Effects of hyperinsulinaemia on the cardiovascular responses to graded hypovolaemia in normal and diabetic subjects

1988 ◽  
Vol 75 (1) ◽  
pp. 85-92 ◽  
Author(s):  
A. R. Scott ◽  
T. Bennett ◽  
I. A. MacDonald
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Normal Male ◽  
Euglycaemic Clamp ◽  
Arterial Blood ◽  
Hyperinsulinaemic Euglycaemic Clamp

1. Two experiments were carried out. The first with five normal male subjects was placebo controlled and single blind, each subject being studied on two occasions. Lower body subatmospheric pressure (LBSP) was used to assess the cardiovascular effects of graded hypovolaemia before and during either a hyperinsulinaemic, euglycaemic clamp or a placebo clamp using 0.9% (w/v) NaCl only. 2. During hyperinsulinaemia, resting systolic blood pressure rose and was accompanied by forearm vasodilatation. Forearm blood flow (FABF) and heart rate (HR) were higher at each level of LBSP during than before hyperinsulinaemia. In addition, hyperinsulinaemia was accompanied by a small increase in noradrenaline, but packed cell volume did not change. 3. In the second experiment, the effects of a hyperinsulinaemic euglycaemic clamp on the cardiovascular responses to LBSP were assessed in seven diabetic subjects with peripheral and autonomic neuropathy. 4. In contrast to the normal subjects, there was a slight fall in systolic blood pressure during the clamp but no effect was noted on HR or FABF. Mean arterial blood pressure was lower at each level of LBSP during hyperinsulinaemia compared with the pre-elamp period. Packed cell volume fell during the clamp and plasma noradrenaline rose. In one of the diabetic subjects, a precipitous fall in blood pressure occurred during hyperinsulinaemia when LBSP of 10 mmHg (1.3 kPa) was applied, this manoeuvre having been well tolerated before the clamp. 5. The mode of action of hyperinsulinaemia is not clear, but there was, however, no evidence that a fall in plasma volume had occurred.

scholarly journals The effects of underfeeding for 7 d on the thermogenic and physiological response to glucose and insulin infusion (hyperinsulinaemic euglycaemic clamp)

1990 ◽  
Vol 64 (2) ◽  
pp. 427-437 ◽  
Author(s):  
I. W. Gallen ◽  
I. A. Macdonald
Keyword(s):  
Blood Pressure ◽  
Metabolic Rate ◽  
Glucose Uptake ◽  
Glucose Oxidation ◽  
Insulin Infusion ◽  
Cardiovascular Responses ◽  
Glucose Disposal ◽  
Euglycaemic Clamp ◽  
Healthy Women ◽  
Hyperinsulinaemic Euglycaemic Clamp

The effect of underfeeding for 7 d (at 60 kJ/kg ideal body-weight) on the thermic and physiological responses to glucose and insulin infusions (hyperinsulinaemic euglycaemic clamp) was studied in six healthy women. Underfeeding had no significant effect on baseline metabolic rate, heart rate, forearm blood flow, diastolic blood pressure, blood intermediary metabolites, plasma insulin or catecholamines, but reduced both respiratory exchange ratio (RER; control (C) 0.86 (SE 0.02), underfed (U) 0.75 (SE 0.01)P< 0.01) and systolic blood pressure (by approximately 10 mmHg,P< 0.01). Baseline forearm glucose uptake and oxygen consumption were similar in both states. During the final 30 min of the glucose and insulin infusion, metabolic rate rose by 0.43 (SE 0.05) kJ/min in the C state, but no rise was seen in the U state (P< 0.01). Glucose disposal rate (C 47.9 (SE 1.8), U 47.3 (SE 4.1) μmol/kg per min) and storage rate (C 27.5 (SE 2.4), U 31.6 (SE 3.6) μmol/kg per min) were similar in both states, but glucose oxidation rate was reduced in the U state (C 20.5 (SE 1.7), U 15.4 (SE 0.7) μmol/kg per min;P< 0.05). RER rose to a higher value in the C state than in the U state (C 0.97 (SE 0.2), U 0.80 (SE 0.01);P< 0.01). During hyperinsulinaemia, the forearm glucose uptake and O2consumption rose in both states. No significant differences were seen in the cardiovascular responses to hyperinsulinaemia in either state. Thus underfeeding abolishes the rise in thermogenesis and reduces glucose oxidation during glucose and insulin infusions in healthy women, but does not affect the glucose disposal or storage rates or the other measured responses.

