Biomedical subjects

L Girling

Publications and source records attributed to L Girling.

12 recordsLinked to original sources

PubMed1988

Effects of altered left atrial pressure on pulmonary vascular pressure-flow relationships.

We studied the effects of changes in pulmonary capillary wedge pressure (PCWP) on the slope (incremental resistance) and the extrapolated pressure intercept (PI) of the mean pulmonary artery pressure (PAP)-cardiac output (CO) relationship. Multipoint plots of PAP against CO were obtained in intact anesthetized dogs. Group 1 consisted of six dogs entirely in West zone 3 and group 2 of four dogs with mixed West zone 2-3. The four conditions studied were the following: 1) fixed low PCWP, 2) fixed high PCWP, 3) variable PCWP, and 4) time-control repeat of condition 1. The PI significantly exceeded PCWP at fixed low PCWP (group 1, 9.3 vs. 11.1 mmHg, group 2, 6.6 vs. 3.9 mmHg). PI became identical to PCWP only at fixed high PCWP in group 1 (19 +/- 2.0 vs. 19 +/- 1.1 mmHg). Thus PCWP reflects the effective vascular outflow pressure when PCWP is fixed and high. For both groups of dogs in condition 3, when PCWP was varied with CO, the slope of the resulting PAP-CO plot was significantly greater than when PCWP was constant. Also in 9 of 10 dogs, PI was less than PCWP when PCWP was varied. These findings demonstrate that when changes in PCWP are allowed to occur during the generation of a pulmonary artery pressure-flow plot, the resulting slope and intercept, as defined by a Starling resistor model, do not accurately represent the incremental resistance and outflow pressure of the pulmonary vasculature.

Analysis of Variance↗

PubMed1986

Pulmonary vascular pressure-flow relationship in canine oleic acid pulmonary edema.

We tested the hypothesis that the increased impedance to flow in canine oleic acid (OA) lung injury is predominantly due to an increase in effective downstream pressure (EDP), obtained by extrapolating to zero flow the linear portion of the pulmonary artery pressure (PAP)/flow (Q) relationship. PAP-Q coordinates were obtained in eight anesthetized, O2-ventilated dogs by varying Q through systemic arteriovenous fistulae. PAP-Q lines were obtained before and approximately 5 h after injection of OA. A second group of six dogs served as a time control (TC) group. There was a linear relationship between PAP and Q in both experimental and control groups (mean r value 0.948). The presence of pulmonary edema in the OA group caused the EDP to almost double, from 7 to 12 mmHg (P less than 0.01). In contrast, EDP remained constant in TCs. Incremental vascular conductance (IVC), slope of the PAP/Q line, decreased (P less than 0.05) a similar amount in both groups. The above findings are consistent with the modeling of the pulmonary circulation according to a Starling resistor in that large amounts of edema changed EDP but not incremental conductance.

Animals↗

PubMed1986

Pulmonary vascular effects of hydralazine in a canine preparation of pulmonary thromboembolism.

Pulmonary arterial pressure (PAP)-flow coordinates were obtained in 14 anesthetized dogs before and after pulmonary hypertension was induced with autologous blood clots. Cardiac output (CO) was altered by systemic arteriovenous fistulas. The PAP-CO coordinates were always rectilinear. Before emboli, the mean vascular closing or outflow pressure (the pressure intercept of the PAP-CO line) was 8.8 +/- 2.1 (SD) mm Hg. Emboli increased PAP (15.1 +/- 1.6 to 36.5 +/- 3.5 mm Hg; p less than .001) and decreased CO (3.8 +/- 0.6 to 2.4 +/- 0.8 liters X min-1; p less than .001). Incremental resistance (the slope of the PAP-CO line) only increased slightly. On the other hand, the marked increase in PAP was predominantly due to an increase in effective outflow pressure (from 8.8 +/- 2.1 to 28.6 +/- 3.6; p less than .001). Hydralazine was administered in a dose sufficient to double CO. This did not affect PAP and caused an inconsistent and small decrease in incremental resistance. However, a consistently significant decrease in effective outflow pressure, averaging 23%, was observed. In this canine preparation of pulmonary hypertension the predominant effect of hydralazine appears to be a decrease in the mean vascular closing or outflow pressure.

