT), with a different mechanism of action. A synergism in BT prolongation has been reported and is currently considered an argument for not recommending their combination. However, a profound suppression of platelet function might be a desirable counterpart of a marked prolongation of BT, with a possible use in selected clinical situations. We therefore studied ex vivo platelet function (aggregation by ADP 0.5-1-2.5 μM; adrenaline 0.75-2.5 μM; collagen 1.5-150 μg/ml; arachidonic acid 1 mM; PAF 1 μM; adrenaline 0.17 μM + ADP 0.62 μM; serum thromboxane ([TX]B2 generation) and BT (Mielke) in 6 patients with stable coronary artery disease receiving such combination. Patients underwent sequential laboratory evaluations at baseline, after 7 days of T 250 mg b.i.d., before and after the intravenous administration of ASA 500 mg, respectively, and, finally, after a minimum of 7 days of sole ASA oral administration (50 mg/day). The experimental design, therefore, allowed a comparison of T and ASA effects (2nd and 4th evaluation), and an assessment of the combination effect (3rd evaluation). Platelet aggregation in response to all doses of ADP was depressed more by T than by ASA. Conversely, responses to adrenaline, and arachidonate were affected more by ASA than by T. For all other agents, differences were not significant. T + ASA combination was more effective (p <0.05) than either treatment alone in depressing responses to high-dose collagen (% over control, mean ± SEM: T: 95 ± 3; ASA: 96 ± 5; T + ASA: 89 ± 4). Serum TXB2 (basal, ng/ml: 380 ± 54) did not change with T (372 ± 36), dropped to <1 ng/ml on ASA injection and slightly re-increased to 9.1 ± 3.1 ng/ml on oral low-dose ASA. BT (basal 7.4 ± 0.6 min) was affected similarly by T (9.2 ± 0.8) or ASA (9.7 ± 0.9) alone, but increased to 15.0 ± 0.7 min on combination treatment (106% increase over control). Thus, the strong synergism in BT prolongation by ASA-T combination has a counterpart in the inhibition of platelet function in response to strong stimuli such as high-dose collagen, not otherwise affected significantly by single-drug treatment. This effect is a possible rationale for the clinical evaluation of T + ASA combination.

A New Hafnium-Beryllium System Prioduced by Ion Implantation and Annealing Techniques

1983 ◽  
Vol 27 ◽  
Author(s):  
J.C. Soares ◽  
A.A. Melo ◽  
M.F. DA Silva ◽  
E.J. Alves ◽  
K. Freitag ◽  
...  
Keyword(s):  
Ion Implantation ◽  
Single Crystals ◽  
Room Temperature ◽  
Low Dose ◽  
Correlation Method ◽  
High Dose ◽  
Tetrahedral Sites ◽  
Time Differential ◽  
Before And After ◽  
Beryllium Foil

ABSTRACTLow and high dose hafnium imolanted beryllium samoles have been prepared at room temperature by ion implantation of beryllium commercial foils and single crystals. These samples have been studied before and after annealing with the time differential perturbed angular correlation method (TDPAC) and with Rutherford backscattering and channeling techniques. A new metastable system has been discovered in TDPAC-measurements in a low dose hafnium implanted beryllium foil annealed at 500°C. Channeling measurements show that the hafnium atoms after annealing, are in the regular tetrahedral sites but dislocated from the previous position occupied after implantation. The formation of this system is connected with the redistribution of oxygen in a thin layer under the surface. This effect does not take place precisely at the same temperature in foils and in single crystals.

Effects of Ambulation and Nondependent Transfers on Vital Signs in Patients Receiving Norepinephrine

2017 ◽  
Vol 26 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Rosario Arcaya Nievera ◽  
Ann Fick ◽  
Hilary K. Harris
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Physical Therapy ◽  
Arterial Pressure ◽  
Low Dose ◽  
Vital Signs ◽  
Activity Level ◽  
Significant Difference ◽  
Before And After ◽  
Norepinephrine Dose

