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J M López Novoa

Publications and source records attributed to J M López Novoa.

11 recordsLinked to original sources
PubMed1998

[Role of endogenous nitric oxide (NO) in pulmonary vascular adaptation to one-lung ventilation during thoracic surgery].

To determine whether endogenous production of nitric oxide (NO) increases during one-lung lung ventilation (OLV) and to observe its possible influence on pulmonary vascular resistance (PVR). The experimental group consisted of 19 patients undergoing chest surgery with OLV, with monitoring by Swan-Ganz catheter. Hemodynamic parameters were measured and peripheral venous blood samples were taken at the start of surgery and 10 minutes after starting OLV. The control group consisted of 13 patients with comparable clinical characteristics undergoing chest surgery with conventional lung ventilation. In this group samples of peripheral venous blood were taken at the start of surgery and at a moment comparable to the sampling of the experimental group. NO was assessed by quantitative colorimetry as the concentration of nitrites in venous blood. Nitrite concentration in the experimental group was higher during OLV (12.7 +/- 10.1 muMol/ml) than initially (7.1 +/- 5.4 muMol/ml) (p < 0.05). Nitrite concentration was similar at the two moments sampled in the control group (8.7 +/- 2.8 muMol/ml at the start of surgery and 8.1 +/- 3.2 muMol/ml in the second sample taken). Mean percent increase in nitrite concentration in the experimental group was 93.7 +/- 117%; mean percent change in the control group was 3.9 +/- 23% (p < 0.001). PVR during OLV (134 +/- 45 din.s.cm-5) is lower than at the start of surgery (163 +/- 37 din.s.cm-5, p < 0.05). During OLV endogenous production of NO, measured as nitrite concentration in plasma, increases. PVR decreases, possibly because of the increase in nitrite concentration.

Colorimetry↗
PubMed1998

Effect of cyclosporin A on rat smooth-muscle cell proliferation.

Cyclosporin A (CsA) is a potent immunosuppressive agent that has significantly improved graft survival in organ- and bone-marrow-transplant recipients. However, in the context of graft transplantation, CsA has been suggested to potentiate vascular disease by stimulating smooth-muscle cell (SMC) proliferation. As previous studies on the effect of CsA on smooth-muscle proliferation have afforded conflicting results, we conducted an in vitro study of the effect of two concentrations of CsA--10(-6) M (corresponding to the maximal concentration in patients) and 10(-7) M (corresponding to trough concentrations)--on cultured rat SMC proliferation, as assessed by [3H]thymidine incorporation into DNA and measuring cell number by a colorimetric method based on the quantitative staining of cell nuclei. In the presence of 0.5% fetal calf serum (FCS), 10(-6) M CsA induced an increase in [3H]thymidine incorporation into DNA (from 614.44 +/- 67.76 to 1,472.6 +/- 177.63 cpm/well; p < 0.05) with no increase in the number of cells. A cytotoxic effect for this dose was ruled out owing to the absence of significant levels of lactate dehydrogenase (LDH) activity in the supernatant. CsA, 10(-7) M, induced an increase in both [3H]thymidine incorporation into DNA (from 614.44 +/- 67.76 to 1,220.91 +/- 145.59 cpm/well) and cell number (82.49 +/- 6.16 to 165.79 +/- 10.48 cells x 10[3]; p < 0.05). In the presence of 10% FCS, the highest CsA concentration increased [3H]thymidine incorporation to 2,115.91 +/- 224.06 cpm/well, with no significant changes in cell number. However, the lowest CsA concentration increased both [3H]thymidine incorporation (to 3.752.58 +/- 525.06 cpm/well) and cell number (to 181.27 +/- 14.2 cells x 10[3]). These findings suggest that the proliferative effect of CsA on SMCs is variable and that it depends on the concentration of the drug, in support of the discordant results reported previously.

Animals↗
PubMed1997

Role of atrial natriuretic factor, hemodynamic changes and renal nerves in the renal effects of intraperitoneal morphine in conscious rats.