Animals↗

PubMed1986

Hemodynamic management in clinical acute hypoxemic respiratory failure. Dopamine vs dobutamine.

We investigated short-term hemodynamic effects of dopamine and dobutamine in eight patients with acute hypoxemic respiratory failure. We tested the hypothesis that for a similar increase in cardiac output, left ventricular filling pressure (pulmonary capillary wedge pressure [PCWP]) would increase with dopamine and decrease with dobutamine. Dopamine increased cardiac output (p less than 0.05), stroke volume (p less than 0.05), and PCWP (p less than 0.01). Cardiac output increased almost 20 percent when PCWP increased 50 percent with dopamine. In contrast, despite a mean 30 percent increase in cardiac output with dobutamine (p less than 0.01), PCWP decreased. In six of these patients, left ventricular end-diastolic volumes and end-systolic volumes were measured using scintigraphic techniques. In all patients, end-diastolic volume increased with dopamine (p less than 0.05); and in four of six, end-systolic volume increased. In contrast, with dobutamine, in five of six patients, end-diastolic volume decreased; and in all six patients, end-systolic volume decreased. There was a small increase in intrapulmonary shunt with both drugs. We conclude that if an inotropic agent is required to increase cardiac output in patients with acute hypoxemic respiratory failure, dobutamine is probably preferred over dopamine.

Acute Disease↗

PubMed1985

Acute cardiopulmonary effects of nitroglycerin in canine oleic acid pulmonary edema.

In a canine model of acute respiratory failure, the authors investigated acute cardiopulmonary effects of nitroglycerin (TNG) and compared the results with those obtained after phlebotomy. Oleic acid increased intrapulmonary shunt (Qs/Qt) from 7.4 to 31% (P less than 0.001) and decreased (P less than 0.01) cardiac output (CO). In the presence of assumed low-pressure pulmonary edema, TNG was infused to decrease mean blood pressure (BP) by 40%; this was associated with a 26% decrease (P less than 0.05) in CO. Qs/Qt increased from 31 to 42% (P less than 0.01). There was a slight increase (P less than 0.01) in pulmonary vascular resistance (PVR) with TNG, and mean pulmonary artery pressure (PAP) decreased (P less than 0.05). In contrast, when CO was decreased by a similar amount with phlebotomy, mean Qs/Qt did not significantly change. There were similar changes in PVR and PAP and mixed venous O2 tension with TNG and phlebotomy. Accordingly, current results rule out increased flow, increased PVO2, and mechanical alterations in pulmonary vascular pressures as contributory to the increase in Qs/Qt with TNG. Alternatively, the increase in Qs/Qt with TNG may be explained by a direct pharmacologic decrease in pulmonary hypoxic vasoconstriction and/or by nonspecific pharmacologic effects.

Animals↗

PubMed1985

Effects of reduced resistive afterload on left ventricular pressure-volume relationship.

In seven anesthetized, beta-blocked dogs, we investigated the effects of a reduction in systemic vascular resistance (SVR) on left ventricular (LV) systolic mechanics. LV pressure and volumes (scintigraphic techniques) were measured in base-line condition, after opening one and then two arteriovenous fistulas (AVF). Volume was infused to maintain LV end-systolic pressure (LVESP). Despite a constant ESP, the mean end-systolic volume (LVESV) fell from 42 to 31 ml (P less than 0.025) when the SVR fell from 81 to 48 units (P less than 0.0025), and the LVESV fell further to 24 ml (P less than 0.0025) when the SVR was decreased to 30 units (P less than 0.025). In six similarly prepared dogs, aortic flow was measured, and when resistive afterload decreased, instantaneous flow increased. Since end-diastolic volume was not significantly changed when resistive afterload decreased, instantaneous LV volume decreased despite constant systolic LV pressure. In two of these dogs, LV pressure-volume (PV) trajectories were drawn for the ejection period. When SVR decreased there was a marked leftward shift of the PV trajectory as the end of ejection was approached. It is concluded that at a given contractile state and ventricular pressure, alterations in resistive load directly affect rate and extent of ventricular shortening.

