Central and peripheral haemodynamic effects of hyperglycaemia, hyperinsulinaemia, hyperlipidaemia or a mixed meal

2003 ◽  
Vol 105 (6) ◽  
pp. 715-721 ◽  
Author(s):  
Andreas FUGMANN ◽  
Jonas MILLGÅRD ◽  
Mahziar SARABI ◽  
Christian BERNE ◽  
Lars LIND
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Venous Occlusion ◽  
Mixed Meal ◽  
Hyperglycaemic Clamp ◽  
Calf Blood Flow ◽  
Haemodynamic Changes

The aim of the present study was to evaluate the haemodynamic changes during hyperinsulinaemia, hyperglycaemia or hypertriglyceridaemia in relation to those following a mixed meal. Ten subjects were subjected to hypertriglyceridaemia (3.9 mmol/l) for 2 h by an infusion of Intralipid® and heparin. Nine subjects received a hyperglycaemic clamp (12.5 mmol/l) with octreotide and low-dose insulin infusion to maintain normoinsulinaemia (10 m-units/l). Ten subjects received saline for 2 h as a control and, thereafter, 2 h of normoglycaemic hyperinsulinaemic clamp (80 m-units/l). Finally, ten subjects were evaluated for 2 h following an ordinary mixed meal. Calf blood flow was measured by venous occlusion plethysmography and cardiac index by thoracic bioimpedance. Both the mixed meal and normoglycaemic hyperinsulinaemia lowered total peripheral resistance, and increased calf blood flow and cardiac index, whereas blood pressure decreased (P<0.05-0.001). Both hyperglycaemia and hypertriglyceridaemia increased calf blood flow, but blood pressure was unchanged. Total peripheral resistance was unchanged in hypertriglyceridaemia, whereas hyperglycaemia induced a significant increase. Normoglycaemic hyperinsulinaemia induced a haemodynamic pattern similar, but to a lesser extent, to the pattern seen following a mixed meal. Hyperinsulinaemia seems to be a major mediator of the haemodynamic response, but other factors are obviously also of great importance. Hypertriglyceridaemia and hyperglycaemia induced haemodynamic responses that are not similar to those seen following a mixed meal.

Central Haemodynamics and Plasma Prostaglandin E2 in Borderline and Sustained Essential Hypertensive Patients before and after Indomethacin

1981 ◽  
Vol 61 (s7) ◽  
pp. 323s-325s ◽  
Author(s):  
M. E. Safar ◽  
A. F. Hornych ◽  
J. A. Levenson ◽  
A. Ch. Simon ◽  
G. M. London ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Hypertensive Patients ◽  
Arterial Blood ◽  
Before And After ◽  
Haemodynamic Changes ◽  
Normotensive Subjects ◽  
Pg E2

1. In basal conditions, plasma arterial prostaglandin (PG) E2 was significantly increased in borderline hypertensive patients (BH) (28.5 ± 6.7 pg/ml) in comparison with sustained essential hypertensive patients (EH) (11.6 ± 3.2 pg/ml) and in comparison with control normotensive subjects (NTS) (5.8 ± 1.4 pg/ml). 2. Plasma arterial PGE2 was positively significantly correlated with cardiac index and negatively significantly correlated with total peripheral resistance in basal conditions. 3. Indomethacin induced more pronounced haemodynamic changes in borderline than in sustained hypertensive patients, with a significant increase in arterial blood pressure and total peripheral resistance and a significant decrease in stroke volume and cardiac index. 4. Indomethacin significantly decreased arterial PGE2 in borderline hypertensive patients. The decrease was less important in sustained hypertensive patients. 5. In the overall population, a significant positive correlation between arterial PGE2 concentration and cardiac index was observed before and after indomethacin treatment. 6. The study suggests an important role of PGE2 in the regulation of cardiac output (positive inotropic effect) and blood pressure of essential hypertensive patients.

