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Biomedical subjects

G E Plante

Publications and source records attributed to G E Plante.

At least 19 recordsLinked to original sources
PubMed1992

Endothelin-1 enhances vascular permeability in conscious rats: role of thromboxane A2.

The purpose of the present experiments was to study the effects of endothelin-1 (ET-1) on vascular permeability and the involvement of the cyclooxygenase metabolites in the vascular responses to ET-1. Bolus intravenous injection of ET-1 (0.1-1.0 nmol/kg) into conscious rats induced immediate hypotension lasting for 30 s followed by sustained dose-dependent hypertension. A low dose of ET-1 (0.1 nmol/kg) did not modify the hematocrit value but the 1.0-nmol/kg dose increased the hematocrit value from 39.7 to 44.4%. Pretreatment of the animals with BM-13505 (1 mg/kg), a thromboxane A2 (TxA2) receptor antagonist, prolonged the duration of the hypotensive response to ET-1 (1.0 nmol/kg) but had no effect on the pressor response. Pretreatment with OKY-046 (10 mg/kg), a TxA2 synthesis inhibitor, or indomethacin (10 mg/kg), a cyclooxygenase inhibitor, had no significant effect on ET-1-induced changes in blood pressure. Evans blue dye extravasation, a marker of vascular permeability, increased up to 235% over control levels in specific vascular beds including the upper and lower bronchi, stomach, duodenum and kidney of ET-1 (1.0 nmol/kg)-treated animals. Pretreatment of the animals with BM-13505, OKY-046 or indomethacin reduced by 60-100% the Evans blue extravasation in these tissues. These results suggest that the effect of ET-1 on vascular permeability is partly mediated and/or modulated by the secondary release of TxA2, whereas its action on arterial blood pressure appears to be independent from prostanoid release in conscious rats.

Animals↗
PubMed1992

Phosphoramidon blocks big-endothelin-1 but not endothelin-1 enhancement of vascular permeability in the rat.

1. Changes in vascular permeability following intravenous injections of human big-endothelin-1 (big-ET-1) and endothelin-1 (ET-1) were measured by extravasation of Evans blue dye (EB, 20 mg kg-1) in selected tissues. 2. A low dose of big-ET-1 (40 pmol kg-1) failed to alter vascular permeability but a dose of 400 pmol kg-1 increased EB extravasation in the trachea, upper and lower bronchi, and lung parenchyma by 55 to 69% (P < 0.05). Vascular permeability was also enhanced in the liver, spleen, kidney, heart, and diaphragm by 20, 14, 41, 25, and 67%, respectively (P < 0.05). 3. Upon injection of ET-1 (400 pmol kg-1), EB extravasation increased in the upper and lower bronchi, lung parenchyma, liver, pancreas, kidney, heart, and diaphragm. 4. Administration of ET-1 and big-ET-1 was not associated with significant systemic responses. 5. Pretreatment with phosphoramidon (PA) blocked the response to big-ET-1 in all tissues examined but this inhibitor failed to alter the response to ET-1. 6. We conclude from these results that the dose-dependent increase in vascular permeability induced by big-ET-1 in various tissues follows its conversion to ET-1 by the endothelin converting enzyme, a PA-sensitive process.

Animals↗
PubMed1992

The role of B1- and B2-kinin receptors in the renal tubular and hemodynamic response to bradykinin.