Animals↗

PubMed1985

Treatment of canine permeability pulmonary edema: short-term effects of dobutamine, furosemide, and hydralazine.

The effects of treatment of oleic acid pulmonary edema with dobutamine, furosemide, and hydralazine on cardiopulmonary function in 24 dogs were investigated. Pulmonary capillary wedge pressure (PCWP) was adjusted to approximately 7 mm Hg; 45 min after oleic acid (0.08 ml/kg), dogs were randomly divided into a control group, in which PCWP was maintained at approximately 7 mm Hg, and into treatment groups as described above. Mean time-averaged PCWP was 2.3 mm Hg in dogs treated with dobutamine, 4.1 mm Hg with furosemide, and 4.4 mm Hg with hydralazine. Four hours of treatment with dobutamine and furosemide significantly (p less than .01) reduced accumulation of lung water compared with the control and hydralazine groups. Qs/Qt was lower (p less than .05) with dobutamine and furosemide compared with the other groups. In dogs given hydralazine, cardiac output (CO) and systemic vascular resistance (SVR) remained constant over the 4 hr treatment interval. In contrast, in all other groups, SVR increased and CO decreased (both p less than .05). The short-term pulmonary effects of the above drugs are probably explained by differences in PCWP and/or by regional pulmonary vascular effects.

Analysis of Variance↗

PubMed1985

Effects of vasodilators on canine cardiopulmonary function when a decrease in cardiac output complicates an increase in right ventricular afterload.

In canine oleic acid pulmonary edema, we investigated acute cardiopulmonary effects of nitroprusside (NP) before (NP1), and after (NP2) pulmonary vascular resistance (PVR) was increased via glass bead embolization. In the setting of increased PVR and reduced cardiac output (CO), acute cardiopulmonary effects of NP and hydralazine were compared. Oleic acid increased (p less than 0.05) pulmonary shunt (Qs/Qt) from 15 to 24%, but did not alter PVR. Cardiac output decreased (p less than 0.01) 31% with oleic acid from 4.2 to 2.9 1 X min-1 and systemic vascular resistance (SVR) increased (p less than 0.01). When PVR was normal, NP reduced (p less than 0.05) blood pressure (BP) from 148 to 123 mmHg, decreased SVR 31%, and increased (p less than 0.05) CO and Qs/Qt. Glass bead embolization increased (p less than 0.001) PVR from 2.2 to 20 mgHg X 1-1 X min and reduced (p less than 0.01) CO 23%, from 2.6 to 2 L/min. The Qs/Qt did not increase with embolization. In contrast to effects of NP1, when RV afterload was increased, CO fell (p less than 0.05) with NP2 from 2 to 1.6 1 X min-1. Alternatively, hydralazine improved cardiopulmonary function. In the setting of increased RV afterload, SVR and PVR decreased (p less than 0.01) 48 and 29%, respectively, with hydralazine. Corresponding to the decrease in resistance, CO increased (p less than 0.001) 84% with hydralazine, from 1.9 to 3.5 1 X min-1. Also, BP and Qs/Qt remained constant and arterial O2 tension increased (p less than 0.05) with hydralazine, from 113 to 152 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1984

Volume expansion versus norepinephrine in treatment of a low cardiac output complicating an acute increase in right ventricular afterload in dogs.

The authors investigated the effects of treatment on ventricular performance when cardiac output (CO) was reduced significantly because of an acute increase in pulmonary vascular resistance (PVR). In eight anesthetized, ventilated dogs, the effects of volume expansion (100 ml 6% dextran) on ventricular performance were determined before and after PVR was elevated. Resistance was increased by microembolization of the pulmonary vascular bed with glass beads (80-100 microns). When PVR was normal, volume expansion increased (P less than 0.05) stroke volume (SV) and mean blood pressure (BP). Alternatively, when RV afterload was increased, volume resulted in RV failure, i.e., decrease in SV (P less than 0.01) from 9.1 to 6.3 ml and a decrease (P less than 0.05) in mean BP from 97 to 65 mmHg, despite increased right ventricular end diastolic pressure (RVEDP) (P less than 0.05). Right ventricular dysfunction occurred with volume expansion, despite constant PVR and a decrease (P less than 0.01) in mean pulmonary artery pressure (PAP). In contrast to volume, norepinephrine infusion decreased biventricular filling pressures (P less than 0.01) and increased (P less than 0.01) SV from 6.2 to 11.3 ml. Accordingly, when RV afterload is increased significantly, even a relatively small increase in blood volume may result in RV dysfunction. Alternatively, inotropic agents with pressor effects may be the treatment of choice to increase CO when RV afterload is increased.