Circulating Dopamine: Its Effect on the Plasma Concentrations of Catecholamines, Renin, Angiotensin, Aldosterone and Vasopressin in the Conscious Dog

1981 ◽  
Vol 61 (4) ◽  
pp. 417-422 ◽  
Author(s):  
S. G. Ball ◽  
M. Tree ◽  
J. J. Morton ◽  
G. C. Inglis ◽  
R. Fraser
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Control Period ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Dopamine Infusion ◽  
Renin Angiotensin ◽  
Arterial Blood

1. Six male beagle dogs with carotid loops were infused with sodium chloride solution (150 mmol/l: saline) during control observations followed by dopamine infusion at various rates. Arterial blood samples were drawn during the control period and at the end of each period of dopamine infusion for the measurement of plasma dopamine, noradrenaline, adrenaline, renin, angiotensin II, aldosterone, vasopressin, electrolytes and packed cell volume. Blood pressure and pulse were recorded throughout. 2. The rate of infusion and plasma dopamine levels were closely correlated (r = 0.99, P < 0.001). Plasma dopamine levels two to 20 times basal values produced no significant change in any of the other variables measured; levels 200 times basal values caused a significant increase (P < 0.05) in plasma renin concentration; levels 2000 times basal values were associated with significant increases (P < 0.05) in plasma renin and angiotensin II, packed cell volume and blood pressure, without significant changes in other measurements. 3. Circulating dopamine is unlikely to be important in the control of sodium and water metabolism.

Differential Blood Pressure and Hormonal Effects after Glucose and Xylose Ingestion in Chronic Autonomic Failure

1989 ◽  
Vol 77 (1) ◽  
pp. 85-92 ◽  
Author(s):  
C. J. Mathias ◽  
D. F. da Costa ◽  
C. M. McIntosh ◽  
P. Fosbraey ◽  
R. Bannister ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Area Under Curve ◽  
Autonomic Failure ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Oral Glucose ◽  
Postprandial Hypotension ◽  
Hormonal Effects

1. To investigate whether carbohydrate contributes to postprandial hypotension in autonomic failure, the cardiovascular, biochemical and hormonal effects of oral glucose and an iso-osmotic solution of oral xylose were studied on separate occasions in six patients with chronic autonomic failure. The effects of oral glucose were also studied in eight normal subjects. 2. In the patients oral glucose lowered blood pressure substantially (−34 ± 7% at 60 min, area under curve −24.9 ± 3.5%, P < 0.001) and for a prolonged period (− 25 ± 4% at 120 min). Plasma noradrenaline levels did not change. In the normal subjects blood pressure was unchanged and plasma noradrenaline rose, suggesting a compensatory increase in sympathetic nervous activity. 3. In the patients xylose caused a smaller and more transient fall in blood pressure (−15 ± 6% at 90 min, area under curve −8.9 ± 4%, P < 0.05) with a non-significant elevation in packed cell volume (36.7 ± 1.8 to 38.2 ± 1.8). It was therefore unclear if xylose was exerting osmotic effects within the bowel which contributed to the small blood pressure fall. Packed cell volume did not change in either the patients or normal subjects after glucose. 4. In the patients and normal subjects plasma insulin rose after glucose. Insulin levels were unchanged after xylose. Levels of pancreatic polypeptide and neurotensin, a potential vasodilator, rose in the patients only. The latter rose to a similar extent after both glucose and xylose, making it unlikely that neurotensin alone accounted for the hypotension. 5. These studies indicate that the carbohydrate components of a meal, and in particular those causing insulin release, contribute to postprandial hypotension in patients with autonomic failure.

Cardiovascular responses to ice-cold showers

1964 ◽  
Vol 19 (6) ◽  
pp. 1145-1150 ◽  
Author(s):  
William R. Keatinge ◽  
Malcolm B. McIlroy ◽  
Alan Goldfien
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cold Water ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Sympathetic Nervous

