Journal articles: 'Hemodynamic effects of insulin'

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Schmetterer, L., M. Muller, P. Fasching, C. Diepolder, A. Gallenkamp, G. Zanaschka, O. Findl, et al. "Renal and Ocular Hemodynamic Effects of Insulin." Diabetes 46, no. 11 (November 1, 1997): 1868–74. http://dx.doi.org/10.2337/diab.46.11.1868.

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Schmetterer, L., M. Muller, P. Fasching, C. Diepolder, A. Gallenkamp, G. Zanaschka, O. Findl, et al. "Renal and ocular hemodynamic effects of insulin." Diabetes 46, no. 11 (November 1, 1997): 1868–74. http://dx.doi.org/10.2337/diabetes.46.11.1868.

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Ferrannini, E., D. Santoro, R. Bonadonna, A. Natali, O. Parodi, and P. G. Camici. "Metabolic and hemodynamic effects of insulin on human hearts." American Journal of Physiology-Endocrinology and Metabolism 264, no. 2 (February 1, 1993): E308—E315. http://dx.doi.org/10.1152/ajpendo.1993.264.2.e308.

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Myocardial muscle is considered to be a target tissue for insulin action, but direct measurements of insulin's effects on cardiac hemodynamics and intermediary metabolism in humans are scarce. We combined great cardiac vein (GCV)/arterial catheterization with the euglycemic insulin clamp technique and thermodilution in six healthy middle-aged (53 +/- 2 yr) volunteers. In the fasting state, the myocardium extracted free fatty acid (FFA), lactate, pyruvate, glycerol, and beta-hydroxybutyrate (6.4 +/- 0.8, 6.2 +/- 1.0, 0.58 +/- 0.12, 0.44 +/- 0.15, and 11 +/- 2 mumol/min, respectively) and consumed 0.26 +/- 0.02 mmol/min oxygen. As fasting plasma insulin (73 +/- 6 pmol/l) was raised and clamped at 503 +/- 16 pmol/l for 100 min while maintaining euglycemia (approximately 5 mmol/l), arterial levels of lactate and pyruvate rose (by 121 and 159%, respectively), whereas FFA, glycerol, and beta-hydroxybutyrate fell (by 69, 48, and 85%, respectively, all P < 0.001). Correspondingly, net myocardial uptake of glucose, lactate, and pyruvate increased to 18.9 +/- 3.5, 32.0 +/- 2.3, and 2.7 +/- 0.5 mumol/min, respectively, whereas net extraction of circulating FFA, glycerol, and beta-hydroxybutyrate was abolished (all P < 0.001). The stimulation of lactate and pyruvate uptake was the result of both increased arterial supply and enhanced myocardial extraction ratio (from 19 +/- 3 to 51 +/- 6% for lactate, from 26 +/- 5 to 44 +/- 5% for pyruvate, P < 0.001 for both). This shift from fat to carbohydrate fuel usage occurred in the absence of changes in oxygen consumption, heart rate, GCV blood flow, aortic pressures, coronary vascular resistance, and left ventricular end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cohen, A. J., D. M. McCarthy, and J. S. Stoff. "Direct hemodynamic effect of insulin in the isolated perfused kidney." American Journal of Physiology-Renal Physiology 257, no. 4 (October 1, 1989): F580—F585. http://dx.doi.org/10.1152/ajprenal.1989.257.4.f580.

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The hemodynamic effect of insulin was examined in isolated perfused kidneys. Experiments were designed to study the effect of the hormone on basal hemodynamics and in the presence of angiotensin II (ANG II). Physiological insulin concentrations caused both renal vasodilation and increased glomerular filtration rate (GFR) during basal perfusion periods and attenuated the vasoconstrictor action of ANG II while limiting the ANG II-induced reduction of GFR. Insulin also increased fractional sodium reabsorption and diminished the natriuretic effect of ANG II. The addition of insulin to perfusions in which ANG II was infused from the start caused renal vasodilation, although supraphysiological concentrations were required. Kidneys perfused with hyperoncotic albumin to prevent filtration similarly demonstrated a vasodilatory effect of insulin that did not require glomerular filtration. Inhibition of prostaglandin (PG) synthesis with indomethacin prevented the vasodilatory effects of insulin. These data support the hypothesis that insulin causes renal vasodilation by a PG-dependent process.

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Stojiljkovic, Milos P., Da Zhang, Heno F. Lopes, Christine G. Lee, Theodore L. Goodfriend, and Brent M. Egan. "Hemodynamic effects of lipids in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 6 (June 1, 2001): R1674—R1679. http://dx.doi.org/10.1152/ajpregu.2001.280.6.r1674.

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Evidence suggests lipid abnormalities may contribute to elevated blood pressure, increased vascular resistance, and reduced arterial compliance among insulin-resistant subjects. In a study of 11 normal volunteers undergoing 4-h-long infusions of Intralipid and heparin to raise plasma nonesterified fatty acids (NEFAs), we observed increases of blood pressure. In contrast, blood pressure did not change in these same volunteers during a 4-h infusion of saline and heparin. To better characterize the hemodynamic responses to Intralipid and heparin, another group of 21 individuals, including both lean and obese volunteers, was studied after 3 wk on a controlled diet with 180 mmol sodium/day. Two and four hours after starting the infusions, plasma NEFAs increased by 134 and 111% in those receiving Intralipid and heparin, P < 0.01, whereas plasma NEFAs did not change in the first group of normal volunteers who received saline and heparin. The hemodynamic changes in lean and obese subjects in the second study were similar, and the results were combined. The infusion of Intralipid and heparin induced a significant increase in systolic (13.5 ± 2.1 mmHg) and diastolic (8.0 ± 1.5 mmHg) blood pressure as well as heart rate (9.4 ± 1.4 beats/min). Small and large artery compliance decreased, and systemic vascular resistance rose. These data raise the possibility that lipid abnormalities associated with insulin resistance contribute to the elevated blood pressure and heart rate as well as the reduced vascular compliance observed in subjects with the cardiovascular risk factor cluster.

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Bradley, Eloise A., Michael G. Clark, and Stephen Rattigan. "Acute effects of wortmannin on insulin's hemodynamic and metabolic actions in vivo." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (March 2007): E779—E787. http://dx.doi.org/10.1152/ajpendo.00407.2006.

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Wortmannin, an inhibitor of phosphatidylinositol 3-kinase, was systemically infused during a hyperinsulinemic euglycemic clamp to investigate its effects in vivo. Rats were infused under anesthesia with saline, 10 or 20 mU·min−1·kg−1 insulin, wortmannin (1 μg·min−1·kg−1) + saline, or wortmannin + insulin (10 mU·min−1·kg−1); wortmannin was present for 1 h before and throughout the 2-h clamp. Femoral blood flow (FBF), glucose infusion rate to maintain euglycemia (GIR), glucose appearance (Ra), glucose disappearance (Rd), capillary recruitment by 1-methylxanthine metabolism (MXD), hindleg glucose uptake (HLGU), liver, muscle, and aorta Akt phosphorylation (P-Akt/Akt), and plasma insulin concentrations were determined. Plasma insulin increased from 410 ± 49 to 1,680 ± 430 and 5,060 ± 230 pM with 10 and 20 mU·min−1·kg−1 insulin, respectively. Insulin (10 and 20 mU·min−1·kg−1) increased FBF, MXD, GIR, Rd, and HLGU as well as liver, muscle, and aorta P-Akt/Akt and decreased Ra (all P < 0.05). Wortmannin alone increased plasma insulin to 5,450 ± 770 pM and increased Ra, Rd, HLGU, and muscle P-Akt/Akt without effect on blood glucose, FBF, MXD liver, or aorta P-Akt/Akt. Wortmannin blocked FBF, MXD, and liver P-Akt/Akt increases from 10 mU·min−1·kg−1 insulin. Comparison of wortmannin + 10 mU·min−1·kg−1 insulin and 20 mU·min−1·kg−1 insulin alone (both at ∼5,000 pM PI) showed that wortmannin fully blocked the changes in FBF and Ra and partly those of GIR, Ra, Rd, HLGU, and muscle P-AKT/Akt. In summary, wortmannin in vivo increases plasma insulin and fully inhibits insulin-mediated effects in liver and aorta and partially those of muscle, where the latter may result from inhibition of insulin-mediated increases in blood flow and capillary recruitment.