Animals↗

PubMed1984

Direct effects of nitroprusside do not alter gas exchange in canine oleic acid edema.

The authors investigated why intrapulmonary shunt (QS/QT) increases with sodium nitroprusside (SNP) in canine oleic acid pulmonary edema. To determine the effects of flow alone on QS/QT, a peripheral arteriovenous fistula with a variable resistor was employed to increase cardiac output (Q) 26 and 52% above base line in a stepwise fashion (P less than 0.01). To examine the direct effects of SNP, distinct from changes in flow, the drug was given to produce matched increments in Q in each dog (P less than 0.01). To control for time, base-line measurements were obtained before and after each intervention, the sequence of which was alternated. At each increment in Q, SNP and the arteriovenous fistula increased QS/QT a similar amount. The mixed venous O2 tension (P-vO2) followed Q similarly in each group. Pulmonary vascular resistance (PVR) fell more (P less than 0.01) with SNP than with the arteriovenous fistula at identical Q and P-vO2. The authors conclude that, in this model, a direct pharmacological effect of SNP does not contribute to the deterioration in QS/QT. In fact, SNP exerts a pulmonary vasoactive effect that does not adversely affect gas exchange.

Analysis of Variance↗

PubMed1984

Effects of dopamine on cardiopulmonary function and left ventricular volumes in patients with acute respiratory failure.

We investigated cardiopulmonary effects of dopamine in patients with acute respiratory failure. Specifically, we wished to test the hypothesis that left ventricular filling pressure (Pcwp) would increase when cardiac output (CO) increased with dopamine. Dopamine (range, 5.5 to 20 micrograms/kg/min) increased blood pressure (BP) (p less than 0.001) Pcwp, CO, and stroke volume (SV) (p less than 0.005). Mean Pcwp increased (p less than 0.005) 45% with dopamine, from 11 to 16 mmHg. Qs/Qt increased with dopamine in association with an increase in mixed venous O2 tension, and arterial O2 tension remained constant. In 8 of these patients, left ventricular end-diastolic volume (LVEDV) and end-systolic volume (ESV) were measured using scintigraphic techniques. The LVEDV increased (p less than 0.01) in each patient after the administration of dopamine, and the mean change was from 134 to 163 ml. Although BP and LV afterload increased in each patient, there was no consistent change in LVESV after dopamine administration, i.e., ESV decreased in 1 patient, remained constant in 3, and increased in 4. Accordingly, because afterload increased in all patients and ESV did not, dopamine probably increased contractility. Because EDV increased in all patients, we concluded that the increase in SV with dopamine is explained by a combination of inotropic and peripheral vascular effects.

Acute Disease↗

PubMed1984

Treatment of shock in a canine model of pulmonary embolism.

Despite the high mortality (greater than 30%) associated with hypotension complicating pulmonary embolism, previous studies have not systematically investigated how best to treat shock resulting from pulmonary embolism. In 24 dogs, we measured relevant hemodynamic parameters before and after shock was produced by intravenously injected autologous blood clots. When systemic blood pressure fell to 70 mmHg, dogs were randomly divided into groups and treated blindly for 1 h. All control dogs and all dogs treated with volume and isoproterenol died. In contrast, all dogs treated with noradrenaline were resuscitated and remained hemodynamically stable for 1 h. This effect of noradrenaline was significant (p less than 0.01, Fisher's exact test). Noradrenaline improved right ventricular performance by increasing blood pressure and improving right ventricular perfusion and/or by a direct increase in contractility. We conclude that in a canine model of pulmonary embolism and shock, noradrenaline may be the drug of choice for acute resuscitation.

Animals↗