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PubMed1976

Permeability of the small intestine after intra-arterial injection of histamine-type mediators and irradiation.

Permeability and selectivity of rabbit small intestine were estimated by a perfusion technique after intra-arterial injection of histamine-type mediators and intestinal irradiation. It was shown that the histamine-type mediators caused an increase in capillary permeability which produced an overall moderate increase in transmucosal permeability with a moderate loss of selectivity. Local intestinal irradiation caused a very marked increase in permeability and a profound loss of selectivity. It was felt that this was produced partly by an increase in capillary permeability but largely by damage to the epithelial basement membrane. It is concluded that the intestinal capillary endothelium is both rate-limiting and selective, though not to a major degree in either case. The epithelial basement membrane, however, appears to be both rate-limiting and markedly selective.

Animals↗
PubMed1986

Effect of cinnarizine on IgE antibody mediated allergic reaction in mice and rats.

The effect of cinnarizine on immunoglobulin E (IgE) antibody mediated allergic reactions in mice and rats was investigated. Nifedipine and tranilast were used as comparative drugs. The dye leakage caused by IgE antibody mediated passive cutaneous anaphylaxis (PCA) in mouse ear was clearly inhibited by cinnarizine administered both orally and intraperitoneally. The inhibitory action of cinnarizine for PCA was as potent as nifedipine and superior to tranilast. Cinnarizine clearly inhibited the increase in capillary permeability caused by histamine and calcium ionophore A 23187 (A 23187) but not by LTD4 in mouse ear. Nifedipine inhibited the increases of capillary permeability caused by A 23187, histamine and LTD4. Tranilast inhibited A 23187 induced vasculitis but not histamine or LTD4-induced reaction. Cinnarizine had no significant effect on the release of histamine caused by antigen or A 23187 from rat peritoneal mast cells. Nifedipine and tranilast inhibited the release of histamine caused by both antigen and A 23187 from rat peritoneal mast cells.

Animals↗
PubMed1996

Increased delivery of a new cisplatin analogue (254-S) in a rat brain tumor by an intracarotid infusion of bradykinin.

The intracarotid infusion of bradykinin has been shown to selectively increase capillary permeability in a brain tumor without affecting either normal brain capillary permeability or the systemic blood pressure. We examined whether the intracarotid infusion of bradykinin could selectively increase the delivery of a new watersoluble antitumor agent, cis-diammine glycolato-platinum (254-S, 303.2 mol. wt.), to transplanted RG2 glioma in rats. The platinum contents in the brain, tumor tissues and plasma were measured using an atomic absorption spectrophotometer. The transfer ratio of 254-S from plasma to the tissues was calculated and expressed as the volume of plasma containing platinum per g tissue (Dp, microliter g-1). Intracarotid bradykinin infusion at a rate of 20 micrograms kg-1 min-1 increased the delivery of 254-S in the tumor tissue by 1.3-fold when compared with intracarotid infusion of 0.9% saline (48.78 +/- 18.11 vs. 37.12 +/- 12.53; p < 0.05). In normal brain tissue including the ipsilateral cortex, the contralateral basal ganglia and the contralateral cortex, bradykinin did not significantly increase the delivery of 254-S in comparison with 0.9% saline (12.28 +/- 9.53 vs. 10.70 +/- 5.05, 4.96 +/- 3.54 vs 4.96 +/- 4.80, 7.64 +/- 4.10 vs. 13.07 +/- 11.38, respectively). These results indicate that the intracarotid infusion of bradykinin selectively increases the delivery of 254-S to the brain tumor without affecting the normal brain. This method may, therefore, enhance the antitumor effect of 254-S for the treatment of brain tumors and also reduce neurotoxicity in the normal brain.

Animals↗
PubMed1978

Plasma volume in isosmotic hypervolaemia.

The Evans-blue distribution volume, haematocrit, and plasma protein concentration were investigated in non-hydrated (control), hydrated, and acutely nephrectomized hydrated, anaesthetized dogs. In control anaesthetized dogs a decrease of the plasma protein level was observed as part of the plasma proteins was lost into the extravascular space and did not return into the circulating plasma during the experimental period. Under the effect of hydration, the Evans-blue distribution volume increased significantly, while the haematocrit and plasma volume did not change. The phenomenon was ascribed to an increase in capillary permeability. During hydration following acute nephrectomy, the Evans-blue distribution volume increased but the haematocrit disecreased and the circulating plasma volume increased. It is concluded that a material (or materials) orginating from the kidney may influence capillary permeability.