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Hashimoto, Seiji, Tomochika Maoka, Tetsuya Kawata, Toshio Mochizuki, Takao Koike, and Takashi Shigematsu. "Roles of Insulin Receptor Substrates (IRS) in renal function and renal hemodynamics." PLOS ONE 15, no. 12 (December 3, 2020): e0242332. http://dx.doi.org/10.1371/journal.pone.0242332.

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We have reported previously that renal hemodynamic abnormalities exist in the prediabetic stage of type II diabetic rats. At this prediabetic stage these rats have hyperinsulinemia, insulin resistance and metabolic syndrome. It is well known that insulin resistance is frequently associated with renal abnormalities, but the mechanism underlying this association has remained speculative. Although insulin is known to modify renal hemodynamics, little is known about the roles of insulin receptor substrates (IRS1, IRS2) in the renal actions of insulin. To address this issue, the effects of insulin on renal function and renal hemodynamics were investigated in C57BL/6 (WT: wild type), insulin receptor substrate 1- knockout (IRS1–/–), and IRS2-knockout (IRS2–/–) mice. IRS2–/–mice had elevated glucose level as expected. 24-h urine collections and serum creatinine revealed that creatinine clearance did not significantly differ between these groups. Albuminuria was found in IRS1–/–and IRS2–/–groups. We examined the effects on the IRS during the administration of Losartan, which is widely used for diabetic nephropathy. After the administration of Losartan the IRS displayed improved renal hemodynamics. Moreover, the subjects were also given Pioglitazone, which improves insulin resistance. Losartan significantly reduced albuminuria in both groups. Pioglitazone also showed similar results. We assessed the autoregulatory responses of the total renal blood flow (RBF), the superficial (SBF) and the deep renal cortical blood flow (DBF) with stepwise reductions of renal perfusion pressure (RPP), which was induced by a manual clamp on the abdominal aorta. During the clamp induced reductions of the RPP by 10 to 20mm HG, RBF, SBF and the DBF fell significantly more in the IRS1 and IRS2 than in the WT mice. Furthermore micropuncture studies showded that compared to the WT tubuloglomerular feedback (TGF) responses of the stop flow pressure (Psf) were reduced in both the IRS1 -/- and IRS2 -/-. The results of the IRS1 and IRS2 mice displayed the pressence of hemodynamic abnormalities. Losartan and Pioglitazone have shown the potential to improve these abnormalities. In conclusion the results indicate that IRS plays a major role in the stimulation of renal functions and renal hemodynamics in type type II diabetes.

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Pitre, M., A. Nadeau, and H. Bachelard. "Insulin sensitivity and hemodynamic responses to insulin in Wistar-Kyoto and spontaneously hypertensive rats." American Journal of Physiology-Endocrinology and Metabolism 271, no. 4 (October 1, 1996): E658—E668. http://dx.doi.org/10.1152/ajpendo.1996.271.4.e658.

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The insulin-mediated vasodilator effect has been proposed as an important physiological determinant of insulin action on glucose disposal in normotensive humans. The present study was designed to further examine the acute regional hemodynamic effects of insulin in different vascular beds and to explore the relationships between insulin vascular effects and insulin sensitivity during euglycemic hyperinsulinemic clamps in conscious normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The rats were instrumented with intravascular catheters and pulsed Doppler flow probes to measure blood pressure, heart rate, and regional blood flows. In WKY rats, the euglycemic infusion of insulin (4 and 16 mU.kg-1.min-1) causes vasodilations in renal and hindquarter vascular beds but no changes in mean blood pressure, heart rate, or superior mesenteric vascular conductance. In contrast, in SHR, the same doses of insulin produce vasoconstrictions in superior mesenteric and hindquarter vascular beds and, at high doses, increase blood pressure. Moreover, at the lower dose of insulin tested, we found a reduction in the insulin sensitivity index in the SHR compared with the WKY rats. The present findings provide further evidence for an association between insulin sensitivity and insulin-mediated hemodynamic responses.

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Sánchez-Lozada, Laura G., Edilia Tapia, Pablo Bautista-García, Virgilia Soto, Carmen Ávila-Casado, Iliana P. Vega-Campos, Takahiko Nakagawa, Lin Zhao, Martha Franco, and Richard J. Johnson. "Effects of febuxostat on metabolic and renal alterations in rats with fructose-induced metabolic syndrome." American Journal of Physiology-Renal Physiology 294, no. 4 (April 2008): F710—F718. http://dx.doi.org/10.1152/ajprenal.00454.2007.

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Increased fructose consumption is associated with hyperuricemia, metabolic syndrome, and renal damage. This study evaluated whether febuxostat (Fx), an investigational nonpurine, and selective xanthine oxidase inhibitor, could alleviate the features of metabolic syndrome as well as the renal hemodynamic alterations and afferent arteriolopathy induced by a high-fructose diet in rats. Two groups of rats were fed a high-fructose diet (60% fructose) for 8 wk, and two groups received a normal diet. For each diet, one group was treated with Fx (5–6 mg·kg−1·day−1 in the drinking water) during the last 4 wk (i.e., after the onset of metabolic syndrome), and the other received no treatment (placebo; P). Body weight was measured daily. Systolic blood pressure and fasting plasma uric acid (UA), insulin, and triglycerides were measured at baseline and at 4 and 8 wk. Renal hemodynamics and histomorphology were evaluated at the end of the study. A high-fructose diet was associated with hyperuricemia, hypertension, as well as increased plasma triglycerides and insulin. Compared with fructose+P, fructose+Fx rats showed significantly lowered blood pressure, UA, triglycerides, and insulin ( P < 0.05 for all comparisons). Moreover, fructose+Fx rats had significantly reduced glomerular pressure, renal vasoconstriction, and afferent arteriolar area relative to fructose+P rats. Fx treatment in rats on a normal diet had no significant effects. In conclusion, normalization of plasma UA with Fx in rats with metabolic syndrome alleviated both metabolic and glomerular hemodynamic and morphological alterations. These results provide further evidence for a pathogenic role of hyperuricemia in fructose-mediated metabolic syndrome.

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Stonestreet, B. S., E. Le, and D. J. Berard. "Circulatory and metabolic effects of beta-adrenergic blockade in the hyperinsulinemic ovine fetus." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1098—H1106. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1098.

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Offspring of women with poorly controlled diabetes exhibit hypoxemia, elevated catecholamine concentration at birth, and an increased incidence of fetal death. Experimental fetal hyperinsulinemia results in increased catecholamine concentration and hemodynamic changes including increased combined ventricular output and vasodilation of select fetal organs. We hypothesized that insulin-induced catecholamine-mediated beta-adrenergic stimulation supports some of these hemodynamic changes in the hyperinsulinemic ovine fetus. To study this, 24 chronically instrumented fetal sheep receiving insulin for 24 h were exposed to beta-(propranolol),beta 1-(metoprolol), and beta 2-(ICI 118,551) adrenergic blockade. Insulin infusion resulted in hyperinsulinemic-hypoglycemia, a surge in epinephrine and norepinephrine concentration, and increases in the combined ventricular output and regional blood flow to the heart, adrenal glands, kidney, gastrointestinal tract, liver, fat, muscle, carcass, and placenta. In the hyperinsulinemic state, beta-adrenergic blockade was associated with significant reductions in the combined ventricular output and blood flow to fat, carcass, lungs, and the placenta; beta 1-blockade was associated with reductions in the combined ventricular output and blood flow to the lungs; and beta 2-adrenergic blockade was associated with reductions in blood flow to muscle and lungs. Because beta-adrenergic blockade was associated with reductions in placental blood flow during hyperinsulinemia, oxygen and glucose metabolism were also compromised. We conclude that in the hyperinsulinemic-hypoglycemic normoxemic ovine fetus, insulin-induced catecholamine-mediated hemodynamic changes are modulated in part by beta-adrenergic receptor stimulation.

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Clark, Michael G., Michelle G. Wallis, Eugene J. Barrett, Michelle A. Vincent, Stephen M. Richards, Lucy H. Clerk, and Stephen Rattigan. "Blood flow and muscle metabolism: a focus on insulin action." American Journal of Physiology-Endocrinology and Metabolism 284, no. 2 (February 1, 2003): E241—E258. http://dx.doi.org/10.1152/ajpendo.00408.2002.