Bradykinin (BK) is known to induce diuresis (UV), natriuresis (UNaV), and increased renal blood flow (RPF) with little or no change in glomerular filtration rate (GFR). In this study, BK is infused alone and concurrently with B1- or B2-kinin receptor antagonists into the left kidney of pentobarbital-anesthetized dogs. The intrarenal infusion of BK (bolus: 0.5 microgram/kg, followed by a sustaining dose: 0.05 micrograms.kg-1.min-1) affected left kidney function only. In the left kidney, UV increased from 0.42 +/- 0.21 to a maximum of 1.88 +/- 0.55 ml/min (P less than 0.01) and UNaV rose from 55 +/- 13 to 160 +/- 17 mueq/min (P less than 0.01), while RPF was enhanced from 86 +/- 11 to 125 +/- 24 ml/min (P less than 0.05), and GFR remained unchanged. When a B1-receptor antagonist ([Leu8]-des-Arg9-BK; 2.0 micrograms.kg-1.min-1) was infused concurrently with BK, the increase in urine flow was not different from BK alone. UNaV was transiently attenuated by 50% in this group (P less than 0.05). A B2-receptor antagonist (D-Arg0,[Hyp3,D-Phe7]-BK; 2.0 micrograms.kg-1.min-1) infused with BK significantly (P less than 0.05) and selectively inhibited by 50% the maximal diuresis provoked by BK alone. UNaV in this group was not different from that induced by BK alone. Finally, the concurrent infusion of either B1- or B2-antagonist completely inhibited the rise in RPF observed when BK was infused alone. We conclude that BK infused into the renal artery of dogs in vivo can alter UV and UNaV independently of global renal hemodynamic (RPF and GFR) changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Renal permeability alteration precedes hypertension and involves bradykinin in the spontaneously hypertensive rat.

Vascular permeability disorders have been described in experimental models, as well as in human hypertension. We recently described the fact that vascular permeability to albumin is heterogeneous in the normal rat. In the present study, we examine the contents of Evans blue dye (EB) bound to albumin in selected organs of unanesthetized Wistar Kyoto (WKY) and in spontaneously hypertensive rats (SHR) at various stages of development of hypertension. EB was injected in the caudal vein of paired 4, 8, 12, and 16-wk-old WKY and SHR. Rats were killed 10 min after EB injection and extraction of the marker was measured in selected tissues. In additional 4 and 16-wk-old animals, bradykinin B1 and B2 receptor antagonists (BKA) were also injected with EB. Renal contents of EB bound to albumin were higher in the SHR than in the WKY: 196 +/- 9, 202 +/- 10, 182 +/- 7, and 196 +/- 9, compared with 158 +/- 8, 155 +/- 7, 138 +/- 7, and 118 +/- 6 micrograms/g dry tissue, in the 4, 8, 12, and 16-wk-old rats, respectively. In the 4-wk-old SHR and WKY, blood pressure values were normal and comparable, yet the alteration in EB permeability was already present in the SHR. Both BKA failed to alter the renal EB extravasation in the WKY, but the B2-BKA restored the renal permeability to control levels in the SHR. We conclude that a selective defect in the renal vascular permeability to EB developed in the SHR. Since this finding precedes hypertension and is corrected by a selective B2-BKA, it is suggested that bradykinin is involved at an early stage of the disease in the SHR.

Animals↗
PubMed1991

Sodium-phosphate cotransport and vascular reactivity.

Inorganic phosphate (PO4) alters vascular reactivity in vivo as well as in vitro. In the latter condition, low PO4 reduces, while high PO4 augments reactivity. We used phosphonoformate (PFA), a phosphaturic compound, binding the renal Na-PO4 co-transporter, to examine the existence of such a transport mechanism in selected vascular smooth muscles (VSM). Strips of aorta (A), mesenteric artery (MA), and vein (MV) were obtained from normal rabbits. All tissues were either superfused in normal PO4 (Group 1: 3 mg/dL), then in modified low PO4 (Group 2: 0 mg/dL) or high PO4 (Group 3: 9 mg/dL) Ringer's solutions. The effect of angiotensin II (AII: 10-11 to 10-8M) was tested on each tissue preparation, and contraction values obtained in the presence of PFA (18.5 micrograms/ml:0.018 ml/min) were compared to control responses in the absence of the drug. In Group 1, the contractions of A were reduced by 23% during PFA, for higher doses of AII only, compared to controls (p less than 0.01). Similarly, the contractions of MA in the presence of PFA were reduced at higher doses of AII, by 22% (p less than 0.01). Finally, the contractions of MV were reduced by 75% (p less than 0.01) for all doses of AII. In Group 2, there was no difference in vascular tissue contraction between controls and PFA, whereas in Group 3, the reduction in A, MA, and MV contractions in PFA-treated tissues were approximately twice as extensive as in Group 1 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1990

Role of eicosanoids in PAF-induced increases of the vascular permeability in rat airways.