Animals↗
PubMed1978

The permeability of single capillaries to potassium ions.

This paper reports a description of methods for determining the diffusional permeability to potassium ions of single capillaries in the frog mesentery. By means of micropipettes, injections or infusions were delivered into a single capillary. The subsequent concentration variations in and about the capillary were followed with K(+)-sensitive microelectrodes. A theoretical analysis is provided which give a quantitative frame of reference for evaluating the observed time-concentration curves in terms of capillary permeability. The advantage of single capillary studies is that the surface area through which diffusion occurs is known as is the concentration difference across the capillary membrane. Three different techniques are: (a) the "single injection" method which represents an application of the indicator diffusion technique where a high-K(+) bolus is injected into a single capillary; (b) the "sack" method which determines the rate of K(+) disappearance from within and immediately outside an occluded capillary segment, after a brief increase in intracapillary K(+) concentration; and (c) the "interstitial diffusion" method which records time and spatial distribution of K(+) in the interstitial space after a step-change in intracapillary K(+) concentration. The methods gave an average potassium permeability of the capillary membrane of 67x10(-5) cm s(-1) (SD: 23, n=26) at room temperature. These figures are clearly higher than those previously reported in mammalian capillary studies using whole-organ techniques. In terms of the pappenheimer pore model, this estimate of capillary permeability is consistent with the behavior of a membrane with a thickness of 1.0 mum which possesses equivalent pores with a radius of 110 A, a fractional pore area of 0.3 percent, and a pore density of 8 mum(-2).

Animals↗
PubMed1980

Simultaneous measurements of capillary filtration and diffusion capacities during graded infusions of noradrenaline (NA) and 5-hydroxytryptamine (5-HT) into the rat hindquarter vascular bed.

The relationships between capillary diffusion capacity (PS) for Cr-EDTA respective capillary filtration capacity (CFC) and vascular resistance during graded intraarterial infusions of NA and 5-HT into the artificially constant flow perfused rat hindquarter vascular bed were investigated. During maximal vasodilatation PS for Cr-EDTA was some 5.5--5.7 ml/min x 100 g, CFC some 0.04 ml/min x mmHg x 100 g, while vascular resistance was 2.8 mmHg x ml-1 x min x 100 g (PRU100) and isogravimetric capillary pressure 12.8 mmHg on an average. Setting out from maximal vasodilatation, increasing doses of NA and 5-HT produced graded reductions in capillary surface area as reflected by progressive decreases in both PS for Cr-EDTA and CFC. These changes occurred simultaneously with progressive increases in both pre- and postcapillary resistances, causing elevations in both arterial and capillary hydrostatic pressures and hance in capillary fluid filtration at constant flow. Capillary hydrostatic pressure increased maximally to 45 mmHg (calculated for NA) and vascular resistance to some 21 mmHg x ml-1 x min x 100 g on an average. PS for Cr-EDTA decreased maximally to some 0.7--1 ml/min x 100 g for both NA and 5-HT and furthermore, the relationships between PS for Cr-EDTA and PRU100 for NA respective 5-HT were almost identical. This was taken to indicate that capillary surface area for nutritional exchange is affected similarly by both drugs. However, the CFU-PRU100 relationship was shifted towards some 30--50% higher CFC values for 5-HT than for NA at almost every level of vasoconstriction. This might suggest that 5-HT besides reducing capillary surface area also induced moderate increases in capillary permeability though increases in number and/or radius of large pores (gaps) (cf. Rippe, Kamiya & Folkow 1978). Even during NA-induced vasoconstriction, when virtually no changes in capillary permeability occurred, PS for Cr-EDTA was reduced to a relatively greater extent than CFC, the discrepancy being most pronounced during marked vasoconstriction. The significance of this finding is discussed.

Animals↗
PubMed1986

The effect of imidazole in endotoxin shock in dogs.