The aim of the present study was to investigate the role of renal nerves and atrial natriuretic factor (ANF) in the mechanisms responsible for the diuresis and antinatriuresis induced by morphine in rats in a normal state of hydration. Male Wistar rats weighing 350-400 g were divided into two groups: one group was subjected to bilateral renal denervation, whereas the other consisted of sham-operated controls. The animals were placed in individual metabolic cages, and morphine (1.25, 2.5, 5.0 or 10.0 mg/kg body weight) or vehicle (0.5 ml isotonic saline) was injected intraperitoneally. Urine was collected hourly for 1 h before and 3 h after morphine injection. The lower doses of morphine (1.25 and 2.5 mg/kg body weight) induced a transient increase in urine output (from 1.17+/-0.12 to 2.49+/-0.34 and from 0.78+/-0.08 to 1.71+/-0.18 microl/min, respectively). The diuretic response to these doses was similar in bilaterally denervated rats. Higher doses (5.0 and 10.0 mg/kg body weight) induced a marked but transient reduction in the urinary flow rate during the first hour (from 0.90+/-0.11 to 0.48+/-0.05 and from 1.37+/-0.17 to 0.45+/-0.08 microl/min, respectively), followed by a delayed diuretic effect. The antidiuretic action of morphine was not observed in bilaterally denervated rats. In control rats, morphine induced a dose-dependent decrease in sodium excretion 1 h after administration, an effect that was blunted in the denervated group. The lower morphine doses (1.25 and 2.5 mg/kg body weight) elicited a transient increase in the glomerular filtration rate (GFR) in both control (from 1.23+/-0.12 to 1.67+/-0.17 and from 1.28+/-0.14 to 2.41+/-0.18 ml/min) and bilaterally denervated rats (from 1.29+/-0.14 to 1.66+/-0.17 and from 1.18+/-0.22 to 1.72+/-0.19 ml/min), whereas the higher doses (5.0 and 10.0 mg/kg body weight) produced a marked, transient GFR decrease in the controls (from 1.25+/-0.11 to 0.43+/-0.05 and from 1.13+/-0.17 to 0.47+/-0.08 ml/min) and bilaterally denervated animals (from 1.48+/-0.16 to 0.74+/-0.09 and from 1.22+/-0.15 to 0.73+/-0.06 ml/min), although the reduction was less pronounced with renal denervation. Morphine induced a transient, dose-dependent reduction in blood pressure (from 114+/-1 to 71+/-6 mm Hg at 10.0 mg/kg body weight) and a dose-dependent elevation of plasma ANF. No differences in plasma ANF were observed between control and denervated animals under basal conditions (60+/-7 vs. 42+/-6 pg/ml) or after injection of 2.5 or 5.0 mg/kg of morphine (155+/-11 vs. 167+/-9 and 360+/-9 vs. 401+/-9 pg/ml, respectively). Our data suggest that the renal responses to intraperitoneal morphine administration derive from the integration of several different actions: (1) increased ANF release; (2) decreased arterial pressure; (3) subsequent activation of renal sympathetic activity, and (4) the direct effect of morphine on tubular function.

Analgesics, Opioid↗
PubMed1993

Renal catabolism of truncated glucagon-like peptide 1.

We have searched for the contribution of the kidney to the catabolism of glucagon-like peptide-1 (7-36)amide or tGLP-1 by analyzing the disappearance of the [125I]tGLP-1 both in vivo, from the plasma of bilaterally nephrectomized (BNX), ureteral-ligated (BUL) and normal rats and in vitro from the perfusate of an isolated rat kidney system. Also, we have measured the degradation of the peptide by the isolated renal tubules. Results from in vivo studies demonstrated that the disappearance half-time (t1/2) of [125I]tGLP-1 was significantly lower in the control than in BUL or BNX rats with the metabolic clearance rate (MCR) being higher in the control than in BUL and BNX group; no difference was found for both parameters between BUL and BNX rats. The urinary excretion of the peptide was negligible. The data from the isolated kidney experiments showed a disappearance of the peptide, which was not due to its spontaneous degradation nor to enzymes released from the kidney to the perfusate. Degradation of the peptide also occurred in the presence of isolated tubules. It was dependent upon the concentration of tubules. This could possibly be due to the action of the brush border-associated peptidases. In conclusion, our results demonstrate that, in the rat, the kidney removes the exogenous tGLP-1 from the peripheral circulation, by a mechanism that involves glomerular filtration and tubular catabolism.

