Biomedical subjects

R Naeije

Publications and source records attributed to R Naeije.

At least 109 records · Page 6Linked to original sources

PubMed1989

Systemic and regional hemodynamic effects of isosorbide dinitrate in patients with liver cirrhosis and portal hypertension.

In a group of 17 cirrhotic patients with portal hypertension, we have investigated the effects of 5 mg sublingual administration of isosorbide dinitrate (IDN) on central hemodynamics, on regional (hepatic and renal) hemodynamics and on blood gases. Fifteen min after drug administration, we observed a decrease in the right atrial mean pressure from 4 +/- 1 to 3 +/- 1 mmHg (mean +/- S.E.M., P less than 0.02) and of pulmonary arterial wedge pressure from 7 +/- 1 to 4 +/- 1 mmHg (P less than 0.001) with decreases of the cardiac index from 4.2 +/- 0.2 to 3.7 +/- 0.2 l/min/m2 (P less than 0.001) and the mean arterial pressure from 89 +/- 4 to 72 +/- 3 mmHg (P less than 0.001) and an increase in heart rate from 86 +/- 4 to 94 +/- 5 beats/min (P less than 0.001). Arterial PO2 decreased from 73 +/- 2 to 66 +/- 2 mmHg (P less than 0.001). As a consequence of both cardiac index and arterial PO2 reductions, O2 transport to the tissues was reduced from 602 +/- 32 to 518 +/- 26 ml/min.m2 (P less than 0.001). The hepatic venous pressure gradient decreased from 17 +/- 1 to 14 +/- 1 mmHg (P less than 0.001) and hepatic vein PO2 did not change. The hepatic blood flow (HBF) determined in 7 patients remained unchanged. Renal blood flow (RBF) determined in 5 patients decreased from 0.76 +/- 0.11 to 0.68 +/- 0.11 l/min (P less than 0.001). In conclusion, isosorbide dinitrate reduces portal hypertension in patients with liver cirrhosis without compromising hepatic perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Redistribution of cardiac output to the kidneys by tertatolol does not involve prostaglandins.

Renal perfusion has been shown to be preserved or improved during treatment by tertatolol in patients with arterial hypertension. The aims of the present study were (1) to document the central and renal hemodynamic effects of tertatolol in normal subjects and (2) to look for a possible interaction between tertatolol and products of the cyclooxygenase pathway of arachidonic acid metabolism. Five mg of tertatolol, 1 g aspirin, 5 mg tertatolol together with 1 g aspirin, and placebo were administered to 8 healthy volunteers at 1 week intervals in a random order and in a double-blind fashion. Cardiac output was measured by cardiac Doppler echography and renal blood flow and glomerular filtration rate by constant infusion techniques using I123-iodohippurate and Cr51-EDTA respectively. Measurements were performed before and then successively 2 and 4 h after oral intake of drugs or placebo. Tertatolol alone or with aspirin significantly decreased heart rate and cardiac output (P less than .05) without change in blood pressure, renal blood flow or glomerular filtration rate. The renal fraction of cardiac output was increased by tertatolol alone or with aspirin (P less than .05). Either placebo or aspirin alone had no effect. Thus tertatolol redistributes cardiac output to the kidneys in normal subjects as previously reported in hypertensive patients. This favorable effect on renal hemodynamics appers unlikely to be mediated by a local release of vasodilating prostaglandins.

Adrenergic beta-Antagonists↗

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

Pharmacological doses of atrial natriuretic factor do not inhibit canine hypoxic pulmonary vasoconstriction.

It has been recently suggested that atrial natriuretic factor (ANF) might be involved in the physiological regulation of pulmonary circulation. Therefore, we investigated the pulmonary hemodynamic response to 20-min infusions of 0.05, 0.1, and 0.2 micrograms kg-1 min-1 of alpha human ANF in five dogs alternatively ventilated with hyperoxic (FIO2 0.4) and hypoxic (FIO2 0.1) gas mixtures. Cardiac output was held constant by the inflation of a balloon in the inferior vena cava or by opening of an arteriovenous femoral fistula, in order to discriminate between active and passive changes in pulmonary arterial pressure (Ppa). Hypoxia increased Ppa from 14 +/- 3 to 24 +/- 3 mm Hg (mean +/- SE, p less than 001). Circulating ANF and guanosine 3',5'-cyclic monophosphate (cGMP) were increased to 1,326 +/- 299 pmol L-1 (normal is less than 10 pmol L-1) and 75.5 +/- 5.8 pmol ml-1 (normal is less than 15 pmol ml-1) respectively, at the highest infused dose. After ANF infusion, heart rate (HR), Ppa, pulmonary capillary wedge pressure (Ppw), and right atrial pressure (Pra) did not change either in hyperoxia or hypoxia. Systemic arterial pressure (Psa) decreased after ANF, but only in hypoxia. Thus, ANF at pharmacological doses associated with a 100-150-fold increase in plasma levels proved to be a poor vasodilator and, in particular, did not inhibit hypoxic pulmonary vasoconstriction (HPV). These results do not support the speculation that ANF might be an endogenous vasodilating modulator of pulmonary vascular tone in the dog.

Animals↗

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

Pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis.

To determine and to quantify the pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis, we measured in 10 cirrhotics blood gases, P50, hemodynamics, ventilation, and the distribution of ventilation-perfusion ratios (VA/Q) using the multiple inert gas elimination technique. Seven patients had an arterial hypoxemia (PaO2 = 69 +/- 6 mm Hg, mean +/- SD), and three patients were normoxemic (PaO2 = 89 +/- 6 mm Hg). In each hypoxemic patient, the VA/Q distributions were characterized by the presence of low VA/Q units. A negative logarithmic correlation was found between the dispersion of the blood flow distribution and the arterial PO2. An acute inspiratory hypoxia (FIO2, 0.125) elicited an increase in pulmonary vascular resistance by 58.5% in the hypoxemic group and by 81.6% in the normoxemic one (p = NS between the two groups). The percent change in pulmonary vascular resistance induced by hypoxia was not correlated with the percent change in the dispersion of the blood flow distribution. A theoretical analysis showed that the mean arterial PO2 of 69 mm Hg of the hypoxemic group differed from a normal reference value of 96 mm Hg as a result of the combined effects of reduced hemoglobin (-4 mm Hg), increased P50 (+4 mm Hg), increased ventilation (+10 mm Hg), low VA/Q (-35 mm Hg), and true shunt (-2 mm Hg). These results show that the "hypoxemia of liver cirrhosis" is essentially caused by VA/Q mismatching, which is not explained by an abnormal hypoxic pulmonary vasoconstriction.

Adult↗

PubMed1989

[Pulmonary circulation and autonomic nervous system].

The function of the autonomic innervation of the pulmonary vasculature remains incompletely understood. Recent studies have contributed to a better understanding of pressure-flow relationships within the pulmonary circulation in intact dog experimental models. This methodological approach has been used to show that, in normal hyperoxic or moderately hypoxic lungs, the sympathetic nervous system exerts a net vasodilatating effect, while the parasympathetic nervous system does not seem to participate to the regulation of vasomotor tone. These results underscore that research in "traditional" physiology still is implicated in ongoing progress in physiopathology and therapeutics.

Animals↗

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↗