The effect of imidazole, a thromboxane A2 inhibitor, in endotoxin shock in dogs was studied. Thromboxane A2 is a vasoconstrictor and enhances platelet and neutrophil aggregation. The purpose of this study was to examine the hemodynamic modifications of endotoxin shock with imidazole. Thirty dogs were studied, all receiving 1 X 10(8) live Escherichia coli/kg over a 30-minute period. The dogs were divided into three groups of ten dogs each. The first group received no treatment. The second group received a concomitant infusion of imidazole 25 mg/kg per hour. In a third group the imidazole infusion was delayed for 1 hour after the E. coli infusion. Mean arterial pressure (MAP), pulmonary wedge pressure (PWP), central venous pressure (CVP), cardiac output (CO), and systemic vascular resistance (SVR) were measured at 30-minute intervals. Hemoglobin (HGB), white blood count (WBC), a-A gradient (a-A grad), A-V 02 difference (AV02 diff), and fluid requirements were measured at 60-minute intervals. The endotoxin shock response in untreated control dogs was characterized by significant changes over time in MAP and SVR (decreased), and CO and a-A grad (increased). The imidazole group was significantly different, as the MAP and SVR did not decrease and the CO did not increase as in the control group. The control group required significantly more fluids than the imidazole group, while the HGB remained stable suggesting more capillary permeability in the control group. The delayed treatment group was statistically similar to the control animals. These data suggest that imidazole significantly modifies the hemodynamic response to endotoxin shock and may reduce the associated capillary permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Therapy for microcirculatory disorders in severe acute pancreatitis: comparison of delayed therapy with ICAM-1 antibodies and a specific endothelin A receptor antagonist.

Many of the complications in severe acute pancreatitis result from the amplifying effects of microcirculatory disruption. The pathogenesis of these microcirculatory disorders is multifactorial and involves various vasoactive mediators. Thus questions arise as to which vasoactive mediators are most important and how long after the onset of disease vasoactive mediator blockade may be effective. The present study compares the effect of delayed therapy with two vasoactive mediator antagonists, previously tested with promising results in other studies in a well-established rodent model of severe acute pancreatitis. Twelve hours after induction of acute pancreatitis, rats were randomized to therapy with intracellular adhesion molecule-1 (ICAM-1) antibody (2 mg/kg IA-29), endothelin A receptor antagonist (ET-RA) (40 mg/kg LU 135252), or saline solution (volume equivalent). After 12 hours of fluid resuscitation, animals underwent repeat laparotomy for intravital microscopic determination of capillary blood flow, leukocyte rolling, and capillary permeability in the pancreas and colon. Other measurements included cardiorespiratory parameters, hematocrit, pleural effusions, ascites, urine production, and survival. Compared to saline treatment, both ICAM antibody and ET-RA significantly enhanced capillary blood flow in the pancreas and colon, reduced leukocyte rolling, and stabilized capillary permeability. These beneficial effects on microcirculation were associated with decreased fluid loss into the third space and improved renal function and survival. Although both antagonists likewise enhanced capillary blood flow and reduced leukocyte rolling, ET-RA was significantly more effective than ICAM antibody in counteracting capillary leakage, thereby further reducing fluid sequestration. The present study confirms the beneficial effects of endothelin and ICAM antagonists in severe acute pancreatitis, even with delayed therapy, suggesting that both compounds are candidates for further clinical testing. Selective endothelin A receptor blockade appears to be especially attractive for clinical use not only because it was superior to ICAM antibody in the present study but also because of its favorable pharmacologic properties and (preliminary) positive results in clinical phase 2 studies currently underway for other diseases.