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The vascular system controls the delivery of nutrients and hormones to muscle, and a number of hormones may act to regulate muscle metabolism and contractile performance by modulating blood flow to and within muscle. This review examines evidence that insulin has major hemodynamic effects to influence muscle metabolism. Whole body, isolated hindlimb perfusion studies and experiments with cell cultures suggest that the hemodynamic effects of insulin emanate from the vasculature itself and involve nitric oxide-dependent vasodilation at large and small vessels with the purpose of increasing access for insulin and nutrients to the interstitium and muscle cells. Recently developed techniques for detecting changes in microvascular flow, specifically capillary recruitment in muscle, indicate this to be a key site for early insulin action at physiological levels in rats and humans. In the absence of increases in bulk flow to muscle, insulin may act to switch flow from nonnutritive to the nutritive route. In addition, there is accumulating evidence to suggest that insulin resistance of muscle in vivo in terms of impaired glucose uptake could be partly due to impaired insulin-mediated capillary recruitment. Exercise training improves insulin-mediated capillary recruitment and glucose uptake by muscle.

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Karstoft, Kristian, Stefan P. Mortensen, Sine H. Knudsen, and Thomas P. J. Solomon. "Direct effect of incretin hormones on glucose and glycerol metabolism and hemodynamics." American Journal of Physiology-Endocrinology and Metabolism 308, no. 5 (March 1, 2015): E426—E433. http://dx.doi.org/10.1152/ajpendo.00520.2014.

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The objective of this study was to assess the insulin-independent effects of incretin hormones on glucose and glycerol metabolism and hemodynamics under euglycemic and hyperglycemic conditions. Young, healthy men ( n = 10) underwent three trials in a randomized, controlled, crossover study. Each trial consisted of a two-stage (euglycemia and hyperglycemia) pancreatic clamp (using somatostatin to prevent endogenous insulin secretion). Glucose and lipid metabolism was measured via infusion of stable glucose and glycerol isotopic tracers. Hemodynamic variables (femoral, brachial, and common carotid artery blood flow and flow-mediated dilation of the brachial artery) were also measured. The three trials differed as follows: 1) saline [control (CON)], 2) glucagon-like peptide (GLP-1, 0.5 pmol·kg−1·min−1), and 3) glucose-dependent insulinotropic polypeptide (GIP, 1.5 pmol·kg−1·min−1). No between-trial differences in glucose infusion rates (GIR) or glucose or glycerol kinetics were seen during euglycemia, whereas hyperglycemia resulted in increased GIR and glucose rate of disappearance during GLP-1 compared with CON and GIP ( P < 0.01 for all). However, when normalized to insulin levels, no differences between trials were seen for GIR or glucose rate of disappearance. Besides a higher femoral blood flow during hyperglycemia with GIP (vs. CON and GLP-1, P < 0.001), no between-trial differences were seen for the hemodynamic variables. In conclusion, GLP-1 and GIP have no direct effect on whole body glucose metabolism or hemodynamics during euglycemia. On the contrary, during hyperglycemia, GIP increases femoral artery blood flow with no effect on glucose metabolism, whereas GLP-1 increases glucose disposal, potentially due to increased insulin levels.

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Rattigan, Stephen, Lei Zhang, Hema Mahajan, Cathryn Kolka, Stephen Richards, and Michael Clark. "Factors Influencing the Hemodynamic and Metabolic Effects of Insulin in Muscle." Current Diabetes Reviews 2, no. 1 (February 1, 2006): 61–70. http://dx.doi.org/10.2174/157339906775473653.

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Shevchuk, Sergii, and Володимир Корчинський. "HORMONAL AND VEGETATIVE FACTORS OF INSULIN RESISTANCE IN PATIENTS WITH HYPERTENSION." Problems of Endocrine Pathology 77, no. 3 (September 14, 2021): 91–98. http://dx.doi.org/10.21856/j-pep.2021.3.13.

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The combination of arterial hypertension (AH) and insulin resistance (IR) significantly increases the risk of cardiovascular complications. Research objective: Studying indices of carbohydrate metabolism, activity of renin-angiotensin-aldosterone system, calcium-regulating hormones, adrenal glucocorticoid function, the condition of the autonomic nervous system and their possible interrelation with hemodynamic parameters in AH patients with different insulin sensitivity. A comprehensive study of hormonal profile was held with use of radio immune method and that of central hemodynamics with use of echocardiography in 72 patients with arterial hypertension stage II, 1-2 degrees, male (mean age – 54.1±3.4 years), with a body mass index up to 30 kg / mІ and verified insulin resistance (IR), in 32 patients of which insulin resistance (IR) was revealed, and in 40 patients its absence was fixed. Insulin resistance was verified by the value of HOMA-IR in excess of 2,77. To assess the condition of the autonomic nervous system, studies of heart rate variability were performed. It is established that patients with hypertension with IR had increased level of plasma renin activity, levels of angiotensin II, cortisol, insulin, parathyroid hormone, decreased parasympathetic and increased sympathetic tonus. According to the results of factor analysis, AH with insulin resistance has a distinctive structure of neurohumoral regulation of the main indicators of central hemodynamics and interhormonal interactions; the direct regulatory effects of angiotensin II, insulin, progesterone, parathyroid hormone on the indicators of central hemodynamics, modulation of presorption action increases. The study not only revealed peculiarities of neurohumoral profiles in patients with hypertension depending on insulin resistance, but also determined distinctive features in structure of the regulatory process of central hemodynamics and interhormonal interactions. This should be taken into account when prescribing antihypertensive therapy.

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Shevchuk, Sergii, and Володимир Корчинський. "HORMONAL AND VEGETATIVE FACTORS OF INSULIN RESISTANCE IN PATIENTS WITH HYPERTENSION." Problems of Endocrine Pathology 77, no. 3 (September 14, 2021): 91–98. http://dx.doi.org/10.21856/j-pep.2021.3.13.

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The combination of arterial hypertension (AH) and insulin resistance (IR) significantly increases the risk of cardiovascular complications. Research objective: Studying indices of carbohydrate metabolism, activity of renin-angiotensin-aldosterone system, calcium-regulating hormones, adrenal glucocorticoid function, the condition of the autonomic nervous system and their possible interrelation with hemodynamic parameters in AH patients with different insulin sensitivity. A comprehensive study of hormonal profile was held with use of radio immune method and that of central hemodynamics with use of echocardiography in 72 patients with arterial hypertension stage II, 1-2 degrees, male (mean age – 54.1±3.4 years), with a body mass index up to 30 kg / mІ and verified insulin resistance (IR), in 32 patients of which insulin resistance (IR) was revealed, and in 40 patients its absence was fixed. Insulin resistance was verified by the value of HOMA-IR in excess of 2,77. To assess the condition of the autonomic nervous system, studies of heart rate variability were performed. It is established that patients with hypertension with IR had increased level of plasma renin activity, levels of angiotensin II, cortisol, insulin, parathyroid hormone, decreased parasympathetic and increased sympathetic tonus. According to the results of factor analysis, AH with insulin resistance has a distinctive structure of neurohumoral regulation of the main indicators of central hemodynamics and interhormonal interactions; the direct regulatory effects of angiotensin II, insulin, progesterone, parathyroid hormone on the indicators of central hemodynamics, modulation of presorption action increases. The study not only revealed peculiarities of neurohumoral profiles in patients with hypertension depending on insulin resistance, but also determined distinctive features in structure of the regulatory process of central hemodynamics and interhormonal interactions. This should be taken into account when prescribing antihypertensive therapy.

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Uchida, Kazuhiko, Kazuhide Ogino, Masaki Shimoyama, Ichiro Hisatome, and Chiaki Shigemasa. "Acute hemodynamic effects of insulin-sensitizing agents in isolated perfused rat hearts." European Journal of Pharmacology 400, no. 1 (July 2000): 113–19. http://dx.doi.org/10.1016/s0014-2999(00)00359-9.

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Svinth-Johansen, Christoffer, Mark Reinhard, and Per Ivarsen. "Hemodynamic Response to Glucose-Insulin Infusion and Meals during Hemodialysis." Kidney and Blood Pressure Research 45, no. 2 (2020): 249–62. http://dx.doi.org/10.1159/000506012.

