Biomedical subjects

M Leeman

Publications and source records attributed to M Leeman.

At least 73 records · Page 4Linked to original sources

PubMed1990

Effects of embolus size on hemodynamics and gas exchange in canine embolic pulmonary hypertension.

We examined the effects of different-sized glass-bead embolization on pulmonary hemodynamics and gas exchange in 12 intact anesthetized dogs. Pulmonary hemodynamics were evaluated by multipoint pulmonary arterial pressure (Ppa)/cardiac output (Q) plots before and 60 min after sufficient amounts of 100-microns (n = 6 dogs) or 1,000-microns (n = 6 dogs) glass beads to triple baseline Ppa were given and again 20 min after 5 mg/kg hydralazine in all the animals. Gas exchange was assessed using the multiple inert gas elimination technique in each of these experimental conditions. Embolization increased both the extrapolated pressure intercepts (by 6 mmHg) and the slopes (by 5 mmHg.l-1.min.m2) of the linear Ppa/Q plots, together with an 80% angiographic pulmonary vascular obstruction. These changes were not significantly different in the two subgroups of dogs. However, arterial PO2 was most decreased after the 100-microns beads, and arterial PCO2 was most increased after the 1,000-microns beads. Both bead sizes deteriorated the distribution of ventilation (VA)/perfusion (Q) ratios, with development of lung units with higher as well as with lower than normal VA/Q. Only 100-microns beads generated a shunt. Only 1,000-microns beads generated a high VA/Q mode and increased inert gas dead space. Hydralazine increased the shunt and decreased the slope of the Ppa/Q plots after 100-microns beads and had no effect after 1,000-microns beads. We conclude that in embolic pulmonary hypertension, Ppa/Q characteristics are unaffected by embolus size up to 1,000 microns.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Restored hypoxic pulmonary vasoconstriction by peripheral chemoreceptor agonists in dogs.

Hypoxic stimulation of the peripheral chemoreceptors inhibits hypoxic pulmonary vasoconstriction (HPV). On the other hand, almitrine, a peripheral chemoreceptor agonist, has been reported in some studies to enhance HPV. To further explore this apparent contradiction, we investigated the effects of two different low intravenous doses of almitrine on pulmonary arterial pressure (Ppa) versus cardiac index (Q) plots in 32 pentobarbital-anesthetized dogs ventilated alternatively in hyperoxia (FIO2, 0.4) and in hypoxia (FIO2 0.1). HPV, defined as a hypoxia-induced increase in Ppa over the entire range of Q studied, from 2 to 5 L/min/m2, was elicited in 16 dogs. In the first eight of these "responders," almitrine 2 micrograms/kg/min had no vascular effect, and in the other eight, almitrine 4 micrograms/kg/min inhibited HPV. In 16 other dogs, hypoxia did not affect Ppa over the entire range of Q. In these "nonresponders," almitrine 2 micrograms/kg/min (n = 8) as well as 4 micrograms/kg/min (n = 8) restored HPV. To answer the question whether the ability to restore HPV would be specific to almitrine, we administered intravenously the structurally unrelated chemoreceptor agonist doxapram at the dose of 20 micrograms/kg/min to an additional group of eight "nonresponders," and this treatment also restored HPV. Intravenous infusion of the malic acid solution solvent of almitrine had no effect on Ppa/Q plots in a final group of eight "nonresponders". We conclude that low dose almitrine and doxapram restore HPV in dogs with a naturally absent hypoxic pulmonary pressor response, probably by a direct effect at the pulmonary vessels.

Almitrine↗

PubMed1989

Absence of parasympathetic control of pulmonary vascular pressure-flow plots in hyperoxic and hypoxic dogs.