Purpose To assess the safety of mobilizing patients receiving low-dose norepinephrine (0.05 μg/kg per min) by examining mean arterial pressure and heart rate before and after activity with parameters set by the physician. Background Norepinephrine is a peripheral vasoconstrictor administered for acute hypotension. During activity, blood flows to the periphery to supply muscles with oxygen, which may oppose the norepinephrine vasoconstriction. The safety of mobilizing patients receiving norepinephrine is unclear. Methods Heart rate, mean arterial pressure, norepinephrine dose, and activity performed were extracted retrospectively from charts of 47 cardiothoracic surgery patients during the first patient transfer to chair or ambulation with norepinephrine infusing. Mean arterial pressure and heart rate were compared before and after physical therapy (paired t tests). Differences among norepinephrine doses and physical activity levels were evaluated (Kruskal-Wallis test). Results Forty-one of the 47 patients (87%) tolerated the activity within safe ranges of vital signs. The change in patients’ mean arterial pressure from before to after activity was not significant (P = .16), but a significant increase in heart rate occurred after activity (P &lt; .001). A Kruskal-Wallis test showed no significant difference in the norepinephrine dose and activity level (χ2 = 6.34, P = .17). No instances of cardiopulmonary or respiratory arrest occurred during any physical therapy sessions. Conclusions Infusion of low-dose norepinephrine should not be considered an automatic reason to keep patients on bed rest.

Spontaneous pressure-flow patterns in the kidney of conscious rats

1993 ◽  
Vol 265 (6) ◽  
pp. H2151-H2159 ◽  
Author(s):  
S. Skarlatos ◽  
P. J. Metting ◽  
S. L. Britton
Keyword(s):  
Arterial Pressure ◽  
Cardiac Cycle ◽  
Flow Patterns ◽  
Renal Circulation ◽  
Physiological Mechanisms ◽  
Pressure Flow ◽  
Ganglionic Blockade ◽  
Conscious Rats ◽  
Mechanical Intervention ◽  
Arterial Pressure Regulation

We have developed a model that permits a quantitative analysis of the contribution of different mechanisms to the spontaneously occurring pressure-flow patterns of a vasculature. In this study we evaluated the spontaneous relationship between arterial pressure (P) and renal blood flow (F) in resting conscious rats during control conditions, autonomic ganglionic blockade (hexamethonium), and nonselective alpha-adrenoreceptor blockade (phentolamine). In a total of 250 trials in 29 rats, we measured the average P and F for each cardiac cycle over 13-min periods (approximately 4,000 cardiac cycles/trial). The P and F values for each cardiac cycle were expressed as percentage change from each 13-min average (beat-to-beat changes). The slope and angle of each consecutive beat-to-beat P-F change were calculated and collated into one of eight zones representing the physiological mechanisms responsible for the concurrent spontaneous changes in P and F. Our results reveal that, in the absence of any chemical or mechanical intervention (control), the renal circulation demonstrated a baroreflex-like P-F pattern approximately 38% of the time. An autoregulatory-like P-F pattern occurred, at the most, 35% of the time. Autonomic ganglionic blockade significantly (P < 0.05) decreased the baroreflex-like pattern and increased the presence of P-F patterns indicative of autoregulation. alpha-Adrenoreceptor blockade resulted in a P-F pattern that was qualitatively similar to that produced by hexamethonium, but with considerably more variability. These results indicate that, in the resting conscious undisturbed state, the autonomic nervous system exerts a tonic influence on the renal circulation that facilitates arterial pressure regulation via a baroreflex-like pattern.

Hemodynamic effects of vasopressin compared with angiotensin II in conscious rats

1987 ◽  
Vol 252 (3) ◽  
pp. H628-H637 ◽  
Author(s):  
J. W. Osborn ◽  
M. M. Skelton ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Fold Increase ◽  
Adrenergic Blockade ◽  
Ganglionic Blockade ◽  
Conscious Rats ◽  
Potent Vasoconstrictor

The mechanisms whereby arginine vasopressin influences hemodynamic and autonomic function were investigated in conscious rats. In normal rats, 60-min intravenous infusions produced dose-related increases of arterial pressure and total peripheral resistance with marked decreases of both heart rate and cardiac output. Cholinergic blockade with methscopolamine attenuated the bradycardia at higher doses of vasopressin, whereby the fall of cardiac output was not affected. beta-Adrenergic blockade with atenolol attenuated the fall of heart rate seen with lower doses of vasopressin but did not prevent the fall of cardiac output. Ganglionic blockade with methscopolamine and hexamethonium resulted in nearly a 60-fold enhancement of vasopressin pressor sensitivity. This was related to a greater rise of peripheral resistance, since the fall of cardiac output was not altered compared with normal rats. Hemodynamic responses to angiotensin II were determined in other groups of conscious, normal rats and rats with ganglionic blockade. Peripheral resistance increased in the normal rats, whereas the related decreases in cardiac output and heart rate were only 30% of the responses seen with equipressor doses of vasopressin. Ganglionic blockade increased pressor activity only two- to eightfold compared with the 60-fold increase observed with vasopressin. We conclude that vasopressin is a more potent vasoconstrictor than angiotensin II, decreases cardiac output independent of neural mechanisms, and results in withdrawal of sympathetic vascular tone to buffer rises of arterial pressure.