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Introduction: Intradialytic nutrition may improve nutritional status and reduce mortality in patients on maintenance hemodialysis (HD) but has been associated with adverse events, mainly hemodynamic instability. Some dialysis centers therefore restrict intradialytic meals. In 2 clinical studies, we investigated the effects of intradialytic glucose-insulin infusion (GII) and meal intake on blood pressure (BP), pulse wave velocity (PWV), pulse wave analysis (PWA), and cardiac output (CO). PWA yielded augmentation index standardized with heart rate 75 (AIx@HR75). Methods: In the GII study, 12 nondiabetic HD patients had BP, PWV, PWA, and CO measured during 3 HD sessions: standard HD, HD with glucose infusion, and HD with GII. In the Meal study, 12 nondiabetic patients had BP and PWA measured on 3 study days: meal alone (non-HD), meal and HD, 2 meals and HD. Twelve matched healthy controls completed the non-HD day. Findings: In the GII study, glucose or GII had no additional effects on hemodynamic parameters compared with standard HD. HD resulted in a decrease in systolic BP of 13%, in diastolic BP of 9%, in AIx@HR75 of 17%, and CO of 18%. PWV was reduced by only 5%. In the Meal study, a meal alone did not change BP, whereas the combined influence of HD and meal intake reduced systolic BP with 22% and diastolic BP with 19%. Furthermore, AIx@HR75 decreased by 37% on HD days and by 36% in controls, but was unaffected on non-HD days. Discussion: In the GII study, HD significantly reduced BP, AIx@75, and CO, whereas PWV remained almost constant. No additional effects were observed by concomitant GII during HD. BP reductions seemed larger in the Meal study compared with the GII study. Taken together, HD per se appears as the main discriminant for intradialytic hypotension but in hemodynamically unstable patients the timing and route of nutrition provision should be considered carefully.

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Mélançon, Sébastien, Hélène Bachelard, Mylène Badeau, Frédéric Bourgoin, Maryse Pitre, Richard Larivière, and André Nadeau. "Effects of high-sucrose feeding on insulin resistance and hemodynamic responses to insulin in spontaneously hypertensive rats." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 6 (June 2006): H2571—H2581. http://dx.doi.org/10.1152/ajpheart.01002.2005.

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This study was designed to investigate the effects of a sucrose diet on vascular and metabolic actions of insulin in spontaneously hypertensive rats (SHR). Male SHR were randomized to receive a sucrose or regular chow diet for 4 wk. Age-matched, chow-fed Wistar-Kyoto (WKY) rats were used as normotensive control. In a first series of experiments, the three groups of rats had pulsed Doppler flow probes and intravascular catheters implanted to determine blood pressure, heart rate, and blood flows. Insulin sensitivity was assessed during a euglycemic hyperinsulinemic clamp performed in conscious rats. In a second series of experiments, new groups of rats were used to examine glucose transport activity in isolated muscles and to determine endothelial nitric oxide synthase (eNOS) protein expression in muscles and endothelin content in vascular tissues. Sucrose feeding was shown to markedly enhance the pressor response to insulin and its hindquarter vasoconstrictor effect when compared with chow-fed SHR. A reduction in eNOS protein content in muscle, but no change in vascular endothelin-1 protein, was noted in sucrose-fed SHR when compared with WKY rats, but these changes were not different from those noted in chow-fed SHR. Similar reductions in insulin-stimulated glucose transport were observed in soleus muscles from both groups of SHR when compared with WKY rats. In extensor digitorum longus muscles, a significant reduction in insulin-stimulated glucose transport was only seen in sucrose-fed rats when compared with the other two groups. Environmental factors, that is, high intake of simple sugars, could possibly potentiate the genetic predisposition in SHR to endothelial dysfunction and insulin resistance.

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Cozzolino, Domenico, Raffaello Furlan, Domenico Gruosso, Cristiana Di Maggio, Emanuele Miraglia del Giudice, Roberto Torella, and Dario Giugliano. "Effects of a Mixed Meal on Hemodynamics and Autonomic Control of the Heart in Patients with Type 1 Diabetes." Journal of Clinical Endocrinology & Metabolism 95, no. 1 (January 1, 2010): 194–200. http://dx.doi.org/10.1210/jc.2009-1663.

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Abstract Context: Food intake induces relevant cardiovascular changes together with parallel increases in cardiac sympathetic activity and insulin plasma levels in man. Objective: We evaluated hemodynamics, neurohormones, and cardiac autonomic control after eating in patients with type 1 diabetes, a disease characterized by the absence of basal and stimulated insulin production. Design and Setting: Fifteen type 1 diabetic patients and 15 healthy controls underwent blood sampling, electrocardiogram, blood pressure and respiration recordings, and heart rate variability analysis while recumbent, during the 70° head-up tilt, and 20 min after a mixed meal; on another occasion, diabetic patients were also studied 20 min after a mixed meal preceded by their scheduled bolus of exogenous insulin. Spectrum analysis of RR interval provided the indices of sympathetic (LFRR) and vagal (HFRR) modulation of the sinoatrial node. Results: At baseline, no significant differences were found between groups, except for metabolic parameters. Compared with baseline, heart rate, plasma catecholamines, and LFRR significantly (P < 0.005) increased, whereas HFRR significantly (P < 0.0001) decreased during the tilt in all subjects. Compared with baseline, plasma norepinephrine, heart rate, and LFRR significantly (P < 0.05) increased, whereas HFRR significantly (P < 0.02) decreased after eating in controls but not in diabetic patients (with and without insulin administered before eating). In both controls and diabetic patients, no relationship between postprandial changes of insulin and LFRR and HFRR was found. Conclusions: Hemodynamic, neurohormonal, and cardiac neural responses to eating are abnormal in type 1 diabetic patients, independently of insulin.

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Chubenko, Е. А., О. D. Belyaeva, Е. А. Bazhenova, Т. L. Karonova, А. V. Kozlenok, S. Е. Nifontov, O. O. Bolshakova, О. А. Berkovich, and Е. I. Baranova. "Pleiotropic effects of moxonidine." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 16, no. 4 (August 28, 2010): 351–55. http://dx.doi.org/10.18705/1607-419x-2010-16-4-351-355.

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Background. Imidazoline receptor agonist moxonidine besides its antihypertensive effect, can increase insulin sensitivity, reduce leptin level, improve lipid metabolism. However, the efficacy, tolerability and pleiotropic effects of moxonidine in postmenopausal women with essential hypertension (EH) and metabolic syndrome (MS) are not well established, and it was the objective of this study. Design and methods. 30 postmenopausal women with EH and MS (52,5 ± 0,4 years old) were included. Moxonidine was administered (400-600 mkg/day) for 12 weeks. Waist circumference (WC), hip circumference (HC), WC/HC ratio, body mass index (BMI), insulin, leptin level, glucose, lipid profile of blood serum, index of insulin resistance (HOMA-IR) and index of functional activity of pancreatic beta cells (HOMA-FB), echocardiography, intima-media thickness (IMT) of common carotid arteries (CCA). Results. Moxonidine therapy was associated with blood pressure (BP) decrease, body weight and BMI decrease, high-density lipoprotein (HDL) cholesterol and HOMA-FB index increase. Left atrium diameter and volume decreased, left ventricular diastolic function improved. Conclusions. Moxonidine is an effective antihypertensive drug for the treatment of postmenopausal hypertensive women with MS, which improves a range of metabolic, hemodynamic parameters and leads to the decrease of left atrium volume and diameter.

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Sommerfield, Andrew J., Ian B. Wilkinson, David J. Webb, and Brian M. Frier. "Vessel wall stiffness in type 1 diabetes and the central hemodynamic effects of acute hypoglycemia." American Journal of Physiology-Endocrinology and Metabolism 293, no. 5 (November 2007): E1274—E1279. http://dx.doi.org/10.1152/ajpendo.00114.2007.

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Objective: To examine the effects of intravenous insulin and acute hypoglycemia on arterial wall stiffness and central hemodynamic responses in adults with and without type 1 diabetes. Research Design and Methods: In 30 young male volunteers [10 nondiabetic ( Group 1); 10 with type 1 diabetes, <5 yr duration ( Group 2); 10 with type 1 diabetes, >15 yr duration ( Group 3)], intravenous insulin was administered to provoke an acute autonomic reaction (R) to hypoglycemia. Heart rate, peripheral blood pressure, and pulse wave analysis (radial artery) were monitored. Augmentation index (AIx), a measure of arterial wall stiffness and wave reflection, and central arterial pressure were recorded. Results: At baseline, no significant differences were observed between Groups 1 and 2 in either AIx or in central arterial pressure, but in Group 3, both measures were significantly higher. All three groups exhibited similar responses to intravenous infusion of insulin and to hypoglycemia: AIx fell progressively from baseline to R, peripheral systolic blood pressure increased, and central systolic pressure decreased. Conclusion: Compared with age- and sex-matched nondiabetic controls, people who had type 1 diabetes for a long duration had increased stiffness of vessel walls. The opposing responses in peripheral and central systolic pressures during hypoglycemia may be related to the reduction in AIx, which causes diminished amplification of the systolic pressure wave. Changes in AIx are probably mediated by a direct action of insulin on arterial endothelium, or changes in heart rate. These functional changes may contribute to the increased cardiovascular morbidity that is associated with type 1 diabetes of long duration.