1. Platelet activating factor (PAF; 1.0 and 5.0 micrograms kg-1) injected in the tail vein of unanaesthetized rats dose-dependently increased the vascular permeability of the trachea, upper and lower bronchi (up to 400%) as measured by the extravasation of Evans blue dye. The permeability of the parenchyma was not affected by PAF treatment. 2. Pretreatment of the animals with an intravenous injection of the PAF antagonist BN-52021 (10 mg kg-1) abolished almost totally the vascular permeability changes elicited by PAF injection (5.0 micrograms kg-1). 3. Pretreatment of the animals with intravenous injections of inhibitors of thromboxane formation, indomethacin (10 mg kg-1) and compound OKY-046 (10 mg kg-1), and thromboxane antagonist, compound L-655,240 (5 mg kg-1), partially reduced PAF effects in the airways (from 28 to 69%). The thromboxane mimic U-44069 (5.0 micrograms kg-1) did not modify the vascular permeability of rat airways. The effect of a low dose of PAF (0.1 microgram kg-1) on the vascular permeability of the trachea and bronchi (but not of the parenchyma) was potentiated by compound U-44069 (5.0 micrograms kg-1) or noradrenaline (400 ng kg-1) whereas the effect of a high dose of PAF (5.0 micrograms kg-1) was not affected. 4. Neither the peptidoleukotriene antagonist MK-571 (10 mg kg-1) nor the 5-lipoxygenase inhibitor, L-663,536 (10 mg kg-1) given before the injection of PAF (5.0 micrograms kg-1) affected the protein extravasation in rat lung tissues. 5. These data suggest that the effect of PAF on rat vascular permeability is partly modulated by thromboxane formation although thromboxanes have no direct effect on the permeability. Thromboxane may act via a vasoconstriction that increases hydrostatic pressure and potentiates the extravasation elicited by PAF effect on endothelial cells. 6. Leukotrienes do not appear to be involved in the changes of rat airway permeability induced by PAF.

Animals↗
PubMed1990

Tumor necrosis factor primes the effects of platelet-activating factor on rat vascular permeability.

The extravasation of Evans blue dye injected in the rat tail vein (EB, 20 mg/kg) was used as a measure of vascular permeability. When the animals were treated with tumor necrosis factor (TNF, 200 micrograms/kg), EB dye was recovered in much larger quantities than in controls in all organs, and especially in the trachea, lower bronchi, lung parenchyma, spleen, pancreas and duodenum (100% increases and over). The EB contents of higher bronchi, heart, liver and kidneys were less marked. The injection of TNF (200 micrograms/kg) 60 min before an injection of platelet-activating factor (PAF, 0.1 micrograms/kg) produced a synergism in many organs. The increases varied from 176 to 574% for the trachea, bronchi, lung parenchyma, pancreas, kidneys and duodenum. The increases in EB contents of the heart, spleen and liver were 86, 96 and 38% respectively. Human recombinant interleukin (IL-1 alpha, up to 400,000 U/kg) did not modify vascular permeability by itself nor primed the effect of PAF in our model. The combination of TNF and IL-1 alpha did not produce effects larger than those of TNF alone. These results further confirm the proinflammatory effects of PAF and its complex interactions with cytokines.

Animals↗
PubMed1979

[Shunt glomerulonephritis: clinical and histopathological manifestations].

In patients with cerebrospinal fluid internal shunts, immune complex glomerulonephritis sometimes develops. Of two new cases the first was classic, while the second was in an adult who had had a ventriculoatril shunt for 8 years; furthermore, the patient had acute renal failure and is the first to have been reported to have Peptococcus septicemia. Shunt glomerulonephritis is characterized by the following: (a) its occurrence following, most often, Staphylococcus albus infection in a patient who usually has a ventriculoatrial shunt; (b) transitory improvement of the symptoms by antibiotherapy only; and (c) full recovery if the prosthesis is removed. Laboratory studies show a low serum concentration of the C3 component of complement, the presence of cryoglobulins and a positive rheumatoid factor test. These abnormalities are reversible with removal of the prosthesis. Optical microscopy of a renal biopsy specimen in the two cases showed cellular proliferation of the glomerular tuft, electron microscopy demonstrated subepithelial deposits and immunofluorescent studies revealed intramembranous and intramesangial immune complexes. These features are similar to those observed in experimental nephritis induced in animals by foreign protein.

