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N Viires

Publications and source records attributed to N Viires.

25 records · Page 2Linked to original sources
PubMed1983

Diaphragmatic contractility enhanced by aminophylline: role of extracellular calcium.

We have studied the effects of aminophylline on diaphragmatic contractility in 12 anesthetized dogs. The phrenic nerves were stimulated supramaximally (20 Hz, 0.1 ms) with electrodes placed around the fifth roots, and the transdiaphragmatic pressure (Pdi) generated at functional residual capacity (FRC) was measured with balloon catheters. Constancy of FRC was monitored by measuring the end-expiratory transpulmonary pressure, the dogs being occluded at FRC before the stimulations. The electrical activity of the diaphragm (Edi) during the stimulations was recorded with electrodes inserted in both hemidiaphragms. Phrenic stimulations during an infusion of aminophylline (10 mg/kg in 5 min) increased Pdi by 25 +/- 8% of control values, whereas the Edi remained unchanged. This potentiating effect of aminophylline was abolished when an identical dose was injected during a continuous infusion of a calcium blocker (verapamil, 0.1 mg X kg-1 X min-1). Infusion of another methylxanthine compound, caffeine (10 mg/kg), also increased Pdi for an identical electrical phrenic nerve stimulation by 21 +/- 6% compared with control values. However, the potentiating effect of caffeine was not abolished by verapamil. We conclude that aminophylline in vivo increases diaphragmatic contractility and that extracellular calcium is necessary for this action, a mechanism not shared by another methylxanthine compound, caffeine.

Aminophylline↗
PubMed1983

Increased ventilation caused by improved diaphragmatic efficiency during aminophylline infusion.

The mechanism underlying the increase in ventilation (VE) observed during aminophylline infusion was investigated in 12 anesthetized spontaneously breathing dogs. Progressive doses of aminophylline were infused every 30 min, leading to plasmatic levels of 10 to 20, 20 to 30, 30 to 50 mg/L. The increase in VE observed while increasing aminophylline plasmatic concentration ranged from 4.2 +/- 6 to 9.5 +/- 1.2 L/min. Concomitantly to VE, we measured an index of the inspiratory neuromuscular output of the diaphragm, the transdiaphragmatic pressure generated at FRC 0.1 s after the onset of a spontaneous inspiration developed against closed airways (Pdi0.1). For each plasmatic level of aminophylline, Pdi0.1 increased as VE (117 +/- 4, 126 +/- 2, 140 +/- 6% of control values for 10 to 20, 20 to 30, 30 to 50 mg/L, respectively). To establish the role played by an improvement in diaphragmatic contractility in the increase in Pdi0.1 with aminophylline, we measured for each plasmatic level of aminophylline the transdiaphragmatic pressure generated at FRC against closed airways during supramaximal stimulation at 10, 20, 50, and 100 Hz of the 2 phrenic nerves (Pdi). Pdi increased while increasing aminophylline plasmatic level for all the frequencies of stimulation. A relationship was found between Pdi and Pdi0.1 at any aminophylline plasmatic level as well as with VE. No change in the mechanical properties of the respiratory system occurred with aminophylline. We conclude that the increase in VE observed after aminophylline administration in our animal model is essentially due to an improvement in diaphragmatic contractility rather than an increase in the central nervous system output.

Aminophylline↗
PubMed1983

Regional blood flow distribution in dog during induced hypotension and low cardiac output. Spontaneous breathing versus artificial ventilation.