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Kapil S. Divekar, Karishma D. Mehta, Pancham Mehta, Payal P. Prajapati, and Kamla H. Mehta. "Comparison of Various Techniques of Anesthesia for Surgical Management of Diabetic Foot." Academia Anesthesiologica International 5, no. 2 (December 16, 2020): 62–65. http://dx.doi.org/10.21276/aan.2020.5.2.13.

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Background: Diabetes mellitus is a multisystem disease caused by an absolute or relative deficiency of insulin secretion or resistance or a combination of both. Anesthesia in them is of special concern because of complex polypharmacy, an inappropriate dose of oral hypoglycemic agents or insulin and errors in converting IV insulin to usual medication. The objective is to compare the various techniques of anesthesia for surgical management of diabetic foot in terms of intraoperative hemodynamic stability, perioperative problems related to anesthesia techniques, postoperative analgesia. Subjects and Methods: Sixty adult diabetic patients of both gender of ASA grade II-III, aged 35years undergoing surgical management of diabetic foot were elected and separated into three groups, Group A: general anesthesia with tracheal intubation, Group B: unilateral spinal anesthesia with injection 0.5% bupivacaine heavy 1.5ml (7.5mg), Group C: popliteal nerve block via lateral approach by injecting 30 ml 0.5% bupivacaine. Parameters like pulse rate, mean arterial blood pressure, respiratory rate and SpO2 were recorded at regular intervals. Postoperative pain, perioperative side effects, complications and problems related to anesthetic techniques were noted. The analysis is done by unpaired t-test and chi-square test. Results: Group C patients were hemodynamic stable than Group A and B. Post-op analgesia was prolonged in Group C. Perioperative side effects were more found in Group A. Conclusion: Popliteal nerve block and unilateral spinal anesthesia provide better hemodynamic stability and postoperative analgesia with negligible side effects as compared to general anesthesia for surgical management of diabetic foot.

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Manhylova, T. A., and N. H. Gafarova. "Metabolic and hemodynamic effects of the growth hormone system — insulin-like growth factor." Terapevticheskii arkhiv 87, no. 12 (2015): 128. http://dx.doi.org/10.17116/terarkh20158712128-133.

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Thomassen, A., T. T. Nielsen, J. P. Bagger, and P. Henningsen. "Cardiac Metabolic and Hemodynamic Effects of Insulin in Patients With Coronary Artery Disease." Diabetes 38, no. 9 (September 1, 1989): 1175–80. http://dx.doi.org/10.2337/diab.38.9.1175.

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Hausberg, Martin, Robert P. Hoffman, Virend K. Somers, Christine A. Sinkey, Allyn L. Mark, and Erling A. Anderson. "Contrasting Autonomic and Hemodynamic Effects of Insulin in Healthy Elderly Versus Young Subjects." Hypertension 29, no. 3 (March 1997): 700–705. http://dx.doi.org/10.1161/01.hyp.29.3.700.

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Thomassen, A., T. T. Nielsen, J. P. Bagger, and P. Henningsen. "Cardiac metabolic and hemodynamic effects of insulin in patients with coronary artery disease." Diabetes 38, no. 9 (September 1, 1989): 1175–80. http://dx.doi.org/10.2337/diabetes.38.9.1175.

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Schmidt, Alice, Johannes Pleiner, Georg Schaller, Michael Roden, Susanne Dallinger, Gert Mayer, Leopold Schmetterer, and Michael Wolzt. "Renal hemodynamic effects of somatostatin are not related to inhibition of endogenous insulin release." Kidney International 61, no. 5 (May 2002): 1788–93. http://dx.doi.org/10.1046/j.1523-1755.2002.00320.x.

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Li, Bing, Jian Yao, Kazuko Kawamura, Yukiko Oyanagi-Tanaka, Mari Hoshiyama, Tetsuo Morioka, Fumitake Gejyo, Makoto Uchiyama, and Takashi Oite. "Real-time observation of glomerular hemodynamic changes in diabetic rats: Effects of insulin ARB." Kidney International 66, no. 5 (November 2004): 1939–48. http://dx.doi.org/10.1111/j.1523-1755.2004.00979.x.

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Jung, Chul-Woo, Jin-Tae Kim, and Kook-Hyun Lee. "The Hemodynamic Effects of Insulin Following Overdosage with Levobupivacaine or Racemic Bupivacaine in Dogs." Journal of Korean Medical Science 22, no. 2 (2007): 342. http://dx.doi.org/10.3346/jkms.2007.22.2.342.

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Zanchi, Anne, Christine Perregaux, Marc Maillard, Daniel Cefai, Juerg Nussberger, and Michel Burnier. "The PPARγ agonist pioglitazone modifies the vascular sodium-angiotensin II relationship in insulin-resistant rats." American Journal of Physiology-Endocrinology and Metabolism 291, no. 6 (December 2006): E1228—E1234. http://dx.doi.org/10.1152/ajpendo.00171.2006.

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Glitazones are efficient insulin sensitizers that blunt the effects of angiotensin II (ANG II) in the rat. Sodium chloride is another important modulator of the systemic and renal effects of ANG II. Whether glitazones interfere with the interaction between sodium and the response to ANG II is not known. Therefore, we investigated the effects of pioglitazone on the relationship between sodium and the systemic and renal effects of ANG II in rats. Pioglitazone, or vehicle, was administered for 4 wk to 8-wk-old obese Zucker rats. Animals were fed a normal-sodium (NS) or a high-sodium (HS) diet. Intravenous glucose tolerance tests, systemic and renal hemodynamic responses to ANG II, and the renal ANG II binding and expression of ANG II type 1 (AT1) receptors were measured. The results of our study were that food intake and body weight increased, whereas blood pressure, heart rate, filtration fraction, and insulin levels decreased significantly with pioglitazone in obese rats on both diets. Pioglitazone blunted the systemic response to ANG II and abolished the increased responsiveness to ANG II induced by a HS diet. Pioglitazone modified the renal hemodynamic response to changes in salt intake while maintaining a lower filtration fraction with ANG II perfusion. These effects were associated with a decrease in the number and expression of the AT1 receptor in the kidney. In conclusion, these data demonstrate that the peroxisome proliferator-activated receptor-γ agonist pioglitazone modifies the physiological relationship between sodium chloride and the response to ANG II in insulin-resistant rats.

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Schneider, Stefan, Vanja Sebastian Zander, Tobias Vogt, Vera Abeln, Heiko K. Strüder, Amrei Jacubowski, Heather Carnahan, and Petra Wollseiffen. "Hemodynamic and Neuroendocrinological Responses to Artificial Gravity." Gravitational and Space Research 5, no. 2 (July 21, 2020): 80–88. http://dx.doi.org/10.2478/gsr-2017-0012.

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AbstractThe aim of this study was to determine the hemodynamic and neuroendocrinological responses to different levels and protocols of artificial gravity, especially in comparison to what is expected during a moderate bout of exercise. Ten male participants were exposed to artificial gravity using two different protocols: the first was a centrifugation protocol that consisted of a constant phase of 2 Gz for 30 minutes, and the second consisted of an intermittent phase of 2 Gz for two minutes, separated by resting periods for three minutes in successive order. Near infrared spectroscopy (oxyhemoglobin and deoxyhemoglobin) at the prefrontal cortex, Musculus biceps brachii, and Musculus gastrocnemius, as well as heart rate and blood pressure were recorded before, during, and after exposure to artificial gravity. In order to determine effects of artificial gravity on neuroendocrinological parameters (brain-derived neurotrophic factor, vascular endothelial growth factor, and insulin-like growth factor 1), blood samples were taken before and after centrifugation. During the application of artificial gravity the concentration of oxyhemoglobin decreased significantly and the concentration of deoxyhemoglobin increased significantly in the prefrontal cortex and the Musculus biceps brachii muscle. Participants exposed to the continuous artificial gravity profile experienced peripheral pooling of blood. No changes were observed for brain-derived neurotrophic factor, vascular endothelial growth factor, or insulin-like growth factor 1. Intermittent application of artificial gravity may represent a better-tolerated presentation for participants as hemodynamic values normalize during resting periods. During both protocols, heart rate and arterial blood pressure remained far below what is experienced during moderate physical activity.