Systemic and regional hemodynamic effects of angiotensin-(1–7) in rats

2003 ◽  
Vol 284 (6) ◽  
pp. H1985-H1994 ◽  
Author(s):  
Walkyria O. Sampaio ◽  
Antônio A. S. Nascimento ◽  
Robson A. S. Santos
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Flow Distribution ◽  
High Dose ◽  
Blood Flow Distribution ◽  
Potent Effect

The systemic and regional hemodynamics effects of ANG-(1–7) were examined in urethane-anesthetized rats. The blood flow distribution (kidneys, skin, mesentery, lungs, spleen, brain, muscle, and adrenals), cardiac output, and total peripheral resistance were investigated by using fluorescent microspheres. Blood pressure and heart rate were recorded from the brachial artery. ANG-(1–7) infusion (110 fmol · min−1 · 10 min−1 iv) significantly increased blood flow to the kidney (5.10 ± 1.07 to 8.30 ± 0.97 ml · min−1 · g−1), mesentery (0.73 ± 0.16 to 1.17 ± 0.49 ml · min−1 · g−1), brain (1.32 ± 0.44 to 2.18 ± 0.85 ml · min−1 · g−1), and skin (0.07 ± 0.02 to 0.18 ± 0.07 ml · min−1 · g−1) and the vascular conductance in these organs. ANG-(1–7) also produced a significant increase in cardiac index (30%) and a decrease in total peripheral resistance (2.90 ± 0.55 to 2.15 ± 0.28 mmHg · ml−1 · min · 100 g). Blood flow to the spleen, muscle, lungs, and adrenals, as well as the blood pressure and heart rate, were not altered by the ANG-(1–7) infusion. The selective ANG-(1–7) antagonist A-779 reduced the blood flow in renal, cerebral, mesenteric, and cutaneous beds and blocked the ANG-(1–7)-induced vasodilatation in the kidney, mesentery, and skin, suggesting a significant role of endogenous ANG-(1–7) in these territories. The effects of ANG-(1–7) on the cerebral blood flow, cardiac index, systolic volume, and total peripheral resistance were partially attenuated by A-779. A high dose of ANG-(1–7) (11 pmol · min−1 · 10 min−1) caused an opposite effect of that produced by the low dose. Our results show for the first time that ANG-(1–7) has a previously unsuspected potent effect in the blood flow distribution and systemic hemodynamics.

Circulation in rats with Guerin carcinoma

1975 ◽  
Vol 38 (4) ◽  
pp. 696-701 ◽  
Author(s):  
L. Takacs ◽  
L. A. Debreczeni ◽  
C. Farsang
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cardiac Index ◽  
Evans Blue ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Organ Weight ◽  
Tumor Implantation

After implantation of Guerin carcinoma in rats, cardiac output (by Evans-blue dilution), distribution of the organ fractions of cardiac output (by Sapirsteins's isotope indicator fractionation technique), nutritive blood flow and circulatory resistance of the organs (including the tumor) were studied. The following parameters were altered proportionately to the weight of the tumor (0.39–84.0 g): a) weight of gut and carcass diminished; b) cardiac index increased, blood pressure and total peripheral resistance decreased; c) tumor fraction of cardiac output was augmented; d) blood flow of the organs increased and their circulatory resistance decreased. Hematocrit decreased from 47.2 to 31.0% 20 days after tumor implantation. In rats with tumor the changes of blood flow may be conditioned by both anemia and the decrease in organ weight.

Contribution of Stenosis Resistance to the Rise in total Peripheral Resistance during Experimental Renal Hypertension in Conscious Dogs

1981 ◽  
Vol 61 (6) ◽  
pp. 663-670 ◽  
Author(s):  
W. P. Anderson ◽  
P. I. Korner ◽  
J. A. Angus ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Plasma Renin Activity ◽  
Renal Artery ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Vascular Beds ◽  
Renal Vascular

1. Mild, moderate and severe renal artery stenosis was induced in uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, followed by a return to control values 24 h after cuff deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. in moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. in these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. in mild stenosis the changes in both cardiac output and total peripheral resistance were variable and not statistically significant. in this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. in all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of nonrenal beds.

