Hypertonic Glucose Infusion Research Articles

Protection of the Myocardium with High-Energy Solutions

An approach to intraoperative protection of the myocardium is described that attempts to increase glucose utilization by infusion of high-energy solutions during aortic cross-clamping. Infusion of hypertonic glucose or glucose plus insulin prior to aortic cross-clamping has enhanced contractility and increased high-energy phosphate moieties in animals with induced ischemia. Recent pilot experiments in our laboratory suggest that infusions of creatine may result in increased production of creatine phosphate, which in turn induces phosphorylation of adenosine diphosphate to adenosine triphosphate, possibly enhancing myocardial contractility. The intraoperative clinical benefits of these infusions remain to be proved, however.

Transcapillary Fluid Movements in Sympathectomized Intestine and Skin during Hemorrhagic Hypotension

Net transcapilary fluid exchange in skin tissue (paw) and small intestine was observed during a 90 min period of hemorrhagic hypotension at 50 mm Hg in the cat. Reflex fluid transfer was prevented by regional sympathectomy and chi-adrenergic blockade. Early in hemorrhage, fluid absorption from the extravascular space occurred in both tissues, apparently caused by osmosis. The process was thus co-ordinated in time with a positive arterio-venous osmolar difference, in turn caused by a marked arterial hypersomolality. Experimetnal arterial hyperosomolality of similar magnitude, created by i.v. infusion of hypertonic glucose in non-bled animals, led to transcapillary fluid absorption in both intestine and skin and at rates similar to those in bleeding. Regional hypotsionen per se caused no fluid absorption. Later in hemorrhage (greater than 30 min), plasma fluid moved into the extravascular space both in skin and intestine, apparently due to a gradual increase of cappilary hydrostatic pressure. It is concluded that the arterial hypersomolality during bleeding can cause transcapillary fluid absorption in intestinal and skin tissues, as previously shown for skeletal muscle (Järhult 1973). The hemodynamic significance of this process for plasma volume regulation in hemorrhage is, however, much greater in skeletal muscle than in intestine and skin, mainly due to the much larger total mass of the muscle tissue.

Postoperative hypoglycemia in congenital hypertrophic pyloric stenosis.

One infant with congenital hypertrophic pyloric stenosis developed severe hypoglycemia with lethargy, irritability, cyanosis, and convulsions in the immediate postoperative period after Fredet-Ramstedt pyloromytomy. A likely hypothesis for this mechanism has been reported as hepatic glycogen depletion secondary to malnutrition. Any infant with malnutrition, from whatever cause, should be assumed to have glycogen depletion, and repletion should be started and continued with all intravenous fluids given during the preoperative period. Hypoglycemia should be suspected when an infant develops any unusual or unexplained symptoms or findings in the immediate postoperative period. Prompt and intensive treatment with intravenous hypertonic glucose infusion must be begun and continued until blood glucose determinations remain at a safe level with oral feedings alone.

Rapid hypertonic glucose infusion: Organ location of label after [ 14C]glucose during hemorrhagic shock

Fifty rabbits were bled to a blood pressure of 40 mmHg, and 15 were not bled. [ 14C]Glucose was given intravenously to all animals. Those animals bled also received an equiosmolar dose of 50% glucose or normal saline. In 30 rabbits, the administered osmolar load per kilogram of 50% glucose or saline was constant, regardless of the volume deficit which varies with this shock model. In 10 rabbits, both the osmolar load of 50% glucose or saline and the volume deficit were kept constant. In an additional 10 rabbits, the amount of 50% glucose was increased by a factor of five. Animals were killed after 5, 30, or 60 min of shock. Normal saline increased blood pressure more slowly but the effect was prolonged. Hypertonic glucose rapidly but transiently increased blood pressure in rabbits after hemorrhagic shock. The myocardium of rabbits given 50% glucose did not contain a statistically significant different amount of label than that of rabbits given saline at 5, 30, or 60 min after shock. This suggests that the rapid and transient increase in blood pressure is not mediated by an increased absolute content or tissue uptake of glucose in the myocardium but is related to a rapid extracellular hyperosmotic effect.