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Zhang, Lei, Catherine M. Wheatley, Stephen M. Richards, Eugene J. Barrett, Michael G. Clark, and Stephen Rattigan. "TNF-α acutely inhibits vascular effects of physiological but not high insulin or contraction." American Journal of Physiology-Endocrinology and Metabolism 285, no. 3 (September 2003): E654—E660. http://dx.doi.org/10.1152/ajpendo.00119.2003.

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TNF-α is elevated in many states of insulin resistance, and acutely administered TNF-α in vivo inhibits insulin-mediated hemodynamic effects and glucose uptake in muscle. In this study, we assess whether the inhibitory effects of TNF-α are affected by insulin dose or muscle contraction. Whole body glucose infusion rate (GIR), femoral blood flow (FBF), hindleg vascular resistance, hindleg glucose uptake (HGU), 2-deoxyglucose uptake into muscles of the lower leg (R′g) and hindleg metabolism of infused 1-methylxanthine (1-MX), a measure of capillary recruitment, were determined. Three groups were studied with and without infusion of TNF-α: euglycemic insulin-clamped, one-leg field-stimulated (2 Hz, 0.1 ms at 30 V), and saline-infused control anesthetized rats. Insulin infusions were 3, 10, or 30 mU · kg-1 · min-1 for 2 h. 1-MX metabolism was maximally increased by all three doses of insulin. GIR, HGU, and R′g were maximal at 10 mU and FBF was maximal at 30 mU of insulin. Contraction increased FBF, HGU, and 1-MX. TNF-α (0.5 μg · kg-1 · h-1) totally blocked the 3 and 10 mU insulin-mediated increases in FBF and 1-MX, and partly blocked GIR, HGU, and R′g. None of the increases due to twitch contraction was affected by TNF-α, and only the increase in FBF due to 30 mU of insulin was partly affected. We conclude that muscle capillary recruitment and glucose uptake due to high levels of insulin or muscle contraction under twitch stimuli at 2 Hz are resistant to TNF-α. These findings may have implications for ameliorating muscle insulin resistance resulting from increased plasma TNF-α and for the differing mechanisms by which contraction and insulin recruit capillary flow in muscle.

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Dallinger, Susanne, Anna Sieder, Jeanette Strametz, Michaela Bayerle-Eder, Michael Wolzt, and Leopold Schmetterer. "Vasodilator effects of l-arginine are stereospecific and augmented by insulin in humans." American Journal of Physiology-Endocrinology and Metabolism 284, no. 6 (June 1, 2003): E1106—E1111. http://dx.doi.org/10.1152/ajpendo.00292.2002.

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The amino acid l-arginine, the precursor of nitric oxide (NO) synthesis, induces vasodilation in vivo, but the mechanism behind this effect is unclear. There is, however, some evidence to assume that the l-arginine membrane transport capacity is dependent on insulin plasma levels. We hypothesized that vasodilator effects of l-arginine may be dependent on insulin plasma levels. Accordingly, we performed two randomized, double-blind crossover studies in healthy male subjects. In protocol 1 ( n = 15), subjects received an infusion of insulin (6 mU · kg−1 · min−1for 120 min) or placebo and, during the last 30 min,l-arginine or d-arginine (1 g/min for 30 min). In protocol 2 ( n = 8), subjects receivedl-arginine in stepwise increasing doses in the presence (1.5 mU · kg−1 · min−1) or absence of insulin. Renal plasma flow and glomerular filtration rate were assessed by the para-aminohippurate and inulin plasma clearance methods, respectively. Pulsatile choroidal blood flow was assessed with laser interferometric measurement of fundus pulsation, and mean flow velocity in the ophthalmic artery was measured with Doppler sonography.l-arginine, but not d-arginine, significantly increased renal and ocular hemodynamic parameters. Coinfusion ofl-arginine with insulin caused a dose-dependent leftward shift of the vasodilator effect of l-arginine. This stereospecific renal and ocular vasodilator potency ofl-arginine is enhanced by insulin, which may result from facilitated l-arginine membrane transport, enhanced intracellular NO formation, or increased NO bioavailability.

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Reikerås, O., P. Gunnes, D. Sørlie, R. Ekroth, and O. D. Mjøs. "Hemodynamic and Metabolic Effects of Dopamine and Insulin During Acute Left Ventricular Failure in Dogs." Journal of Cardiovascular Pharmacology 8, no. 2 (March 1986): 303–8. http://dx.doi.org/10.1097/00005344-198603000-00012.

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Kita, Toshihiro, Yoshihiko Suzuki, and Kazuo Kitamura. "Hemodynamic and hormonal effects of exogenous adrenomedullin administration in humans and relationship to insulin resistance." Hypertension Research 33, no. 4 (January 22, 2010): 314–19. http://dx.doi.org/10.1038/hr.2009.236.

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Koskenkari, Juha K., Päivi K. Kaukoranta, Kai T. Kiviluoma, M. J. Pekka Raatikainen, Pasi P. Ohtonen, and Tero I. Ala-Kokko. "Metabolic and Hemodynamic Effects of High-Dose Insulin Treatment in Aortic Valve and Coronary Surgery." Annals of Thoracic Surgery 80, no. 2 (August 2005): 511–17. http://dx.doi.org/10.1016/j.athoracsur.2005.03.024.

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Daoud Naccache, Deeb, Sergey Yalonetsky, and Ronen Bar-Yoseph. "Acute Effects of Insulin on Cardiac Function in Patients with Diabetes Mellitus: Clinical Applicability and Feasibility." International Journal of Endocrinology 2020 (March 17, 2020): 1–8. http://dx.doi.org/10.1155/2020/8134548.

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Background. Insulin promotes glucose consumption as the main cardiac energy source, while increasing myocardial efficiency. The short-term effects of insulin on cardiac function and its potential curative role in an acute diabetological cardiology setting remain unknown. Our study evaluated the role of acute insulin administration in the diabetic heart, its corresponding effective blood insulin level, and the time-course applicability of insulin treatment in a routine clinical setting. Methods. We evaluated a case series of six male (48.1 ± 4.9 y/o) patients with controlled diabetes (HbA1c of 6.6 ± 0.3%) and disease duration of 14.4 ± 6.7 yr. Each subject was evaluated for glucose homeostasis, as well as hemodynamic and echocardiographic (systolic and diastolic) parameters at three points: baseline followed by two successive insulin loads in euglycemic hyperinsulinemic clamp study. Results were analysed using Student’s t-test. Results. The first insulin load led to a physiologic blood insulin level of 145 ± 36 μU/ml, and both systolic (7 mmHg) blood pressure and diastolic (4 mmHg) blood pressure decreased significantly. Left ventricular fractional shortening (LVFS) increased significantly by 11.8%. Diastolic function parameters of mitral annulus movement of the A′ wave increased relative to baseline by 20.0% (27.8% under the second insulin load), A′ medial increased relative to baseline by 30%, and A′ lateral increased relative to baseline by 17%, displayed by tissue Doppler imaging. Conclusions. Insulin acutely affected the diabetic heart at a physiologic level within a 2 h time course. Insulin mainly increased left ventricular systolic function and, to a second degree, improved left ventricular diastolic functions and atrial systole in diabetic subjects. These results may facilitate the development of insulin-based acute treatment in diabetic patients with cardiac morbidity. This trial is registered with NCT02962921.

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Leibel, R. L., E. M. Berry, and J. Hirsch. "Metabolic and hemodynamic responses to endogenous and exogenous catecholamines in formerly obese subjects." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 4 (April 1, 1991): R785—R791. http://dx.doi.org/10.1152/ajpregu.1991.260.4.r785.