Hypoxic stimulation of the peripheral chemoreceptors has been reported to inhibit hypoxic pulmonary vasoconstriction (HPV). This has been explained by a reflex vagal (Chapleau et al., 1988) or sympathetic (Naeije et al., 1989) pulmonary vasodilation. We therefore investigated the effects of bilateral cervical vagotomy and of muscarinic block (atropine sulfate 0.1 mg.kg-1 i.v.) on multipoint pulmonary arterial pressure (Ppa)-cardiac index (Q) plots in 16 sodium pentobarbital-anesthetized dogs ventilated alternately in hyperoxia (fraction of inspired O2, FIO2, 0.4) and in hypoxia (FIO2 0.1). Over the range of Q studied, 2 to 5 L.min-1.m-2, hypoxia increased Ppa and did not change pulmonary capillary wedge pressure (Ppw). After bilateral cervical vagotomy or after atropine, Ppa and Ppw at all levels of Q were not modified either during hyperoxia or during hypoxia. These results show that the parasympathetic system does not affect the global hypoxia-induced pulmonary vasopressor response and thus suggest that the depressor effect of chemoreceptor stimulation on HPV is not vagally mediated.

Animals↗

PubMed1989

Effects of propofol on pulmonary and systemic arterial pressure-flow relationships in hyperoxic and hypoxic dogs.

We have investigated the effects of a continuous infusion (18 mg kg-1 h-1) of the aqueous emulsion formulation of propofol on mean pulmonary arterial (PAP)/cardiac output (O) and mean systemic arterial pressure (SAP)/Q relationships in 15 intact pentobarbitone-anaesthetized dogs subjected to hyperoxia (F/O2 0.4) and hypoxia (F/O2 0.1). Five-point PAP/Q and SAP/Q plots were obtained by opening an arterio-venous femoral fistula or by stepwise inflations of an inferior vena cava balloon. Over the range of Q studied (2-5 litre min-1), hypoxia increased PAP in eight dogs ("responders") and did not affect PAP in seven others ("non-responders"). Hypoxic pulmonary vasoconstriction (HPV) was restored in non-responders by the administration of acetylsalicylic acid (ASA) 1 g i.v. Hypoxia did not affect SAP over the range of Q studied in the responders or in the non-responders treated with ASA. Propofol had no effect on hyperoxic or on hypoxic PAP at all values of Q either in responders or in non-responders with HPV restored by ASA. Propofol did not change Q at uncontrolled flow, but decreased SAP at the lowest Q (2 and 3 litre min-1) during hyperoxia and at all values of Q during hypoxia. The systemic vascular effects were the same in animals of both groups, treated with ASA or not. We conclude that propofol does not influence pulmonary vascular tone and does not inhibit HPV, but reduces systemic vascular tone when venous return or oxygenation is decreased. The haemodynamic response to propofol was not affected by cyclo-oxygenase inhibition.

Anesthetics↗

PubMed1989

Pulmonary vascular responses to surgical chemodenervation and chemical sympathectomy in dogs.

We investigated the effects of surgical peripheral chemoreceptor denervation, chemical sympathectomy with 6-hydroxydopamine (6-OHDA), and the peripheral chemoreceptor stimulant almitrine on multipoint pulmonary arterial pressure-cardiac index (PAP/Q) plots in 30 pentobarbital sodium-anesthetized dogs ventilated alternatively in hyperoxia [fraction of inspired O2, (FIO2) = 0.4] and hypoxia (FIO2 = 0.1). A hypoxic pulmonary vasoconstriction (HPV), i.e., a hypoxia-induced increase in PAP over the entire range of Q studied, from 2 to 5 l.min-1.m-2, was elicited in all the animals. Surgical denervation of the carotid and aortic chemoreceptors in a first group of nine dogs increased PAP at the lowest Q of 2 and 3 l.min-1.min-2 in hyperoxia and increased PAP at all levels of Q in hypoxia, so that HPV was enhanced. Chemical sympathectomy in a second group of eight dogs increased PAP at all levels of Q to a comparable extent in hyperoxia and hypoxia so that HPV remained unchanged. Almitrine (8 micrograms.kg-1.min-1 iv) in a third group of eight dogs increased PAP at all levels of Q in hyperoxia but had no effect on PAP/Q plots in hypoxia, so that HPV was inhibited. Almitrine had these same pulmonary vascular effects when administered to the chemodenervated and the sympathectomized dogs. Sham operation and a 2-h delay in a final group of five dogs had no effect on hyperoxic or hypoxic PAP/Q plots. We conclude that in intact dogs 1) the sympathetic nervous system reduces both hyperoxic and hypoxic pulmonary vascular tone, 2) stimulation of the peripheral chemoreceptors inhibits HPV, and 3) almitrine has direct pulmonary vasoconstricting effects in hyperoxia but not hypoxia.