Acute Disease↗
PubMed2002

The role of endothelial cells in the pathogenesis of ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication of treatment with fertility drugs. Using human lung microvascular endothelial cells (HUMEC-L) as an in-vitro model of OHSS, we have tested the hypothesis that the endothelium is a target of HCG in the pathogenesis of OHSS. Since OHSS is characterized by increased capillary permeability, we have investigated the production and action of vasoactive agents. When HUMEC-L were cultured with high doses of estradiol (E(2)), no significant changes were observed in the secretion of vascular endothelial growth factor (VEGF), interleukin (IL)-6 or IL-1 beta. However, the addition of HCG resulted in a significant increase in the secretion of VEGF and IL-6. Time-course experiments showed that VEGF was secreted within minutes of HCG addition, whereas IL-6 was significantly increased only after 48 h in culture. The secretion of IL-1 beta was unchanged by these hormonal conditions. The presence of HCG receptors was demonstrated in HUMEC-L in basal conditions as well as after the addition of E(2). The expression of VEGF receptors was also investigated. High doses of E(2) were unable to increase the expression of KDR, flt-1 and sfl-t, but the addition of HCG significantly upregulated the KDR concentration in endothelial cells, while no change was observed for flt. Permeability assays demonstrated that while E(2) alone did not change the arrangement of HUMEC-L in vitro, the presence of HCG caused changes in the actin fibres corresponding to increased capillary permeability. Anti-human VEGF antibodies were able to overcome these changes. In conclusion, these experiments show that the endothelium may be a primary target of HCG, causing an acute release of VEGF and a significant increase in IL-6 and resulting in an autocrine-paracrine action that may increase vascular permeability.

Actins↗
PubMed1999

The blood vessel, linchpin of diabetic lesions.

The morbidity and mortality associated with diabetes mellitus are essentially related to the vascular lesions that develop over time in this condition. Both the macrocirculation and microcirculation are involved, and as a consequence, vital organs such as the brain, retina, heart, and kidney and the limbs become damaged. Because microalbuminuria represents the earliest and probably most sensitive indication of endothelial dysfunction in diabetes mellitus, the results of pharmacologic intervention with angiotensin-converting enzyme inhibitors, which treat glomerular hypertension were the first indication of potential beneficial effects in reducing diabetic nephroplasty. The nature of endothelial dysfunction related to diabetes is probably not homogeneous, since microcirculation networks are affected at different periods and with variable intensity. This appears to be the case for the aorta, the heart, segments of the digestive tract, the skin, and the skeletal muscle, the largest consumer of insulin. Although the aorta and large arteries contain a small portion of the total blood volume, their distribution of blood flow (pulse pressure) to peripheral organs may affect endothelial function in the microcirculation. Changes in the structure of conduit arteries, partly responsible for the alteration in compliance characteristics, could well be related to the way these arteries are fed by the vasa vasorum system. This report describes a new in vitro approach to examine capillary permeability in normal and alloxan-induced diabetic rabbits. Preliminary results indicate that the size of terminal arterioles of the vasa vasorum (increased diameter) and the capillary permeability to albumin (markedly enhanced) in this specialized network are profoundly affected in the thoracic aorta obtained from diabetic animals. Albumin extravasation into the interstitial fluid compartment of the aorta is likely to lead to structural and physicochemical changes: in fact, removal of interstitial macromolecules via lymphatic drainage is poor in the blood vessel wall of large arteries. This experimental approach is likely to be useful in the exploration of medications affecting the structure and function of conduit vessels.

Animals↗
PubMed1979

Permeability of retinal capillaries in rats with inherited retinal degeneration.

The permeability of retinal capillaries in RCS rats with inherited retinal degeneration was investigated with horseradish peroxidase used as a tracer. Five-week-old rats showed typical degeneration of photoreceptor cells and accumulation of outer segment debris, but retinal capillaries were not permeable to peroxidase. At 10 weeks of age, capillaries in the inner retina appeared normal, but many in the outer retina were leaky. Peroxidase activity in these latter vessels was demonstrable in the basal laminae of endothelial cells and pericytes and in vesicles on the luminal and abluminal sides of the endothelium. Tracer also permeated the intercellular spaces in the surrounding area. The number of leaky capillaries in the outer retina increased during the course of the dystrophy. The site of the leak in permeable capillaries has not yet been established; it may be due to an alteration of the endothelial cell junctions or of transcellular vesicular transport. In the choriocapillaris, peroxidase permeated Bruch's membrane and the basal infoldings between adjacent pigment epithelial cells; tracer progression along the intercellular spaces was blocked at the zonulae occludens at the apicolateral border. The RCS rat may be a useful model for studying the morphological basis of changes in capillary permeability associated with retinal degeneration.

Animals↗
PubMed1987

Regulation of vascular permeability in cell culture.