Animals↗
PubMed1990

Intravascular and interstitial fluid dynamics in rats treated with minoxidil.

Edema is a major complication of vasodilatory therapy. However, the pathophysiologic mechanisms leading to the formation of vasodilator-mediated edema are insufficiently understood. The present study therefore examined the effect of the chronic administration of the potent arteriolar vasodilator, minoxidil (Mx), on extracellular fluid dynamics in rats. Extracellular volume (ECV), plasma volume (PV), interstitial fluid volume (IV), arterial pressure (AP), and interstitial fluid pressure (IP) were measured in rats treated for 10 days with Mx (1.5 mg/kg/day) and in control animals. In addition to a decreased AP, Mx-treated animals had diminished water and sodium excretion. ECV, PV, and IV and plasma renin concentration (PRC) were also increased in the Mx-treated rats. IP, which was subatmospheric in control rats (-2.6 +/- 0.04 mm Hg), was near zero in Mx-treated animals (-0.2 +/- 0.02 mm Hg, p less than 0.05). Saline ECV expansion (20 min, Ringer infusion, 3% body weight) or rat albumin injection (300 mg/2 ml) induced similar changes in the volume of the extracellular fluid compartments in both groups. However, changes in IP were blunted in Mx-treated rats. These results, therefore, show that Mx-treated rats have changes in interstitial fluid dynamics prior to any macroscopic evidence of edema accumulation. These alterations in the extracellular compartment dynamics may be a consequence of the sustained arteriolar vasodilation induced by Mx.

Aldosterone↗
PubMed1990

[A model of experimental acute pancreatitis in the conscious rat].

We describe an experimental model of acute pancreatitis in conscious rats, based on biliary reflux; sodium deoxycholate was injected while maintaining the common duct (biliary and pancreatic) temporally occluded. A progressive increase of serum amylase, cardiac rate and hematocrit value, as well as a decrease of plasma proteins are characteristic of this experimental model. Blood pressure was maintained until shortly before death, which occurred after 85 minutes. This is a simple model, reliable and reproducible, which requires minimal surgical manipulation.

Acute Disease↗
PubMed1982

Effect of sodium orthovanadate on renal renin secretion in vivo.

The effect of vanadate (0.5 mumol/min) on renin secretory rate (RSR) of the kidney has been studied in nembutal-anesthetized, volume-expanded dogs. Intrarenal vanadate infusion caused a 69.3 +/- 8.8% decrease in RSR. This was accompanied by marked decreases in renal blood flow (RBF), glomerular filtration rate (GFR) and fractional excretion of sodium (FENa). Renal vascular resistance rose from 1.3 +/- 0.09 to 6.1 +/- 2.3 mm Hg/ml/min (P less than .0005). Papaverine infusion partially blunted the effect of vanadate on RSR (RSR only fell to 42. +/- 10% of basal values). The decreases in RBF and GFR were also less and FENa slightly higher than normal. Acetylcholine prevented the effects of vanadate more fully. There was no fall in RBF, GFR or FENa and it basically abolished the fall in RSR which fell only 19.4 +/- 25.3 of control (P = N.S.). Nifedipine (a slow Ca++ channels blocker) also prevented the fall in RBF, GFR and FENa induced by vanadate. RSR did not change significantly (7.8 +/- 10.9%). These results clearly demonstrate that vanadate is a potent inhibitor of renin secretion and suggest that inhibition of smooth muscle Na+, K+, adenasine triphosphatase and changes in the cystosolic concentration of Na and Ca are involved in its mechanism. Changes in perfusion pressure and sodium delivery to the macula densa appear to have little if any role in the inhibition.

Acetylcholine↗