Almitrine↗

PubMed1989

Sinoaortic deafferentation reduces intrapulmonary shunt in dogs with oleic acid lung injury.

Hypoxic stimulation of the peripheral chemoreceptors has been reported to inhibit hypoxic pulmonary vasoconstriction. To evaluate the pathophysiological importance of this observation, we investigated the effects of surgical peripheral chemoreceptor denervation on pulmonary vascular tone and gas exchange in 17 pentobarbital-anesthetized dogs with oleic acid pulmonary edema. Pulmonary arterial pressure-cardiac index (Ppa/Q) plots, blood gases, and intrapulmonary shunt measured by the SF6 method were obtained at base line, after peripheral chemodenervation (n = 9) or after sham operation (n = 8), and again after 0.09 ml.kg-1 intravenous oleic acid. Over the range of Q studied (2-5 l.min-1.m-2), Ppa/Q plots were best fitted as first-order polynomials in most dogs in all experimental conditions. Chemoreceptor denervation increased Ppa at the lowest Q, while sham operation did not affect the Ppa/Q plots. Oleic acid increased Ppa over the entire range of Q and increased intrapulmonary shunt. This latter was measured at identical Q during the construction of the Ppa/Q plots. Chemoreceptor-denervated dogs, compared with sham-operated dogs, had the same pulmonary hypertension but lower intrapulmonary shunt (36 +/- 4 vs. 48 +/- 5%, means +/- SE, P less than 0.04) and venous admixture (43 +/- 4 vs. 54 +/- 3%, P less than 0.02). We conclude that in intact dogs chemoreceptor denervation attenuates the rise in intrapulmonary shunt after oleic acid lung injury. Whether this improvement in gas exchange is related to an enhanced hypoxic pulmonary vasoconstriction is uncertain.

Afferent Pathways↗

PubMed1989

Prostaglandin E1 in the adult respiratory distress syndrome. Benefit for pulmonary hypertension and cost for pulmonary gas exchange.

Prostaglandin E1 (PGE1) has been reported to improve survival in patients with the adult respiratory distress syndrome (ARDS). However, the effects of this pulmonary vasodilating compound on gas exchange have been little documented. We therefore measured hemodynamics, blood gases, and the distributions of ventilation-perfusion ratios (VA/Q), using the multiple inert gas elimination technique, at baseline and during infusion of PGE1 0.02 to 0.04 microgram.kg-1.min-1 in six patients with pulmonary hypertension secondary to ARDS ventilated with 10 cm H2O positive end-expiratory pressure. PGE1 decreased systemic arterial mean pressure (-16%) and pulmonary arterial mean pressure (-15%) and increased cardiac index (+20%) and heart rate (+11%). Arterial PO2 decreased from 99 +/- 6 to 77 +/- 8 mm Hg (p less than 0.01, mean +/- SEM) with no change in mixed venous PO2 and in O2 consumption. PGE1 increased true shunt from 21 +/- 4 to 32 +/- 5% of total blood flow (p less than 0.01) with no significant modification in the pattern of VA/Q distribution. Thus, in ARDS, pulmonary hypertension is reduced by PGE1 at the price of a deterioration in pulmonary gas exchange. The clinical relevance of these findings remains to be evaluated.

Adult↗

PubMed1989

Effects of theophylline and S 9795 on hyperoxic and hypoxic pulmonary vascular tone in intact dogs.