Uptake of materials by the intact liver. The exchange of glucose across the cell membranes.

D-Glucose equilibrates within liver cells. We have studied its process of entry into and exit from these cells with the multiple indicator dilution technique. Labeled red cells (a vascular indicator), labeled sucrose (an extracellular reference), and labeled D-glucose were rapidly injected into the portal vein, and from serially sampled hepatic venous blood, normalized outflow-time patterns were obtained. The labeled red cell curve rises to an early high peak, and decays rapidly; and that for sucrose reaches a later and lower peak and decays less rapidly, but generates an equivalent area. The curve for labeled D-glucose begins with that for labeled sucrose, gradually rises to a peak which is later and substantially lower than that for sucrose, and then decreases slowly. At high glucose levels this curve assumes a squared-off shape, rises fairly quickly to its highest level, at the time of the sucrose peak, and then slowly decreases. Phlorizin and galactose infusion result in the emergence of a pronounced early peak, under the sucrose peak; and the curve for tracer L-glucose approaches that for sucrose. We resolve from the D-glucose curves, by model analysis, two components: throughout material, which has not entered the cells; and exchanging material, which has entered and later returned to the circulation. The analysis provides estimates of the kinetic entrance and exist coefficients; and from these, saturation of both the entrance and exit processes was evident. The characteristic transport parameters were determined. For both entrance and exit, a common Km, 2,170 mg/100 ml, and transport maximum, 5.13 mg s-1 (ml intracellular fluid)-1, were found. Both these values are exceedingly large. Several other phenomena were defined which additionally characterize the transport process: phlorizin and galacose produced competitive inhibition; the transport process was found to be relatively stereospecific; and sudden infusion of hypertonic glucose produced counter-transport of labeled D-glucose.

Letter to the Editor

Quantitative studies to determine the exact amount of insulin received by a patient under the conditions of insulin-glucose therapy for Reye's syndrome would be academically desirable. We admit that some insulin activity can be lost by nonspecific binding to the tubing and glassware. However, we cannot agree that the Reye's syndrome patients treated with "slow" intravenous infusion of hypertonic glucose and insulin may not have received any insulin. Thinner control films were less permeable than thicker control films.

Maximum tubular reabsorption capacity for glucose and renal hemodynamcis during rapid hypertonic glucose infusion in normal and diabetic subjects.

It is demonstrated that the maximum tubular reabsorption capacity for glucose (Tmo) is significantly increased in young patients with diabetes of short duration. (Mean value for diabetics: 419±50 mg/min (n = 10); mean value for normals: 352±64 mg/min (n = 9). GFR is also significantly increased in diabetics. For the whole material there was a clear positive correlation between GFR and Tmc. In the normal subjects GFR was constant during the high glucose level, whereas RPF increased. In the diabetics, RPF was constant but GFR decreased consistently about 9 per cent. In both diabetics and normals there was a decrease in urinary potassium excretion and an increase in urinary sodium excretion during glucose infusion.

Hypertonic glucose infusion during labor: Maternal-fetal serum insulin relationships

Determinations of serum immunoreactive insulin (IRI) were done in venous samples from 22 normal women in labor before and after receiving a 10 minute intravenous infusion of glucose. Serial samples were also obtained from the scalps of their fetuses during the 90 minute period of observations. An early and sustained serum insulin response to the infusion was observed in the mothers, but the fetal IRI response was not evident until 40 minutes after the end of the infusion. The highest fetal IRI values were observed approximately one hour after the fetal blood glucose peak. A transplacental load of glucose to the human fetus seems to produce a delayed IRI response similar to that seen in normal newborn infants after intravenous glucose tolerance tests.

