Effect of hyperosmolality on vascular resistance and lymph flow in the cat ileum

Levine, Stephen B.; Granger, D. Neil; Brace, R. A.; Taylor, A. E.

doi:10.1152/ajpheart.1978.234.1.h14

Cited by 21 publications

(21 citation statements)

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“…Indeed, earlier intravital videomicroscopy studies of the rat's cremaster muscle have shown that the magnitude of arteriolar dilation evoked by hyperosmolar solutions of dextrose, sucrose, or sodium chloride was similar but that the dilation rate constant differs among the three hyperosmolar solutions (2). Other perfusion studies of the dog's forelimb (28) and cat's ileum (29) have found that both the magnitude and the time course of the dilatory effects of hyperosmolar dextrose and sodium chloride solutions differed significantly. These data on the intestinal vasoactivity suggest that hypertonic glucose-based solutions dilate the intestinal microvasculature by at least two mechanisms: One is an instantaneous microvascular vasodilation related to the osmotic stress, and the second is a more insidious, time-dependent vasodilation, stimulated by an energy-dependent transport of glucose into cells.…”

Section: Vascular Reactivitymentioning

confidence: 98%

Disparity in Osmolarity-Induced Vascular Reactivity

Zakaria

Hunt²,

Li³

et al. 2005

Journal of the American Society of Nephrology

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Conventional peritoneal dialysis solutions (PDS) are vasoactive. This study was conducted to identify vasoactive components of PDS and to describe quantitatively such vasoactivity. Anesthetized nonheparinized rats were monitored continuously for hemodynamics while the microvasculature of the jejunum was studied with in vivo intravital microscopy. In separate experiments, vascular reactivity of rat endothelium-intact and -denuded aortic rings (2 mm) was studied ex vivo in a standard tissue bath. In both studies, suffusion of the vessels was performed with filter-sterilized isotonic and hypertonic solutions that contained glucose or mannitol as osmotic agents. PDS served as a control (Delflex 2.25%). Hypertonic glucose and mannitol solutions produced a significant vascular reactivity in aortic rings and instantaneous and sustained vascular relaxation at all levels of the intestinal microvasculature. Similarly, lactate that was dissolved in a low-pH isotonic physiologic salt solution produced significant force generation in aortic rings. Whereas isotonic glucose and mannitol solutions had no vasoactivity in aortic rings, isotonic glucose produced a selective, insidious, and time-dependent vasodilation in the intestinal premucosal arterioles ( C onventional peritoneal dialysis solutions (PDS) dilate visceral and parietal microvasculature by mechanisms possibly related to hyperosmolality, low pH, and the buffer anion system of these solutions (1,2). Studies of hyperosmolar sodium solutions perfused into the intestinal lymph produced vasodilation of submucosal arterioles through a mechanism partially mediated by a hyperosmolality-induced nitric oxide (NO) release (3). Similarly, intravenous infusion of hypertonic galactose or mannitol solutions in pigs increased the baseline hepatic blood flow by 37%, presumably by a mechanism attributed to an osmotic stress (4). Massett et al. (5) found that in vitro infusion of isolated, cannulated, and pressurized skeletal muscle arterioles with hypertonic solutions of glucose, sucrose, or mannitol at an osmolality of 330 mOsmol/kgH 2 O equally dilates these arterioles. This vascular reactivity seems to be an endothelium-dependent response, which is independent of the NO or the cyclooxygenase pathways, but can be nearly abolished by glibenclamide, an ATP-sensitive potassium channel inhibitor. Similar results were obtained with coronary arterioles perfused ex vivo with either hypertonic glucose or sucrose solutions. In these vessels, only glibenclamide caused attenuation of the hypertonic solution-mediated vascular relaxation. In addition, inhibition of inward rectifier potassium channels or calcium activated potassium channels had no effect on hyperosmolality-induced vascular reactivity (6,7). Our recent intravital videomicroscopy of the terminal ileum in rats showed that exposure of the ileum to a conventional PDS produces an instantaneous and sustained vascular relaxation at all levels of the microvasculature, which is essentially associated with doubling of blood flow in the in...

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Section: Vascular Reactivitymentioning

confidence: 98%

Disparity in Osmolarity-Induced Vascular Reactivity

Zakaria

Hunt²,

Li³

et al. 2005

Journal of the American Society of Nephrology

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“…The repercussions of a rise in plasma osmolality of the order of 30 mOsm kg-' on mesenteric resistance and intrahepatic blood distribution are unknown. It has been reported that moderate increases in plasma osmolality, of the order of 5 mOsm kg-', enhance hepatic blood flow by about 10% (Levine et al, 1978;Richardson & Withrington, 1980). On the other hand, Ballet et al (1988) reported that increasing concentrations of AVP were able to augment portal resistances even in the presence of enhanced hepatic blood flow.…”

Section: Resultsmentioning

confidence: 99%

Effect of dehydration and hyperosmolal hydration on lignocaine and metabolites disposition in conscious rabbits