In the literature, it remains uncertain whether methylxanthines inhibit hypoxic pulmonary vasoconstriction. We examined the effects of theophylline and of S 9795, a new methylxanthine derivative, on multipoint mean pulmonary arterial pressure (Ppa)/cardiac index (Q) relationships in 31 intact dogs, ventilated alternately in hyperoxia (fraction of inspired oxygen, FIO2 0.4) and in hypoxia (FIO2 0.1). A sequence of two 5-point Ppa/Q plots at FIO2 0.4 and at FIO2 0.1, consecutively, was performed before and after i.v. administrations of theophylline 10 mg.kg-1 (n = 8) and 25 mg.kg-1 (n = 7), of S 9795 10 mg.kg-1 (n = 8) and of placebo (n = 8). The Ppa/Q plots were rectilinear in all experimental conditions. Over the entire range of Q studied, 2-5 l.min-1.m-2, hypoxia increased Ppa in all animals. Placebo had no effect on these Ppa/Q plots. Theophylline at the lowest dose (plasma levels from 8.4-13.6 micrograms.ml-1) and S 9795 (plasma levels from 3.0-11.2 micrograms.ml-1) did not affect Ppa/Q in hyperoxia or in hypoxia. Theophylline at the highest dose (plasma levels from 17.8-40.4 micrograms.ml-1) reduced hypoxic Ppa at all levels of Q and hyperoxic Ppa at the highest Q, from 3-5 l.min-1.m-2, and inhibited hypoxia-induced increases in Ppa. We conclude that pulmonary vasoconstriction may be preserved after the lowest doses of methylxanthines recommended for the treatment of increased bronchial tone.

Animals↗

PubMed1988

Preserved renal perfusion during beta blockade by tertatolol with and without cyclooxygenase inhibition in normal humans.

The systemic and renal hemodynamic effects of tertatolol, a new noncardioselective beta blocker without partial agonist activity, given alone or in combination with cyclooxygenase inhibition by acetylsalicylic acid (aspirin), were investigated in eight healthy volunteers. Tertatolol 5 mg, aspirin 1 g, tertatolol 5 mg together with aspirin 1 g and placebo were administered at 1-week intervals in a random order and in a double-blind fashion. Cardiac output was measured by Doppler echography and renal blood flow and glomerular filtration rate (GFR) by constant infusion techniques using (123I) iodohippurate and (51Cr) EDTA, respectively. Measurements were performed before and then successively 2 and 4 hours after oral intake of drugs or placebo. Tertatolol decreased cardiac output by 22% (P less than .05) and heart rate by 17% (P less than .05) without change in blood pressure, renal blood flow, and GFR. The same effects occurred when tertatolol was given together with aspirin. Either placebo or aspirin alone had no effect on systemic and renal hemodynamics. These results suggest that cardiac output is redistributed to the kidneys after tertatolol intake in normal humans. This favorable effect on renal hemodynamics is probably not mediated by a local release of vasodilating prostaglandins.

Adult↗

PubMed1988

Acute effects of tertatolol and nadolol on systemic and renal hemodynamics in patients with essential hypertension.

The acute systemic and renal hemodynamic effects of tertatolol, a new noncardioselective beta-blocker without partial agonist activity, were compared to those of an equipotent dose of nadolol in eight patients with essential hypertension. Tertatolol (5 mg) or nadolol (80 mg) were administered orally at an interval of 1 week in a random order as a double-blind, cross-over study. Cardiac output was measured by Doppler echography, and renal blood flow and glomerular filtration rate were measured by constant infusion techniques using 123I-iodohippurate and 51CR-EDTA, respectively. Measurements were performed before and then successively 2 and 4 hours after ingestion of the drugs. Both nadolol and tertatolol decreased blood pressure and cardiac output to a comparable extent. Renal blood flow remained unchanged, so that the renal fraction of cardiac output increased from 14.4 +/- 1.5% to 21.3 +/- 2% after nadolol and from 14.8 +/- 2.4% to 20.5 +/- 1.8% after tertatolol (mean +/- SE, P less than 0.01 before vs. after; nadolol vs. tertatolol was not significant). The glomerular filtration rate remained unchanged, from 68 +/- 9 to 64 +/- 6 mL/min.m2 after nadolol and from 71 +/- 8 to 67 +/- 7 mL/min.m2 after tertatolol (before vs. after and nadolol vs. tertatolol levels were not significant). These results show that both tertatolol and nadolol redistribute cardiac output to the kidneys in patients with essential hypertension.

Adult↗

PubMed1988

Multipoint pulmonary vascular pressure/flow relationships in hypoxic and in normoxic dogs: effects of nitrous oxide with and without cyclooxygenase inhibition.