Regional distribution of blood flow during diving in the duck (Anas platyrhynchos)

1979 ◽  
Vol 57 (5) ◽  
pp. 995-1002 ◽  
Author(s):  
David R. Jones ◽  
Robert M. Bryan Jr. ◽  
Nigel H. West ◽  
Raymond H. Lord ◽  
Brenda Clark
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Regional Distribution ◽  
Peripheral Resistance ◽  
Tissue Blood Flow ◽  
Arterial Blood ◽  
The Brain

The regional distribution of blood flow, both before and during forced diving, was studied in the duck using radioactively labelled microspheres. Cardiac output fell from 227 ± 30 to 95 ± 16 mL kg−1 min−1 after 20–72 s of submergence and to 59 ± 18 mL kg−1 min−1 after 144–250 s of submergence. Mean arterial blood pressure did not change significantly as total peripheral resistance increased by four times during prolonged diving. Before diving the highest proportion of cardiac output went to the heart (2.6 ± 0.5%, n = 9) and kidneys (2.7 ± 0.5%, n = 9), with the brain receiving less than 1%. The share of cardiac output going to the brain and heart increased spectacularly during prolonged dives to 10.5 ± 3% (n = 5) and 15.9 ± 3.8% (n = 5), respectively, while that to the kidney fell to 0.4 ± 0.26% (n = 3). Since cardiac output declined during diving, tissue blood flow (millilitres per gram per minute) to the heart was unchanged although in the case of the brain it increased 2.35 times after 20–75 s of submergence and 8.5 times after 140–250 s of submergence. Spleen blood flow, the highest of any tissue predive (5.6 ± 1.3 mL g−1 min−1, n = 4), was insignificant during diving while adrenal flow increased markedly, in one animal reaching 7.09 mL g−1 min−1. The present results amplify general conclusions from previous research on regional distribution of blood flow in diving homeotherms, showing that, although both heart and brain receive a significant increase in the proportionate share of cardiac output during diving only the brain receives a significant increase in tissue blood flow, which increases as submergence is prolonged.

Effect of Sotalol on Haemodynamics and Renin—Angiotensin—Aldosterone System in Hypertensive Patients

1976 ◽  
Vol 51 (1) ◽  
pp. 9-17 ◽  
Author(s):  
A. Verniory ◽  
M. Staroukine ◽  
F. Delwiche ◽  
M. Telerman
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Excretion Rate ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Hypertensive Patients ◽  
Receptor Blocking ◽  
Plasma Angiotensin

1. Twenty-three hypertensive patients were treated by sotalol, a pure beta-adrenergic receptor blocking agent. The drug produced a significant decrease of blood pressure in nineteen patients. 2. On average, cardiac index decreased but not significantly; heart rate decreased and stroke index increased significantly. Total peripheral resistance varied in both directions. 3. Sotalol determined a fall in plasma renin concentration (only significant in the high-renin group), a fall in plasma angiotensin II concentration and in urinary excretion rate of aldosterone accompanied by a rise in plasma potassium concentration. 4. The fall of blood pressure was not correlated with the decreases of renin and angiotensin II concentrations or excretion rate of aldosterone. However, in the placebo period plasma angiotensin II concentration was significantly correlated with total peripheral resistance; during sotalol treatment the variations of these two parameters seemed also to be correlated. 5. There was a poor correlation between decreases of cardiac output and of blood pressure; it was impossible to foresee the magnitude of the lowering of the blood pressure from the initial cardiac index. 6. The association of a diuretic with sotalol enhanced the hypotensive effect of the beta-receptor blocking drug, without significant increase of plasma renin and angiotensin II concentrations.