Although one of the earliest findings of diabetic retinopathy is altered capillary permeability, metabolic factors in diabetes that may increase the permeability of capillaries to fluorescein are unknown. We have studied the effect of a variety of vascular and retinal cells and hyperglycemia on the diffusion rate of fluorescein. These studies were performed with a cell culture system that mimics the cross-section of a capillary by having two chambers separated with a porous membrane that can support the growth of cells on either side of the membrane. The addition of a confluent layer of endothelial cells or retinal pigmented epithelial (RPE) cells inhibited fluorescein diffusion between the two chambers 20- and 300-fold, respectively, after cells were cultured for greater than 5 days. Exposure of endothelial cells to 400 mg/dl glucose for either 3 or 100 days did not affect the barrier function of these cells. The barrier function of capillary endothelial cells isolated from BB rats with chronic diabetes and from nondiabetic animals did not differ. In contrast to endothelial cells and RPE cells, arterial smooth muscle and pericytes, which are not known to form tight junctions, did not inhibit the diffusion of fluorescein more than 2-fold. Surprisingly, the dual culture of endothelial cells with either retinal pericytes or smooth muscle cells resulted in a 50-fold increase in the rate of fluorescein diffusion, showing a disruption of the endothelial barrier. In summary, the intercellular connections between endothelial and epithelial cells that are responsible for the barrier to fluorescein diffusion are not functionally affected by chronic exposure to hyperglycemia or diabetic conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

The importance of polymorphonuclear leukocytes in lipopolysaccharide-induced superoxide anion production and lung injury: ex vivo observation in rat lungs.

The purpose of this study is to determine if the polymorphonuclear leukocyte (PMN) is a major causative agent for lipopolysaccharide (LPS)-induced lung injury and responsible for the excess production of superoxide anion in the lung. We measured superoxide anion production from the lung and pulmonary capillary permeability in rats with and without PMN depletion. The superoxide anion production from the lung was measured using a purpose-built ex vivo chemiluminescence apparatus. Pulmonary capillary permeability was evaluated by the Evans blue dye extravasation method. PMN sequestration was determined by counting PMNs in histologic tissue specimens using microscopy. All rats received 3 mg/kg LPS intravenously. Examinations were undertaken at 2, 6, and 12 h after the LPS injection. The PMN-depleted group received cyclophosphamide 4 days before the LPS injection, which resulted in a PMN count of less than 200 cells/microliter. In rats without PMN depletion, Evans blue dye extravasation increased significantly at 12 h after the LPS injection; PMN sequestration increased at 2, 6, and 12 h after the LPS injection; and superoxide anion production increased at 6 h and remained elevated at 12 h after the LPS injection. The increased permeability, PMN sequestration, and superoxide anion production were not seen in the PMN-depleted group. The contribution of the xanthine/xanthine oxidase system and alveolar macrophages to the observed superoxide anion production was negligible. We conclude that, in rats, the PMN is a major causative agent in LPS-induced lung injury and is responsible for the excess production of superoxide anion in the lung.

Animals↗
PubMed1990

The effects of neutrophils and phospholipase A2 on transvascular albumin flux in isolated rabbit lungs.

In this study, addition of phospholipase A2 (PLA2) to salt-perfused isolated rabbit lungs containing rabbit polymorphonuclear leukocytes leads to an increase in pulmonary capillary permeability. We add 1.5 X 10(8) polymorphonuclear leukocytes to the perfusate. Next, indomethacin is added to the perfusate and 40 units of PLA2 are infused into the pulmonary arterial inflow of the lungs. At the end of the study, a lung sample is removed for measurement of transvascular albumin flux using I125-albumin as a measure of the permeability-surface area product. Control studies demonstrate no increase in transvascular albumin flux. Addition of a dual cyclooxygenase and lipoxygenase inhibitor, BW755C, to the perfusate prevents the increase in transvascular albumin flux. We conclude that PLA2 interacts with polymorphonuclear leukocytes to increase protein permeability. Since PLA2 can release endogenous arachidonic acid and platelet-activating factor from cells, this suggests that release of such products may contribute to an increase in pulmonary capillary permeability from polymorphonuclear leukocytes. The ability of BW755C to prevent the increase suggests the possibility that lipoxygenase products contribute.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1994

Regulation of vascular permeability by macrophage-derived chemotactic factor produced in Japanese encephalitis.