Chamelian

Lécrivain

Robichaud

et al. 1994

British J Pharmacology

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The present study aimed to investigate the effect of dehydration and hyperosmolal hydration on the disposition of lignocaine and two of its metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX). Lignocaine was infused to three groups of conscious rabbits: controls, rabbits previously deprived of water for 48 h and rabbits receiving an infusion of 2.5% NaCl. In dehydrated and hyperosmolal‐hydrated rabbits, plasma osmolality was 321 ± 1 and 313 ± 1 mOsm kg−1, respectively (P<0.01 compared to controls, 285 ± 1 mOsm kg−1). In dehydrated animals, baseline values of plasma arginine vasopressin (AVP) concentrations and plasma renin activity (PRA) were higher than in controls, i.e. 12.4 ± 1.4 pg ml−1 and 15.4 ± 1.7 ng AI ml−1 h−1 vs. 3.4 ± 0.2 pg ml−1 (P<0.01), and 5.1 ± 0.6 ng AI ml−1 h−1 (P<0.01), respectively; atrial natriuretic peptide (ANP) decreased from 55 ± 11 to 32 ± 4 pg ml−1 (P<0.05). Compared to controls, hyperosmolal hydration only increased AVP to 15.5 ± 0.7 pg ml−1 (P<0.01). Under both experimental conditions, lignocaine plasma concentrations were almost double (P<0.01) those in controls, due to a lower systemic clearance, e.g. 54 ± 3 and 59 ± 1 vs. 96 ± 5 ml min−1 kg−1, respectively. Plasma levels of MEGX increased (P<0.01) only in dehydrated animals, although GX plasma concentrations were augmented (P<0.01) about three fold in both groups of animals. The changes in lignocaine plasma concentrations were correlated with AVP levels (R2 = 0.5168, P<0.001). To document the effect of AVP on hepatic plasma flow, another group of rabbits received on separate occasions two doses of AVP (17 and 84 ng kg−1) while receiving an infusion of indocyanine green. AVP reduced hepatic plasma flow from 38.9 ± 2.7 ml min−1 to 19.6 ± 2.5 ml min−1 (P<0.01). The predicted maximal AVP‐induced decrease in hepatic plasma flow was 19.6 ml min−1 kg−1 (Emax), and AVP concentration eliciting 50% of Emax (ED50) was 28.7 pg ml−1. It is concluded that both dehydration and hyperosmolal hydration alter the disposition of lignocaine and two of its metabolites.

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“…These effects can be reproduced even when rapid injections are given systemically, al though slower infusions cause no demonstra ble effects [24]. Thus these findings, if not fulfilling some local functional requirement [7,18,21], are hard to understand in physio logical terms [17].…”

Section: Discussionmentioning

confidence: 99%

“…TDL flow increased during the hyperosmolar infusions, giving a high degree of correlation with infusion time (r = 0.88 and 0.94, for 1-and 2-M infusions, respectively). These results indicate that hyperosmolar loading has only fluid physiological effects under normotensive conditions.There is considerable evidence in the liter ature to show that induced states of hyperos molality cause striking cardiovascular altera tions [1,16,17], Only one report, however, questions whether the many investigations have merely documented pharmacological and not physiological events, due to the ex …”

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confidence: 99%

“…Most authors agree that the solute chosen to induce hyperosmolality has only minor qualitative significance regarding the effects observed [17]. Although experimentally in duced states of hyperosmolality should be associated with both fluid shifts and/or car diovascular effects, no previous report has successfully documented these interrelated events in the normal intact animal.…”

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confidence: 99%

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Cardiovascular and Lymph Flow Changes Caused by Physiological Hyperosmolar Provocation in Unanesthetized Rats

Quiros¹,

Ware²

1984

Eur Surg Res

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Cardiovascular and thoracic duct lymph (TDL) flow alterations were investigated in non-starved rats, lightly sedated with neuroleptanalgesia, before and after osmolar loading. 0.29-, 1.0- and 2.0-M xylose solutions were infused at the rate of 4 ml × h^–1 for 20 min. Neither control animals receiving 0.29-M infusions (iso-osmolar) nor those which received 1- and 2-M infusions showed any detectable changes in cardiac output, heart rate, total peripheral resistance or any organ and tissue flow. On the other hand, TDL flow increased during the hyperosmolar infusions, giving a high degree of correlation with infusion time (r = 0.88 and 0.94, for 1- and 2-M infusions, respectively). These results indicate that hyperosmolar loading has only fluid physiological effects under normotensive conditions.

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Effect of hyperosmolality on vascular resistance and lymph flow in the cat ileum

Cited by 21 publications

References 0 publications

Disparity in Osmolarity-Induced Vascular Reactivity

Disparity in Osmolarity-Induced Vascular Reactivity

Effect of dehydration and hyperosmolal hydration on lignocaine and metabolites disposition in conscious rabbits

Cardiovascular and Lymph Flow Changes Caused by Physiological Hyperosmolar Provocation in Unanesthetized Rats

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