scholarly journals Lycopene supplementation attenuated xanthine oxidase and myeloperoxidase activities in skeletal muscle tissues of rats after exhaustive exercise

2005 ◽  
Vol 94 (4) ◽  
pp. 595-601 ◽  
Author(s):  
Chieh-Chung Liu ◽  
Chi-Chang Huang ◽  
Wan-Teng Lin ◽  
Chin-Cheng Hsieh ◽  
Shih-Yi Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Xanthine Oxidase ◽  
Low Dose ◽  
Exhaustive Exercise ◽  
Strenuous Exercise ◽  
High Dose ◽  
Sedentary Control ◽  
Muscle Tissues ◽  
Significant Difference

Strenuous exercise is known to induce oxidative stress leading to the generation of free radicals. The purpose of the present study was to investigate the effects of lycopene, an antioxidant nutrient, at a relatively low dose (2·6 mg/kg per d) and a relatively high dose (7·8 mg/kg per d) on the antioxidant status of blood and skeletal muscle tissues in rats after exhaustive exercise. Rats were divided into six groups: sedentary control (C); sedentary control with low-dose lycopene (CLL); sedentary control with high-dose lycopene (CHL); exhaustive exercise (E); exhaustive exercise with low-dose lycopene (ELL); exhaustive exercise with high-dose lycopene (EHL). After 30 d, the rats in the three C groups were killed without exercise, but the rats in the three E groups were killed immediately after an exhaustive running test on a motorised treadmill. The results showed that xanthine oxidase (XO) activities of plasma and muscle, and muscular myeloperoxidase (MPO) activity in group E were significantly increased compared with group C. Compared with group E, the elevations of XO and MPO activities of muscle were significantly decreased in group EHL. The malondialdehyde concentrations of plasma and tissues in group E were significantly increased by 72 and 114 %, respectively, compared with those in group C. However, this phenomenon was prevented in rats of the ELL and EHL groups. There was no significant difference in the GSH concentrations of erythrocytes in each group; however, exhaustive exercise resulted in a significant decrease in the GSH content of muscle. In conclusion, these results suggested that lycopene protected muscle tissue from oxidative stress after exhaustive exercise.

Effect of short-term administration of vasopressin on arterial pressure and norepinephrine turnover in Long–Evans rats

1987 ◽  
Vol 65 (10) ◽  
pp. 2142-2146 ◽  
Author(s):  
R. L. Kline ◽  
K.-Y. Chow ◽  
P. F. Mercer
Keyword(s):  
Arterial Pressure ◽  
Water Intake ◽  
Urine Output ◽  
Plasma Osmolality ◽  
Chronic Administration ◽  
Urine Osmolality ◽  
Cardiovascular Reflexes ◽  
High Dose ◽  
Normal Fluid ◽  
Long Evans

Vasopressin (AVP) in acute experiments has been shown to influence cardiovascular reflexes, but the effect of a more prolonged administration of AVP on the sympathetic nervous system has not been investigated. Long–Evans rats were treated for 7 days with AVP (Pitressin tannate in oil, with single daily doses of 100 or 500 mU∙100 g−1, s.c.) to determine whether AVP alters norepinephrine (NE) turnover in kidney, intestine, or skeletal muscle. Control rats were given equal doses of peanut oil daily. NE turnover was determined by measuring the decline in tissue levels of NE for 8 h after inhibition of tyrosine hydroxylase with α-methyl-p-tyrosine (300 mg∙kg−1, i.p. every 4 h). Measurements of water intake, urine output, and urine osmolality showed that chronic administration of the high dose, but not the low dose, of AVP produced maintained increases in urine osmolality and decreases in water intake and urine output. Body weight, plasma osmolality, plasma electrolytes, and hematocrit were not significantly altered by AVP treatment, but mean arterial pressure was elevated significantly (control, 105 ± 3 mmHg versus AVP, 119 ± 4 mmHg, p < 0.05) (1 mmHg = 133.3 Pa) in the high dose group. Plasma renin activity was decreased slightly, but significantly in rats treated with the high dose of AVP. Compared with results in control animals, there were no statistically significant changes in NE turnover after chronic administration of either the low or the high dose of AVP. The results indicate that administration of AVP for 7 days to rats in normal fluid balance does not result in a decrease in NE turnover in peripheral organs.

scholarly journals Increased thromboxane mediates the adverse renal effects of interleukin-2 in rats.