The authors investigated the effects of 70% nitrous oxide on overall mean pulmonary artery pressure (MPAP)/cardiac index (CI) relationships in 13 intact pentobarbital anesthetized dogs ventilated alternatively in normoxic (fraction of inspired O2, FIO2 0.3) and in hypoxic (FIO2 0.1) conditions. Five-point MPAP/CI plots were constructed by opening an arterio-venous femoral fistula or by stepwise inflations of a balloon in the inferior vena cava. These MPAP/CI plots were rectilinear in all experimental conditions. Over the entire range of CI studied, 1-5 l.min-1.m-2, hypoxia increased MPAP in seven dogs ("responders"), and did not affect MPAP in six other dogs ("nonresponders"). Hypoxic pulmonary vasoconstriction (HPV) was restored in "nonresponders" by administration of 1 g acetylsalicylic acid (ASA) intravenously. In "responders," nitrous oxide partially inhibited HPV. In "nonresponders" with a hypoxic pressor response restored by ASA, nitrous oxide enhanced both normoxic and hypoxic pulmonary vascular tone, and did not affect HPV. These results suggest that pulmonary vascular effects of nitrous oxide depend on preexisting pulmonary vascular tone, and may be modulated by cyclooxygenase products of arachidonic acid metabolism.

Animals↗

PubMed1988

Pulmonary artery pressure: flow relationships in hyperoxic and in hypoxic dogs. Effects of methylprednisolone.

Methylprednisolone has been reported to impair hypoxic pulmonary vasoconstriction in isolated lungs, possibly by inhibiting the generation of vasoconstricting products of arachidonic acid metabolism. We investigated the effects of methylprednisolone on mean pulmonary artery pressure (PAP):cardiac index (Q) relationships in intact pentobarbital anaesthetized dogs ventilated alternatively in hyperoxia (fraction of inspired O2, FiO2 0.4) and in hypoxia (FiO2 0.1). Cardiac output was increased by opening an arterio-venous femoral fistula or reduced by stepwise inflations of a balloon in the inferior vena cava. Five point PAP:Q relationships were found to be rectilinear in all experimental conditions. Over the entire range of Q studied (2 to 5 l/min.m2), hypoxia increased PAP in seven dogs ("responders") and did not affect PAP in three other dogs ("non-responders"). A hypoxic pulmonary pressor response was restored in these three "non-responders" by administration of 1 g acetylsalicylic acid iv. Methylprednisolone 30 mg/kg iv had no effect on hyperoxic and on hypoxic pulmonary vascular tone in the "responders" and in the "non-responders" treated with acetylsalicylic acid. An additional dog pretreated with methylprednisolone 30 mg/kg iv 24 h before the experiment still had a marked hypoxia-induced increase in PAP over the entire range of Q studied. Thus a large dose of methylprednisolone does not affect hypoxic or hyperoxic pulmonary vascular tone in intact dogs. These data do not support the hypothesis that products of arachidonic acid metabolism mediate hypoxic pulmonary vasoconstriction.

Animals↗

PubMed1988

Effects of increased pulmonary vascular tone on gas exchange in canine oleic acid pulmonary edema.

Pulmonary gas exchange was investigated before and after an increase in pulmonary vascular tone induced by administration of acetylsalicylic acid (ASA), indomethacin, or almitrine in 32 pentobarbital-anesthetized and ventilated (fraction of inspired O2 0.4) dogs with oleic acid lung injury. Pulmonary vascular tone was evaluated by five-point pulmonary arterial pressure (PAP)/cardiac index (Q) plots and intrapulmonary shunt was measured using a SF6 infusion. PAP/Q plots were rectilinear in all experimental conditions. In control dogs (n = 8), oleic acid (0.09 ml/kg iv) increased PAP over the range of Q studied (1-5 l.min-1.m-2). At the same Q, arterial PO2 fell from 186 +/- 11 to 65 +/- 8 (SE) Torr and intrapulmonary shunt rose from 5 +/- 1 to 50 +/- 6% 90 min after oleic acid injection. These changes remained stable during the generation of two consecutive PAP/Q plots. ASA (1 g iv, n = 8), indomethacin (2 mg/kg iv, n = 8), and almitrine (8 micrograms.kg-1.min-1 iv, n = 8) produced a further increase in PAP at each level of Q. ASA and indomethacin, respectively, increased arterial PO2 from 61 +/- 4 to 70 +/- 3 Torr (P less than 0.05) and from 70 +/- 6 to 86 +/- 6 Torr (P less than 0.05) and decreased intrapulmonary shunt from 61 +/- 5 to 44 +/- 4% (P less than 0.05) and from 44 +/- 5 to 29 +/- 4% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Almitrine↗

PubMed1988

Pulmonary vascular pressure-flow plots in canine oleic acid pulmonary edema. Effects of prostaglandin E1 and nitroprusside.