The vascular effects of Japanese encephalitis virus (JEV)-stimulated splenic macrophage-derived neutrophil chemotactic factor (MDF) were evaluated in mice. Intraperitoneal injection of MDF in mice resulted in a rapid increase in capillary permeability in a dose-dependent manner as assessed by leakage of intravenously injected radiolabelled albumin ([125I]-albumin) or Evans blue dye. Intradermal inoculation of MDF in rabbits caused [51Cr]-labelled neutrophil emigration and accumulation into injected sites. Peak plasma leakage and neutrophil infiltration were observed at 1 h following MDF inoculation, and plasma leakage was restored by 2.5 h. The increase in capillary permeability was sensitive to pretreatment of mice with avil and ranitidine (H1 and H2 histamine receptor blockers, respectively), resulting in abrogation of the response; indomethacin, a prostaglandin synthetase inhibitor, did not have any effect.

Animals↗
PubMed2005

Adrenoceptor subtypes in the control of burn-induced plasma extravasation.

Burn trauma is known to induce a significant rise in circulating catecholamine levels and despite catecholamines being potent endogenous vasoactive agents with known actions on microvascular permeability, their effect on burn edema has been poorly investigated. The present study in rats investigated the role and importance of adrenergic receptor subtypes in the regulation of basal capillary permeability in normal skin and hyperpermeability in partial- and full-thickness skin burns. Edema was quantified by spectrophotometric analysis of extravasated Evans blue-albumin. Evaluation was based on intravenous administration of the following adrenergic agonists and antagonists: l-phenylephrine (alpha(1)-receptor agonist), prazosin (alpha(1)-receptor antagonist), clonidine (alpha(2)-receptor agonist), yohimbine (alpha(2)-receptor antagonist), prenalterol (beta(1)-receptor agonist), terbutaline (beta(2)-receptor agonist), or propranolol (beta(1)- and beta(2)-receptor antagonist). Results showed increased capillary permeability in normal skin following administration of terbutaline (p<0.01) and yohimbine (p<0.01). In partial-thickness burns, clonidine significantly (p<0.05) reduced edema formation, whereas in full-thickness burns edema was significantly reduced by clonidine (p<0.05) and l-phenylephrine (p<0.01). In conclusion, the inhibition of postburn edema induced by stimulation of alpha(1)-receptors (l-phylephrine) and alpha(2)-receptors (clonidine) could be secondary to increased vascular resistance and reduced tissue perfusion pressure and/or suppressed inflammatory reaction in the burn injury. In the treatment of burn patients, clonidine is particularly interesting since the agent has previously been proven to induce potent analgesia in thermally injured.

Adrenergic Agonists↗
PubMed1990

Temporal effects of dexamethasone on blood-to-brain and blood-to-tumor transport of 14C-alpha-aminoisobutyric acid in rat C6 glioma.

We used quantitative autoradiography (QAR) to evaluate the effect of systemically administered dexamethasone on capillary permeability in brain tumors and surrounding brain. Rats bearing unilateral right hemispheric C6 gliomas were studied at one and twelve hours after 10 mg/kg of intraperitoneal dexamethasone. Capillary permeability was determined by measuring unidirectional blood-to-brain and blood-to-tumor transport of 14C-alpha aminoisobutyric acid (14C-AIB) over fifteen minutes. 14C-AIB entry into tumor, brain adjacent-to-tumor (BAT), and ipsilateral and contralateral cortices was determined and expressed as a unidirectional transfer constant, K. Nontreated tumor K was more than two-fold greater than K for BAT and ten-fold greater than ipsilateral cortical K, confirming substantial barrier disruption in tumor. In addition, the K for BAT was also significantly greater than K for cortex, indicating that the barrier in the peritumoral region was also disrupted. One hour after dexamethasone treatment, tumor K fell to 63% of its pretreatment value (p less than 0.025). By twelve hours post-treatment, tumor K fell to 25% of the untreated value (p less than 0.001) and to 47% of the one-hour value (p less than 0.005). BAT K fell to 29% of its untreated value (p less than 0.02) and to 46% of its one-hour value (p less than 0.02). By 12 hours, ipsilateral cortical K fell to 67% of the untreated cortical value (p less than 0.05). Compared to untreated values, there was no significant difference between contralateral cortical K at either one or twelve hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoisobutyric Acids↗