Adult↗
PubMed1977

Long-term treatment of severe hypertension with minoxidil.

Minoxidil, a new potent hypotensive agent, was used as the primary antihypertensive agent in 11 patients--10 men and 1 woman aged 35 to 54 years with severe hypertension that was refractory to treatment with maximal (or maximally tolerated) doses of conventional antihypertensive agents. Six patients had severely impaired renal function and three of them were undergoing long-term hemodialysis. The patients were given 2.5 to 40 mg/d of minoxidil for periods of 2 to 29 months. All except one who was almost anuric received propranolol and diuretics. Blood pressure was controlled satisfactorily in all patients. In two patients the hypertension became partially resistant after 1 year of treatment. The main side effects were sodium retention, tachycardia and hirsutism. Renal function remained stable or improved and hemodialysis was discontinued in two patients. Minoxidil is a remarkably potent hypotensive with relatively few side effects and seems particularly advantageous in patients with chronic renal failure.

Adult↗
PubMed1977

[Potomania: re-evaluation of the diagnostic tests and unusual presentation with hydronephrosis and megabladder].

Three cases of compulsive polydipsia previously diagnosed as diabetes insipidus are presented. Abnormally dilated bladder and pyelocalyceal systems were accompanying features, as previously described for diabetes insipidus, particularly of renal orign. Results of the hypertonic saline (Hickey-Hare) test were positive in only one case. Results of restriction of liquids followed by intravenous injection of vasopressin (Miller test) favoured a diagnosis of complete diabetes insipidus. These two tests cannot, therefore, exclude compulsive polydipsia. The features suggesting a diagnosis of compulsive water drinking are low plasma osmolality, a decrease in 24-hour urine output following water restriction, and abnormal behaviour. The diagnosis is confirmed by an 18-hour dehydration test done after gradual fluid restriction, which favours partial restoration of the papillary osmotic gradient.

Adolescent↗
PubMed1977

Effects of saline infusion and acute metabolic acidosis and alkalosis on water and electrolyte transport in the human colon.

Both the kidney and colon secrete bicarbonate and transport water and electrolytes. The respective contributions of these two organs to acid-base and electrolyte balance in normal man has thus been studied in eight healthy male volunteers who underwent simultaneous renal clearance studies, and colonic perfusion with a 0.9% saline or 7.2% mannitol solution, during metabolic alkalosis and acidosis, extracellular volume expansion, and control conditions. There was no influence of these acid-base conditions on electrolyte transport in the colon. In the urine, preferential loss of chloride over sodium averaged 81, 143 (P less than 0.001), and 141 (P less than 0.05) muequiv./min, during control, metabolic acidosis, and extracellular volume expansion conditions, respectively. During alkalosis more sodium than chloride was lost (146 muequiv./min) (P less than 0.001). Colonic pH averaged 7.41 during saline and 6.75 (P less than 0.005) during mannitol perfusion. Titratable acid was not produced in the colon during saline perfusion, and averaged 18 muequiv./min during mannitol perfusion. Urinary titratable acid increased from 19 to 25 muequiv./min (P less than 0.01) during volume expansion. With saline perfusion, bicarbonate secretion rate in the colon rose from 249 muequiv./min during control conditions to 289 muequiv./min during metabolic alkalosis (P less than 0.05). More bicarbonate was excreted in the urine during alkalosis when mannitol was introduced in the colon (243 muequiv./min) than when saline was perfused (152 muequiv./min) (P less than 0.05). This study indicates that the response of the human colon is trivial compared with that of the kidney during acute changes in acid-base balance.

Acid-Base Equilibrium↗