We investigated the effects of prostaglandin E1 (PGE1) and of sodium nitroprusside (NP) on multipoint pulmonary arterial pressure (PAP)/cardiac index (Q) plots in 24 pentobarbital-anesthetized and ventilated dogs with pulmonary hypertension secondary to oleic acid lung injury. The PAP/Q plots were rectilinear in all experimental conditions. In control dogs (n = 8), PAP was increased over the entire range of Q studied, from 1 to 4 L/min.m2, 90 min after oleic acid 0.09 ml/kg, and remained so during 2 consecutive 5-point PAP/Q plots, each of them being constructed in about 30 min. Oleic acid increased the extrapolated pressure intercept (p less than 0.001) but not the slope of the PAP/Q plots. Infusion of PGE1 0.4 micrograms/kg.min intravenously (n = 8) reduced PAP at each level of Q, with a reduction of the extrapolated pressure intercept (p less than 0.01) and no change in slope of the PAP/Q plots. In contrast, NP 5 micrograms/kg.min intravenously (n = 8) slightly reduced PAP only at the highest Q studied, without any significant change in extrapolated pressure intercept or slope of PAP/Q plots. Systemic blood pressure was decreased by 21% after PGE1 and by 24% after NP. Neither drug affected Q nor blood gases after oleic acid. The results suggest that pulmonary hypertension secondary to oleic acid pulmonary edema may be due more to an increase in effective outflow pressure of the pulmonary circulation than to an increase in incremental vascular resistance, and that active vasoconstriction contributes to this type of pulmonary hypertension.

Alprostadil↗

PubMed1988

Pulmonary artery pressure--flow plots in hyperoxic and in hypoxic dogs: effects of prostaglandin E1.

The effects of prostaglandin E1 on mean pulmonary artery pressure (Ppa):cardiac index (Q) relationships were investigated in eight anaesthetized dogs, ventilated in hyperoxia (fraction of inspired oxygen (FiO2) 0.4) and in hypoxia (FiO2 0.1). Cardiac output was increased by opening an arterio-venous femoral bypass or reduced by stepwise inflations of a balloon in the inferior vena cava. Five-point Ppa:Q relationships were found to be linear in all experimental conditions. Hypoxia increased Ppa over the entire range of Q studied (1-5l.min-1.m-2). Prostaglandin E1 0.4 microgram.kg-1.min-1 intravenously decreased hyperoxic Ppa for Q ranging from 3-5 l.min-1.m-2, hypoxic Ppa for Q ranging from 2-5 l.min-1.m-2 and attenuated hypoxia-induced increases in Ppa. These results show that prostaglandin E1 is a pulmonary vasodilator in both hyperoxic and hypoxic conditions. At the dose of 0.4 microgram.kg-1, prostaglandin E1 partially inhibits hypoxic pulmonary vasoconstriction.

Alprostadil↗

PubMed1987

The increased expiratory muscle use in upright dogs: role of cardiovascular receptors.