General and Regional Haemodynamic Effects of Intravenous Ergotamine in Man

1983 ◽  
Vol 65 (6) ◽  
pp. 599-604 ◽  
Author(s):  
P. Tfelt-Hansen ◽  
I.-L. Kanstrup ◽  
N. J. Christensen ◽  
K. Winkler
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Plasma Catecholamines ◽  
Peripheral Resistance ◽  
Haemodynamic Effects ◽  
Pressor Effect ◽  
Plasma Adrenaline ◽  
Vascular Beds

1. The effect of intravenous ergotamine on general (blood pressure and cardiac output) and regional (splanchnic, renal and muscular) haemodynamics was studied immediately and 3 h after administration in seven male volunteers. Also plasma catecholamines were determined. 2. An increase in blood pressure with a peak just after administration was observed. The cardiac output was unchanged and the pressor effect of ergotamine was due to an increase in total peripheral resistance. 3. Plasma noradrenaline decreased 65% at the peak of the pressor effect whereas plasma adrenaline was unchanged. 4. Hepatic blood flow decreased 34% just after ergotamine administration and was normal after 3 h. Renal blood flow decreased by 29 and 19%. Calf blood flow was unchanged. These results suggest that different vascular beds in man react differently to ergotamine.

Angiotensin II: nitric oxide interaction and the distribution of blood flow

1993 ◽  
Vol 265 (6) ◽  
pp. R1276-R1283 ◽  
Author(s):  
D. H. Sigmon ◽  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Conscious Rats

Nitric oxide (NO) contributes to the regulation of regional blood flow. Inhibition of NO synthesis increases blood pressure and vascular resistance. Using radioactive microspheres and the substrate antagonist N omega-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg) to block NO synthesis, we tested the hypothesis that there is a significant interaction between the vasodilator NO and the vasoconstrictor angiotensin II, which regulates regional hemodynamics. Further, we investigated the influence of anesthesia on this interaction. L-NAME increased blood pressure, decreased cardiac output, and increased total peripheral resistance in both anesthetized and conscious rats. In anesthetized rats, L-NAME decreased blood flow to visceral organs (i.e. kidney, intestine, and lung) but had little effect on blood flow to the brain, heart, or hindlimb. Treating anesthetized rats with the angiotensin II receptor antagonist losartan (10 mg/kg) attenuated the decrease in cardiac output and the increase in total peripheral resistance without affecting the pressor response to L-NAME. Losartan also attenuated the visceral hemodynamic responses to L-NAME. In conscious rats, L-NAME decreased blood flow to all organ beds. Treating these rats with losartan only marginally attenuated the increase in total peripheral resistance to L-NAME without significantly affecting the pressor response or the decrease in cardiac output. Losartan had no effect on the regional hemodynamic responses to L-NAME. These data suggest that NO-mediated vascular relaxation is an important regulator of total peripheral and organ vascular resistance. (ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular effects produced by L-glutamate stimulation of the lateral hypothalamic area

1989 ◽  
Vol 257 (2) ◽  
pp. H540-H552 ◽  
Author(s):  
S. E. Spencer ◽  
W. B. Sawyer ◽  
A. D. Loewy
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Lateral Hypothalamic Area ◽  
Hypothalamic Area ◽  
Pharmacological Blockade ◽  
Stimulation Of

L-Glutamate microinjections into the tuberal region of the lateral hypothalamic area (LHAt) caused a fall in blood pressure and heart rate in pentobarbital-anesthetized rats. The bradycardia was mediated by both beta-adrenergic and muscarinic mechanisms as demonstrated with pharmacological blockade. The hypotension was due to a decrease in cardiac output, not a decrease in total peripheral resistance. In addition, there was a reduction in coronary blood flow. If heart rate was held constant by pharmacological blockade or by electrical cardiac pacing, L-glutamate stimulation of the LHAt still caused a fall in blood pressure. When the electrically paced model was used, this hypotension was due to a fall in cardiac output. In contrast, with the pharmacological blockade of the heart, the hypotension was due to a decrease in the total peripheral resistance. The cardiac output reduction in the paced condition was not mediated solely by either beta-sympathetic or parasympathetic mechanisms as determined by pharmacological blockade. With heart rate held constant by either drugs or pacing, LHAt stimulation did not alter regional blood flow or resistance in any vascular bed, including the coronary circulation. We conclude that L-glutamate stimulation of the LHAt lowers the cardiac output and heart rate by both parasympathetic and beta-adrenergic mechanisms and elicits hypotension by lowering cardiac output in the naive and electrically paced model.

Sign in / Sign up

Export Citation Format

Share Document