1994 ◽  
Vol 4 (9) ◽  
pp. 1701-1710
Author(s):  
D Rubinger ◽  
E Cohen ◽  
Y Haviv ◽  
J Bernheim ◽  
E Shiloni ◽  
...  
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Low Dose ◽  
Combined Therapy ◽  
Interleukin 2 ◽  
Chronic Administration ◽  
Urinary Sodium Excretion ◽  
Metabolic Effects ◽  
High Dose ◽  
Sodium And Potassium

The capillary leak syndrome with decreased GFR and renal water and sodium retention after recombinant interleukin-2 (IL-2) administration may arise from endothelial activation via an increase in prostaglandin synthesis. This study was undertaken to better define the role of the prostaglandin system in the renal and metabolic effects of IL-2 administration in rats. The chronic administration of IL-2 (100,000 U/kg, thrice daily, ip) resulted in a significant increase in body weight, a decrease in GFR and in the urinary excretion of sodium and potassium, and an increase in the urinary excretion of thromboxane (TXB2). After combined IL-2 and low-dose indomethacin (1.7 mg/kg per day po), a significant decrease in body weight with normalization of GFR, of the urinary excretion of Na, and of urinary TXB2 was noted in animals receiving combined therapy as compared with those receiving IL-2 alone. In contrast, high-dose indomethacin administration (33.3 mg/kg po for the last 3 days of the study) was associated with a further decrease in GFR, enhancement of the sodium and potassium retention, and suppression of prostaglandin E2 excretion. The administration of the thromboxane receptor antagonist SQ 29548 in IL-2-treated rats led to a reversal of the fall in GFR induced by the lymphokine without significant changes in urinary sodium excretion. These results support the hypothesis that thromboxane is an important mediator of the renal and systemic effects of IL-2. These effects are reversed at least partly by low-dose indomethacin, which selectively suppresses thromboxane A2 (TXA2) synthesis, or by TXA2 receptor antagonism.

Efficacy of Low-Dose versus High-Dose Continuous Cyclic Azithromycin Therapy for Preventing Acute Exacerbations of COPD

Respiration ◽  
2021 ◽  
pp. 1-8
Author(s):  
Xavier Pomares ◽  
Concepción Montón ◽  
Daniel Huertas ◽  
Alicia Marín ◽  
Ester Cuevas ◽  
...  
Keyword(s):  
Dose Group ◽  
Low Dose ◽  
Therapy Group ◽  
High Dose ◽  
University Hospitals ◽  
Copd Exacerbations ◽  
Before And After ◽  
Dosing Regimens ◽  
Maximal Medical Therapy ◽  
Severe Copd

<b><i>Background:</i></b> Long-term azithromycin therapy significantly reduces the frequency of COPD exacerbations (ECOPD). However, previous studies have used different dosing regimens, and the efficacy of these regimens has not been compared. <b><i>Objective:</i></b> Compare the efficacy of low-dose with high-dose continuous cyclic azithromycin (CC-A) in severe COPD. <b><i>Methods:</i></b> Patients with severe COPD and repeated exacerbations (ECOPD ≥4 or ≥3 with at least 1 hospital admission in the previous year) were prospectively recruited (January 2017 to December 2019) as a multicenter cohort (from 3 university hospitals in the Barcelona area) and treated with low-dose CC-A: 250 mg 3 times per week (250-CC-A group). This cohort was compared with a historical (January 2007 to December 2013) single-center cohort of severe COPD with frequent ECOPD treated with high-dose CC-A: 500 mg 3 times per week (500-CC-A group). To assess differences in ECOPD prevention according to the administration of low-dose or high-dose CC-A, moderate-to-severe ECOPD was evaluated during the 12-month period before and after starting CC-A therapy. <b><i>Results:</i></b> Fifty-eight patients with severe COPD were evaluated: 37 in the low-dose group and 21 in the high-dose group. The 250-CC-A therapy group achieved a mean reduction in moderate-to-severe ECOPD of 65.6% at 12 months after starting CC-A therapy (with a 61.5% reduction in hospitalizations), while the 500-CC-A group achieved a reduction of 60.5% (with a 44.8% reduction in hospitalizations). No significant differences between 250-CC-A and 500-CC-A dosages were observed in the mean annual reduction of moderate-to-severe ECOPD (<i>p</i> = 0.55) or hospitalizations (<i>p</i> = 0.07) with respect to the year prior to starting CC-A. <b><i>Conclusions:</i></b> Low-dose 250-CC-A therapy over a 1-year period is similar to high-dose 500-CC-A in reducing exacerbation frequency in severe COPD patients with frequent ECOPD despite maximal medical therapy.

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