Hypertonic glucose infusion during labor: Maternal-fetal blood glucose relationships

Maternal-fetal blood glucose relationships were studied in 32 patients in labor before and after an infusion of glucose. Maternal and fetal hyperglycemic responses to the infusion were not parallel. The fetal peak occurred 10 minutes after the maternal, and the fetal glucose levels declined more slowly. There was not a constant glucose gradient or ratio between the materal and fetal compartments. Evidence for placental transfer of glucose by facilitated diffusion is presented and glucose disappearance rates were calculated on mothers and fetuses. A more basic understanding of carbohydrate metabolism in normal and abnormal pregnancies is needed before new therapeutic regimens involving the use of glucose can be evaluated.

Pulmonary blood volume in hemorrhagic shock in the dog and primate.

ARTICLESPulmonary blood volume in hemorrhagic shock in the dog and primateFL Abel, JA Waldhausen, WJ Daly, and WL PearceFL Abel, JA Waldhausen, WJ Daly, and WL PearcePublished Online:01 Nov 1967https://doi.org/10.1152/ajplegacy.1967.213.5.1072MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAcute hemorrhagic shock decreases airway resistance in anesthetized ratSam Bayat, Gergely Albu, Skander Layachi, Flore Portier, Marc Fathi, Ferenc Peták, and Walid Habre1 August 2011 | Journal of Applied Physiology, Vol. 111, No. 2Autonomic activation links CNS oxygen toxicity to acute cardiogenic pulmonary injuryIvan T. Demchenko, S. Yu Zhilyaev, A. N. Moskvin, Claude A. Piantadosi, and Barry W. Allen1 January 2011 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 300, No. 1Chest wall and lung mechanics during acute hemorrhage in anesthetized dogsJournal of Cardiothoracic and Vascular Anesthesia, Vol. 11, No. 5Hypovolemic-Traumatic Shock Models in BaboonsSensitivity of Central Venous Pressure, Pulmonary Capillary Wedge Pressure, and Intrathoracic Blood Volume as Indicators for Acute and Chronic HypovolemiaNew monkey model of severe-volume controlled hemorragic shockResuscitation, Vol. 17, No. 1RETRANSFUSION ACIDOSIS AND VENTILATIONRapid hypertonic glucose infusion: Organ location of label after [14C]glucose during hemorrhagic shockJournal of Surgical Research, Vol. 17, No. 2Retransfusion acidosis after haemorrhagic hypotension in dogsInjury, Vol. 5, No. 3Myocardial Performance in Hemorrhagic Shock in the Dog and PrimateCirculation Research, Vol. 32, No. 4INCREASED CAPILLARY PERMEABILITY TO 125I-LABELED ALBUMIN DURING EXPERIMENTAL HEMORRHAGIC SHOCK*,†30 April 2012 | Transactions of the New York Academy of Sciences, Vol. 35, No. 3 Series IIPulmonary changes in treated hemorrhagic shockThe American Journal of Surgery, Vol. 124, No. 6Pulmonary changes in treated and untreated hemorrhagic shockThe American Journal of Surgery, Vol. 122, No. 5A Computer Analysis of Pulmonary Function in Surgical PatientsThe Annals of Thoracic Surgery, Vol. 11, No. 6Pulmonary changes following hemorrhagic shock and resuscitation in baboonsThe Journal of Thoracic and Cardiovascular Surgery, Vol. 59, No. 3The causes of progressive pulmonary insufficiency in surgical patientsJournal of Surgical Research, Vol. 9, No. 12Peripheral Vascular Response to Simulated Hemorrhagic Shock during Cardiopulmonary Bypass in DogsCirculation Research, Vol. 25, No. 2 More from this issue > Volume 213Issue 5November 1967Pages 1072-1078 Copyright & PermissionsCopyright © 1967 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1967.213.5.1072PubMed4964180History Published online 1 November 1967 Published in print 1 November 1967 Metrics