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Formerly or reduced-obese (RO) subjects exhibit diminished systemic energy requirements for weight maintenance. Based on studies in animals and humans, there is reason to believe that the autonomic nervous system (ANS) plays an important role in coordinate regulation of energy metabolism and may be altered in the RO state. We have, therefore, investigated aspects of autonomic physiology in obese (OB), RO, and never obese (NO) subjects subjected to insulin-mediated hypoglycemia and incremental intravenous infusions of epinephrine. Total catecholamine secretion during insulin-induced hypoglycemia was significantly lower in the RO. The RO showed increased sensitivity to in vivo lipolytic and cardiovascular effects of endogenous and infused catecholamines. In these studies, OB subjects responded more like the NO subjects than did the RO. The RO display characteristic changes in autonomic status that may play a role in their enhanced energy efficiency.

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Forjaz, Cláudia L. M., Paulo R. Ramires, Taís Tinucci, Kátia C. Ortega, Heloísa E. H. Salomão, Edna C. Ignês, Bernardo L. Wajchenberg, Carlos E. Negrão, and Décio Mion. "Postexercise responses of muscle sympathetic nerve activity and blood flow to hyperinsulinemia in humans." Journal of Applied Physiology 87, no. 2 (August 1, 1999): 824–29. http://dx.doi.org/10.1152/jappl.1999.87.2.824.

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Although insulin and exercise cause dramatic changes in physiological parameters, the impact of exercise on neural and hemodynamic responses to insulin administration has not been described. In a study of the effects of a single bout of exercise on blood pressure (BP), muscle sympathetic nerve activity (MSNA), and forearm blood flow (FBF) responses to insulin infusion during the postexercise period, 11 healthy men underwent, in a random order, two hyperinsulinemic euglycemic clamps performed after 45 min of 1) bicycle exercise (50% peak O2 uptake, Exercise session) and 2) seated rest (Control session). Data were analyzed during baseline and steady-state periods. Although insulin levels and insulin sensitivity were similar, baseline plasma glucose levels were significantly lower in the Exercise than in the Control session. Mean BP was significantly lower (3%) and FBF was higher (27%) in the Exercise session. Exercise increased insulin-induced MSNA enhancement (84%) without changing FBF and BP responses to hyperinsulinemia. In conclusion, a single bout of exercise that does not alter insulin sensitivity exacerbates insulin-induced increase in MSNA without changing FBF and BP responses to hyperinsulinemia.

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Hoogenberg, K., W. J. Sluiter, G. Navis, T. W. Van Haeften, A. J. Smit, W. D. Reitsma, and R. P. Dullaart. "Exogenous norepinephrine induces an enhanced microproteinuric response in microalbuminuric insulin-dependent diabetes mellitus." Journal of the American Society of Nephrology 9, no. 4 (April 1998): 643–54. http://dx.doi.org/10.1681/asn.v94643.

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Exogenous norepinephrine (NE) increases intraglomerular pressure in animal experiments, but it is unknown whether NE induces a microproteinuric response in humans. Moreover, it has not been studied whether possible microproteinuric and renal hemodynamic changes induced by NE are altered in insulin-dependent diabetes mellitus (IDDM) complicated by microalbuminuria. Therefore, the microproteinuric and renal hemodynamic responses to exogenous NE infusions were measured in eight matched normoalbuminuric IDDM patients (group D1), microalbuminuric IDDM patients (group D2), and control subjects (group C). As anticipated, mean arterial pressure (MAP)-NE dose-response curves were significantly shifted leftward in groups D1 and D2 compared with group C (P < 0.05), indicating a higher systemic NE responsiveness in IDDM. On separate days, NE or placebo was infused at individually determined NE threshold doses (T; delta MAP = 0 mmHg), 20% pressor doses (20% P; delta MAP = 4 mmHg), and pressor doses (P; delta MAP = 20 mmHg), with measurement of urinary albumin (UalbV), IgG excretion (UIgGV), GFR (by 125I-iothalamate), and effective renal plasma flow (by 131I-hippurate). At NE pressor dose, UalbV and UIgGV rose in all groups (P < 0.05 to 0.01), whereas urinary beta 2-microglobulin was unchanged. The increases in UalbV and UIgGV were more pronounced in the microalbuminuric group than in the other groups (P < 0.05). An NE dose-dependent fall in effective renal plasma flow and rise in filtration fraction were found in all groups (P < 0.05 to 0.001 for all), whereas GFR did not change significantly. The renal hemodynamic dose-response relationship was similar in the groups. In conclusion, exogenous NE acutely promotes glomerular protein leakage, and it is plausible that intraglomerular NE effects contribute to this phenomenon. The microproteinuric response is enhanced in microalbuminuric IDDM despite unaltered renal hemodynamic responsiveness, which may reflect a specific NE response or a general effect of vasopressor stimuli to promote glomerular protein leakage in patients with a preexistent defect in glomerular permselectivity.

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Vehkavaara, Satu, Jukka Westerbacka, Tiina Hakala-Ala-Pietilä, Antti Virkamäki, Outi Hovatta, and Hannele Yki-Järvinen. "Effect of Estrogen Replacement Therapy on Insulin Sensitivity of Glucose Metabolism and Preresistance and Resistance Vessel Function in Healthy Postmenopausal Women1." Journal of Clinical Endocrinology & Metabolism 85, no. 12 (December 1, 2000): 4663–70. http://dx.doi.org/10.1210/jcem.85.12.7034.

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In the present study, we hypothesized that estradiol, via its ability to vasodilate in an endothelium-dependent manner, might enhance vascular effects of insulin. Basal and insulin-stimulated peripheral blood flow and resistance, arterial stiffness, and glucose metabolism were determined in 27 healthy postmenopausal women before and after 12 weeks of treatment with either transdermal or oral estradiol or corresponding placebo preparations. Whole body insulin sensitivity was determined using the euglycemic insulin clamp technique (rate of continuous insulin infusion 1 mU/kg·min), forearm blood flow with a strain-gauge plethysmography, and arterial stiffness using pulse wave analysis. Estradiol therapy increased basal peripheral blood flow (1.5 ± 0.1 vs. 1.9 ± 0.1 mL/dL·min, 0 vs. 12 weeks; P < 0.01), decreased peripheral vascular resistance (65 ± 3 vs. 52± 3 mm Hg/mL/dL·min, respectively; P < 0.01), and diastolic blood pressure (78 ± 2 vs. 75± 2 mm Hg, respectively; P < 0.05) but had no effect on large artery stiffness. Infusion of insulin did not acutely alter peripheral blood flow but diminished large artery stiffness significantly both before and after the 12-week period of estradiol therapy. No measure of acute insulin action (glucose metabolism, blood flow, or large artery stiffness) was altered by estradiol or placebo treatment. These data demonstrate that insulin and estradiol have distinct hemodynamic effects. Physiological doses of estradiol increase peripheral blood flow but have no effects on large artery stiffness, whereas physiological concentrations of insulin acutely decrease stiffness without changing peripheral blood flow. Putative vasculoprotection by estradiol is, thus, not mediated via alterations in arterial stiffness or insulin sensitivity.

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Waldstein, S. R., and H. O. Burns. "GENDER AND INSULIN EFFECTS ON STRESS-INDUCED HEMODYNAMIC RESPONSE, LIPOPROTEIN LIPIDS, AND ANTHROPOMETRICS IN YOUNG ADULTS." Psychosomatic Medicine 60, no. 1 (1998): 135. http://dx.doi.org/10.1097/00006842-199801000-00193.

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Rocchini, Albert P., Robert F. Wilson, Paul Marker, and Tereza Cervenka. "Metabolic and Hemodynamic Effects of a Graded Intracoronary Insulin Infusion in Normal and Fat Anesthetized Dogs." Hypertension 27, no. 3 (March 1996): 354–59. http://dx.doi.org/10.1161/01.hyp.27.3.354.

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Ilercil, A. "The Cardiac and Hemodynamic Effects of Insulin on Non-diabetic American Indians: The Strong Heart Study." Journal of the American College of Cardiology 31, no. 2 (February 1998): 526A. http://dx.doi.org/10.1016/s0735-1097(97)88290-3.

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Ilercil, A., M. J. Roman, M. Paranicas, M. J. O'Grady, T. K. Welty, R. R. Fabsitz, B. V. Howard, E. T. Lee, and R. B. Devereux. "The cardiac and hemodynamic effects of insulin on non-diabetic American Indians: the strong heart study." Journal of the American College of Cardiology 31 (February 1998): 526. http://dx.doi.org/10.1016/s0735-1097(98)80641-4.