Respiratory muscle blood flow and organ blood flow was studied in two groups of dogs with radioactively labeled microspheres to assess the influence of the working respiratory muscles on the regional distribution of blood flow when arterial pressure and cardiac output were lowered by pericardial tamponade. In one group (n = 6), the dogs were paralyzed and mechanically ventilated (Mv), while in the other (n = 6), they were left to breathe spontaneously (Sb). Cardiac output fell to 30% of control values during tamponade in both groups and was maintained constant. None of the dogs was hypoxic. Ventilation in the Sb group peaked after 50 min of hypotension, but remained unchanged in the Mv group. Duplicate measurements of blood flow were made during a control period and after 50 min of tamponade (corresponding to the peak ventilation in Sb). Blood flow to the respiratory muscles increased significantly (P less than 0.001) during tamponade in Sb (diaphragmatic flow increased to 361% of control values), while it decreased in Mv. Although the arterial blood pressure and cardiac output were comparable in the two groups, blood flow distribution during tamponade was different. In Sb, the respiratory muscles received 21% of the cardiac output, compared with only 3% in the Mv group. Thus, by muscle paralysis and Mv, a large fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during low cardiac output state: blood flows to the liver, brain, and quadriceps muscles were significantly higher during tamponade in the Mv group compared with the Sb group. Similarly, blood lactate at all times after the induction of low cardiac output and hypotension was significantly lower in the Mv animals (P less than 0.005).

Animals↗
PubMed1982

Respiratory muscle contribution to lactic acidosis in low cardiac output.

The role of the respiratory muscles in the evolution of experimental low cardiac output and lactic acidosis was studied in 2 groups of dogs. One group (6 dogs) was paralyzed and artificially ventilated, and the other (6 dogs) was breathing spontaneously. Shock was induced by cardiac tamponade; cardiac output during shock amounted to 25 to 35% of control values in both groups. All the spontaneously breathing dogs died from ventilatory failure (mean time, 2 h), whereas the artificially ventilated dogs were still alive 3 h after the onset of cardiogenic shock. At any given time after the onset of shock, arterial pH was significantly lower in the spontaneously breathing dogs than in the artificially ventilated ones. This was due to a greater increase in arterial blood lactate in the spontaneously breathing dogs than in the artificially ventilated ones (9.47 +/- 2.7 versus 4.74 +/- 56 mmoles/L at 2 h, respectively). Greater glycogen depletion associated with higher muscle lactate concentrations were found in the respiratory muscles of the spontaneously breathing dogs when compared with that in the artificially ventilated ones. It is concluded that artificial ventilation in cardiogenic shock decreases substantially the severity of lactic acidosis and prolongs survival.

Abdominal Muscles↗
PubMed1979

Effect of methacholine chloride on rheology and transport of canine tracheal mucus.

The effect of methacholine chloride (M) on tracheal mucus was investigated in three conscious tracheostomized dogs. Aerosols of M in concentrations of 2--32 mg/ml were delivered intratracheally for 1 min. Mucus was sampled with a cytology brush at 2 min postchallenge and at irregular intervals thereafter. The mechanical properties of each sample were determined in the magnetic microrheometer, and correlated with mucociliary transportability as assayed by the frog palate technique. With high doses of M, there was an increase in volume of secretion collected per unit time. The elastic modulus (G') at 2 min postchallenge went up (to 1.5 x 2.3 x control for 16 and 32 mg/ml, respectively) then fell below control before returning to base line after 30 or 45 min. With low doses of M (2--8 mg/ml) the secretion rate was also above control, but only a decrease in G' (to 0.54 x control) was observed. The decrease in G' at low doses did not significantly alter the frog palate transport rate; however, the increase at higher doses did impede mucociliary transport.

Animals↗
PubMed1979

Influence of vagal tone on rheology and transportability of canine tracheal mucus.

The influence of vagal tone on the rheology of tracheal mucus was studied in 6 conscious, tracheostomized dogs. Mucus was sampled via the tracheostomy with a cytology brush before and after administration of atropine. After vagal blockade, a clear decrease in the mucus collection rate was seen. The viscoelastic properties of the mucus were not altered by atropine when control elasticity was high, but when control elasticity was low, administration of atropine led to increased elasticity. In neither case was there a significant change in transportability of the mucus samples. The increase in elasticity from a small initial value was consistent with the blocking of moderate vagal activity, because administration of methacholine in the same group of dogs had been shown to cause a decrease in mucus elasticity.

Animals↗