A shower of ice-cold water (0@#X2013;2.5 C) over the chest caused large increases in systolic and diastolic arterial pressures, pulse pressure, and pulse rate in normal subjects. Cardiac output rose by 59 and 100% in the two subjects in whom it was measured. The changes in pressure were considerably larger than those caused by a cold pressor test or by anxiety. The changes appear to be due to sympathetic nervous reflexes to the heart and blood vessels rather than release of adrenal catecholamines, as plasma epinephrine did not increase and plasma norepinephrine rose only by 0.32 @#X00B5;g/liter. Hyperventilation and evidence of peripheral venoconstriction occurred during the showers, but neither voluntary hyperventilation nor increased venous return from a change in posture produced the changes in blood pressure seen during shower arterial blood pressure; cardiac output; catecholamines; sympathetic nervous reflexes; hyperventilation; peripheral venoconstriction Submitted on March 10, 1964

Haemodynamic and Cerebrovascular Responses to Glycerol Infusion in Dogs

1989 ◽  
Vol 77 (5) ◽  
pp. 535-539 ◽  
Author(s):  
Jiann-Liang Chen ◽  
Yeou-Chih Wang ◽  
Jia-Yi Wang
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Cell Volume ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Packed Cell Volume ◽  
Vessel Diameter ◽  
Serum Osmolarity ◽  
Arterial Blood ◽  
Pial Vessel

1. The response of cerebral blood vessels to hyperosmolar agents in vivo remains controversial, and little is known about the effect of glycerol on cerebral vessels. In this study we investigated the cerebrovascular response to intravenous administration of glycerol (1 g/kg, infused over 25 min) in dogs under pentobarbital anaesthesia. 2. Intracranial pressure, systemic arterial pressure, mean arterial blood pressure, serum osmolarity and packed cell volume were continuously monitored, and blood gases were checked frequently. Through a parietal cranial window, pial vessel diameter was measured by means of a surgical microscope and a video image-analyser. 3. Pial vessel diameter increased gradually with a maximum at 30 min after the beginning of glycerol infusion. The maximum increase in diameter in small (< 100 μm) vessels was 14.3%, whereas that in large (> 100 μm) vessels was 10.3%. There was only a slight increase (< 4%) in pial vessel diameter in vehicle-infused animals. The intracranial pressure decreased drastically after glycerol infusion, whereas the mean arterial blood pressure remained constant. There were correlations between the rise in serum osmolarity, fall in packed cell volume and vasodilatation, indicating that glycerol caused vasodilatation accompanied by plasma volume expansion. 4. Our data suggest that glycerol produces cerebral vasodilatation, which might be beneficial in cerebral ischaemia and vasospasm, in addition to its intracranial pressure-reducing effect on normal or oedematous brain. The degree of vasodilatation was not sufficient to affect the predominant intracranial pressure drop resulting from cerebral dehydration.

scholarly journals A METHOD TO DETERMINE THE PERIPHERAL ARTERIAL BLOOD PRESSURE IN THE MOUSE

1941 ◽  
Vol 74 (1) ◽  
pp. 29-40 ◽  
Author(s):  
Philip D. McMaster
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
Close Agreement ◽  
Carotid Arteries ◽  
Systolic Pressure ◽  
Arterial Blood ◽  
Relative Transparency ◽  
Direct Measurements ◽  
Peripheral Arterial

Advantage has been taken of the relative transparency of the claw of the mouse to devise a method, here described, to measure the blood pressure in the animal's leg. Direct measurements of the systolic blood pressure from the carotid arteries of anesthetized mice have also been made. Simultaneous blood pressure readings by both these methods applied to the same animal showed close agreement. The systolic pressure ranged from 60 to 126 mm. Hg, according to the conditions.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

The relationship of blood flow velocity fluctuations to intracranial pressure B waves

1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Wave Amplitude ◽  
Transcranial Doppler Ultrasound ◽  
Normal Subjects ◽  
Content Type ◽  
Arterial Blood ◽  
Flow Fluctuations

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.

Abstract 12689: Cardiovascular Responses to Energy Drinks in a Healthy Population: The C-energy Study

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Teri M Kozik ◽  
Mouchumi Bhattacharyya ◽  
Teresa T Nguyen ◽  
Therese F Connolly ◽  
Walther Chien ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Vital Signs ◽  
Cardiovascular Responses ◽  
Energy Drinks ◽  
Energy Drink ◽  
Emergency Department Visits ◽  
Qtc Interval ◽  
Cardiac Responses ◽  
Energy Drink Consumption