A change from the supine to upright posture in anesthetized dogs promotes increased expiratory muscle use during breathing. To examine the role of cardiovascular receptors in eliciting this expiratory muscle recruitment, the electromyographic (EMG) activity of the triangularis sterni (TS) and abdominal external oblique (EO) muscles was recorded in seven spontaneously breathing animals during head up tilting and during occlusion of the inferior vena cava. Head up tilting was associated with a reduction in cardiac output, a transient fall in systemic blood pressure, and considerable increases in TS and EO expiratory EMG activity. On an average (mean +/- SE), the amount of TS and EO expiratory activity in the supine posture was 44.7 +/- 12.9 and 10.3 +/- 7.3%, respectively, of the activity recorded in the 80 degree head up posture. When occlusion of the inferior vena cava in the supine animals induced a reduction in cardiac output and a fall in systemic blood pressure that were comparable to those measured during head up tilting, the TS and EO expiratory EMG activity also increased. This activity, however, always remained smaller than that recorded during breathing in the upright posture; for the seven animals, the amount of TS and EO expiratory activity during vena cava occlusion was only 58.4 +/- 5.7 and 17.9 +/- 10.4% of the activity in upright posture, respectively (P less than 0.001 for both muscles). We conclude, therefore, that the reduced venous return and systemic hypotension of the upright posture are not the critical sensory events for promoting the increased expiratory muscle use in this posture. It must, therefore, be elicited by respiratory receptors.

Animals↗

PubMed1987

Influence of cyclo-oxygenase inhibition and of leukotriene receptor blockade on pulmonary vascular pressure/cardiac index relationships in hyperoxic and in hypoxic dogs.

Overall mean pulmonary arterial pressure (MPAP)/cardiac index (CI) relationships were investigated in 13 pentobarbital anaesthetized dogs ventilated consecutively with a fraction of inspired O2 (F1O2) of 0.4 and with a F1O2 of 0.1. This sequence of alternated F1O2 0.4 and F1O2 0.1 was repeated in the dogs with a strong pulmonary pressor response to hypoxia (more than 20% increase in pulmonary vascular resistance) (n = 6) under a continuous infusion of the leukotriene receptor blocker FPL 57231 (2 mg min-1 kg-1), and in the dogs with a weak pressor response to hypoxia (n = 7) after cyclo-oxygenase inhibition by acetylsalicylic acid (1 g intravenously). Five-point MPAP/CI plots were constructed by opening a femoral arteriovenous fistula or by stepwise inflations of an inferior vena cava balloon catheter. The MPAP/CI plots were rectilinear in all experimental conditions. In responders, hypoxia was associated with an increase in MPAP over the entire range of CI studied (1-5 litres min-1 m-2). Infusion of FLP 57231 abolished the vasoconstricting effect of hypoxia. In non-responders, MPAP was not affected by hypoxia over the entire range of CI. After acetylsalicylic acid administration, hypoxia resulted in a significant rise in MPAP from 2 to 5 litres min-1 m-2. Infusion of FLP 57231 decreased mean systemic arterial pressure at both F1O2 0.4 and F1O2 0.1, while acetylsalicylic acid had no effect on systemic haemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Pulmonary hemodynamic response to dopamine and dobutamine in hyperoxic and in hypoxic dogs.

The pulmonary hemodynamic response to dopamine and to dobutamine was investigated in dogs ventilated with hyperoxia (fraction of inspired O2 concentration [FIO2], 0.4 balance nitrogen) and challenged with short periods of inspiratory hypoxia (FIO2 0.125 or 0.1 for 10 min). Dopamine at doses of 5, 10, and 20 micrograms X kg-1 X min-1 (n = 7 dogs) increased cardiac index (CI) and pulmonary artery pressure (PAP) without change in indexed pulmonary vascular resistance (PVRI) at both FIO2 0.4 and 0.125. Hypoxia-induced increases in PVRI were unaffected by dopamine. Dobutamine at doses of 5, 10, and 20 micrograms X kg-1 X min-1 (n = 7 dogs) increased CI, with an increase in PAP without change in PVRI at FIO2 0.4, and at FIO2 0.125 there was no change in PAP and a decrease in PVRI. Hypoxia-induced increases in PVRI were inhibited by dobutamine, partially at 5 and 10 micrograms X kg-1 X min-1, and completely at 20 micrograms X kg-1 X min-1. In two additional groups of seven dogs the effects of reducing FIO2 from 0.4 to 0.1 without and with dopamine or dobutamine either at 10 micrograms X kg-1 X min-1 (n = 7) or at 20 micrograms X kg-1 X min-1 (n = 7) were studied at an unchanged CI obtained by stepwise inflations of a balloon placed in the inferior vena cava. At constant flow both amines increased PVRI at FIO2 0.4 and did not significantly affect hypoxia-induced increases in PVRI.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