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Tapia, Edilia, Magdalena Cristóbal, Fernando E. García-Arroyo, Virgilia Soto, Fabiola Monroy-Sánchez, Ursino Pacheco, Miguel A. Lanaspa, et al. "Synergistic effect of uricase blockade plus physiological amounts of fructose-glucose on glomerular hypertension and oxidative stress in rats." American Journal of Physiology-Renal Physiology 304, no. 6 (March 15, 2013): F727—F736. http://dx.doi.org/10.1152/ajprenal.00485.2012.

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Fructose in sweetened beverages (SB) increases the risk for metabolic and cardiorenal disorders, and these effects are in part mediated by a secondary increment in uric acid (UA). Rodents have an active uricase, thus requiring large doses of fructose to increase plasma UA and to induce metabolic syndrome and renal hemodynamic changes. We therefore hypothesized that the effects of fructose in rats might be enhanced in the setting of uricase inhibition. Four groups of male Sprague-Dawley rats ( n = 7/group) were studied during 8 wk: water + vehicle (V), water + oxonic acid (OA; 750 mg/k BW), sweetened beverage (SB; 11% fructose-glucose combination) + V, and SB + OA. Systemic blood pressure, plasma UA, triglycerides (TG), glucose and insulin, glomerular hemodynamics, renal structural damage, renal cortex and liver UA, TG, markers of oxidative stress, mitDNA, fructokinase, and fatty liver synthase protein expressions were evaluated at the end of the experiment. Chronic hyperuricemia and SB induced features of the metabolic syndrome, including hypertension, hyperuricemia, hyperglycemia, and systemic and hepatic TG accumulation. OA alone also induced glomerular hypertension, and SB alone induced insulin resistance. SB + OA induced a combined phenotype including metabolic and renal alterations induced by SB or OA alone and in addition also acted synergistically on systemic and glomerular pressure, plasma glucose, hepatic TG, and oxidative stress. These findings explain why high concentrations of fructose are required to induce greater metabolic changes and renal disease in rats whereas humans, who lack uricase, appear to be much more sensitive to the effects of fructose.

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Effat, Hassan, Ramy Khaled, Ahmed Battah, Mohamed Shehata, and Waleed Farouk. "Effect of Glucose-Insulin-Potassium Infusion on Hemodynamics in Patients with Septic Shock." Open Access Macedonian Journal of Medical Sciences 9, B (November 23, 2021): 1517–24. http://dx.doi.org/10.3889/oamjms.2021.6641.

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BACKGROUND: Glucose-insulin-potassium (GIK) demonstrates a cardioprotective effect by providing metabolic support and anti-inflammatory action, and may be useful in septic myocardial depression. AIM: The aim of this study was to assess role of GIK infusion in improving hemodynamics in patients with septic shock in addition to its role in myocardial protection and preventing occurrence of sepsis-induced myocardial dysfunction and sepsis-induced arrhythmias. METHODS: This study was conducted on 75 patients admitted to the Critical Care Department in Cairo University Hospital with the diagnosis of septic shock during the period from January 2019 to December 2019. Patients were divided into two groups; first group was managed according to the last guidelines of surviving sepsis campaign and was subjected to the GIK infusion protocol while second group was managed following the last guidelines of surviving sepsis campaign only without adding GIK infusion. RESULTS: Patients in the GIK group showed better lactate clearance (50% vs. 46.7%) and less time needed for successful weaning of vasopressors than the control group (3.57±1.16 vs. 3.6±1.45 days) thought not reaching statistical significance. There was no statistically significant difference between both groups regarding development of septic-induced cardiomyopathy (16.7% in the control group vs. 13.3% in the GIK group); however, patients with hypodynamic septic shock showed better improvement in hemodynamic profile in the GIK group. Sepsis-induced arrhythmias occurred more in patients of the control group than in patients of the GIK group with no statistically significant difference between both groups (33.3% vs. 20%, p = 0.243). Few side effects were developed as a result of using GIK infusion protocol. CONCLUSIONS: GIK may help in improving hemodynamics and weaning of vasopressors in patients with refractory septic shock and those with septic induced cardiomyopathy. The use of GIK was well tolerated with minimal adverse reactions.

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Polak, Kaija, Leopold Schmetterer, Alexandra Luksch, Susanna Gruber, Elzbieta Polska, Vanessa Peternell, Michaela Bayerle-Eder, Michael Wolzt, Michael Krebs, and Michael Roden. "Free fatty acids/triglycerides increase ocular and subcutaneous blood flow." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 1 (January 1, 2001): R56—R61. http://dx.doi.org/10.1152/ajpregu.2001.280.1.r56.

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Elevated plasma free fatty acids (FFA) induce skeletal muscle insulin resistance and impair endothelial function. The aim of this study was to characterize the acute hemodynamic effects of FFA in the eye and skin. A triglyceride (Intralipid 20%, 1.5 ml/min)/heparin (bolus: 200 IU; constant infusion rate: 0.2 IU · kg−1· min−1) emulsion or placebo was administered to 10 healthy subjects. Measurements of pulsatile choroidal blood flow with laser interferometry, retinal blood flow with the blue field entoptic technique, peak systolic and end diastolic blood velocity (PSV, EDV) in the ophthalmic artery with Doppler sonography, and subcutaneous blood flow with laser Doppler flowmetry were performed during an euglycemic somatostatin-insulin clamp over 405 min. Plasma FFA/triglyceride elevation induced a rise in pulsatile choroidal blood flow by 25 ± 3% ( P < 0.001) and in retinal blood flow by 60 ± 23% ( P= 0.0125). PSV increased by 27 ± 8% ( P = 0.001), whereas EDV was not affected. Skin blood flow increased by 149 ± 38% ( P = 0.001). Mean blood pressure and pulse rate remained unchanged, whereas pulse pressure amplitude increased by 17 ± 5% ( P = 0.019). Infusion of heparin alone had no hemodynamic effect in the eye or skin. In conclusion, FFA/triglyceride elevation increases subcutaneous and ocular blood flow with a more pronounced effect in the retina than in the choroid, which may play a role for early changes of ocular perfusion in the insulin resistance syndrome.

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Giugliano, D. "Hemodynamic and Metabolic Effects of Transdermal Clonidine in Patients With Hypertension and Non–Insulin-Dependent Diabetes Mellitus." American Journal of Hypertension 11, no. 2 (February 1998): 184–89. http://dx.doi.org/10.1016/s0895-7061(97)00319-1.

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50

Bochkareva, E. V., O. V. Alexandrovich, P. Yu Bardybakhin, E. K. Butina, N. G. Kucheryavaya, I. N. Ozerova, and V. A. Metelskaya. "Antiischemic effects of metoprolol and the risk of carbohydrate metabolism disturbances in angina patients." Cardiovascular Therapy and Prevention 11, no. 6 (December 20, 2012): 23–28. http://dx.doi.org/10.15829/1728-8800-2012-6-23-28.

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Aim. To study the association between antiischemic effects (AIE) of metoprolol (MP), glucose tolerance, and insulin sensitivity in patients with stable angina (SA). Material and methods. The study included 28 male patients, aged 46-68 years, with stable effort angina, Functional Class II-III, and positive exercise stress test (EST). The time of the ST segment depression by ≥1 mm defined the threshold exercise stress time. MP in a selected dose was administered twice a day, for one month. Its hemodynamic effects were assessed by the dynamics of heart rate (HR), blood pressure (BP), and double product (DP). Glucose tolerance test (GTT) was performed at baseline (before MP administration) and after one month of MP treatment. Tissue insulin sensitivity and insulin resistance (IR) were assessed by ISI0.120 and HOMA-IR parameters, respectively. Results. AIE was registered in 57% of the patients, while 43% failed to demonstrate it. Both groups did not differ by the extent of MP impact on the levels of HR, BP, and DP. The presence or absence of AIE was linked to selected parameters of glucose metabolism. In patients with AIE, the pre-treatment levels of glucose and insulin 2 hours after glucose load were higher (p=0,028 and 0,043, respectively) and ISI1,120 values lower than in patients without AIE (p=0,023). Among participants with AIE, impaired glucose tolerance (IGT) was observed in 4 at baseline and in 8 one month later; among patients without AIE, IGT was not registered. Conclusion. For the first time, the presence of AIE during MP therapy of SA patients was linked to the decreased insulin sensitivity of peripheral tissues (ISI0.120). Paired EST with a single MP dose at baseline provides an opportunity to identify the patients with a higher risk of metabolic disturbances during the longer-term MP treatment.

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Journal articles on the topic 'Hemodynamic effects of insulin'

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