Introduction: Energy drinks are presumed to enhance energy, physical endurance, mood, and boost metabolism. Serious health risks have been reported with energy drink consumption such as myocardial infarction, cardiac arrest, stroke, seizures, and arrhythmias. More than 20,000 emergency department visits related to energy drink consumption were reported in 2011. Little is known about the possible pathophysiological mechanisms and adverse events associated with energy drinks. Unlike the tobacco and alcohol industry, there are limited restrictions regulating the purchasing and marketing of these drinks. Purpose: To determine if consumption of energy drinks alter; vital signs (blood pressure, temperature), electrolytes (magnesium, potassium, calcium), activated bleeding time (ACT), or cardiac responses measured with a 12-lead electrocardiographic (ECG) Holter. Method: Subjects consumed two-16 ounce cans of an energy drink within one hour and remained in the lab where data was collected at base line (BL) and then during four hours post consumption (PC). Vital signs were taken every 30 minutes; blood samples were collected at BL, one, two and four hours PC and ECG data was collected throughout the entire study period. Paired students t-test and a corresponding non-parametric test (Wilcoxon signed rank) were used for analysis of the data. Results: Fourteen healthy young subjects were recruited (mean age 28.6 years). Systolic blood pressure (BL=132, ±7.83; PC= 151, ±11.21; p=.001); QTc interval (BL=423, ±22.74; PC=503, ±24.56; p<.001); magnesium level (BL 2.04, ± 0.09; PC=2.13, ±0.15; p=.05); and calcium level (BL=9.31, ±.28; PC=9.52, ±.22; p=.018) significantly increased from BL. While potassium and ACT fluctuated (increase and decrease) no significant changes were observed. Eight of the fourteen subjects (57%) developed a QTc >500 milliseconds PC. Conclusions: In our sample, consumption of energy drinks increased systolic blood pressure, serum magnesium and calcium, and resulted in repolarization abnormalities. Because these physiological responses can lead to arrhythmias and other abnormal cardiac responses, further study in a larger sample is needed to determine the effects and possible consequences of energy drink consumption.

scholarly journals Acute, local infusion of angiotensin II impairs microvascular and metabolic insulin sensitivity in skeletal muscle

2018 ◽  
Vol 115 (3) ◽  
pp. 590-601 ◽  
Author(s):  
Dino Premilovac ◽  
Emily Attrill ◽  
Stephen Rattigan ◽  
Stephen M Richards ◽  
Jeonga Kim ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Microvascular Blood Flow ◽  
Euglycaemic Clamp ◽  
Hyperinsulinaemic Euglycaemic Clamp ◽  
Skeletal Muscle Glucose Uptake

Abstract Aims Angiotensin II (AngII) is a potent vasoconstrictor implicated in both hypertension and insulin resistance. Insulin dilates the vasculature in skeletal muscle to increase microvascular blood flow and enhance glucose disposal. In the present study, we investigated whether acute AngII infusion interferes with insulin’s microvascular and metabolic actions in skeletal muscle. Methods and results Adult, male Sprague-Dawley rats received a systemic infusion of either saline, AngII, insulin (hyperinsulinaemic euglycaemic clamp), or insulin (hyperinsulinaemic euglycaemic clamp) plus AngII. A final, separate group of rats received an acute local infusion of AngII into a single hindleg during systemic insulin (hyperinsulinaemic euglycaemic clamp) infusion. In all animals’ systemic metabolic effects, central haemodynamics, femoral artery blood flow, microvascular blood flow, and skeletal muscle glucose uptake (isotopic glucose) were monitored. Systemic AngII infusion increased blood pressure, decreased heart rate, and markedly increased circulating glucose and insulin concentrations. Systemic infusion of AngII during hyperinsulinaemic euglycaemic clamp inhibited insulin-mediated suppression of hepatic glucose output and insulin-stimulated microvascular blood flow in skeletal muscle but did not alter insulin’s effects on the femoral artery or muscle glucose uptake. Local AngII infusion did not alter blood pressure, heart rate, or circulating glucose and insulin. However, local AngII inhibited insulin-stimulated microvascular blood flow, and this was accompanied by reduced skeletal muscle glucose uptake. Conclusions Acute infusion of AngII significantly alters basal haemodynamic and metabolic homeostasis in rats. Both local and systemic AngII infusion attenuated insulin’s microvascular actions in skeletal muscle, but only local AngII infusion led to reduced insulin-stimulated muscle glucose uptake. While increased local, tissue production of AngII may be a factor that couples microvascular insulin resistance and hypertension, additional studies are needed to determine the molecular mechanisms responsible for these vascular defects.

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