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Results for “VASCULAR RESISTANCE”

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At least 145 records · Page 8Linked to original sources

PubMed1991

Responsiveness of raised pulmonary vascular resistance to oxygen assessed by pulsed Doppler echocardiography.

OBJECTIVE: To assess whether changes in Doppler echocardiographic indices in the pulmonary artery correlated with changes in pulmonary vascular resistance. DESIGN: Acceleration time, ejection time, maximal flow velocity, and velocity time integrals were measured at the same time as pressure and oxygen saturation measurements in room air and during 10 minutes of oxygen breathing in the catheterisation laboratory. Pulmonary vascular resistance and pulmonary blood flow (Qp) were calculated from catheterisation data by use of the Fick principle. PATIENTS: 14 consecutive patients with a congenital heart defect and a left to right shunt associated with raised pulmonary artery pressure who underwent routine diagnostic cardiac catheterisation to assess their pulmonary vascular resistance. RESULTS: Though pulmonary vascular resistance and systolic pulmonary artery pressure fell significantly during oxygen administration, there was no significant change in the acceleration time or ejection time. Peak velocity increased significantly during oxygen administration. During oxygen breathing Doppler derived measurements of pulmonary flow showed a significant increase in Qp similar to the increase in Qp measured by the Fick principle. There was no significant correlation between the fall in pulmonary vascular resistance and the increase in acceleration time or ejection time, increase in peak velocity, increase in pulmonary artery diameter, or increase in Doppler derived pulmonary blood flow. CONCLUSIONS: Measurements of acceleration and ejection time by Doppler echocardiography did not predict the response of pulmonary artery pressure and resistance to oxygen. Though changes in maximal flow velocity across the pulmonary artery and in Doppler derived pulmonary blood flow measurements became significant during oxygen breathing, the correlation of these changes with fall in pulmonary vascular resistance was poor.

Blood Flow Velocity↗

PubMed1997

Positive end-expiratory pressure increases pulmonary venous vascular resistance in patients after coronary artery surgery.

OBJECTIVE: To investigate the effect of positive and-expiratory pressure (PEEP) on the longitudinal distribution of pulmonary vascular resistance in patients immediately after coronary artery bypass grafting. DESIGN: Prospective, intervention study. SETTING: Postcardiac surgery intensive care unit in a teaching institution. PATIENTS: Twenty patients after elective coronary artery bypass grafting. INTERVENTION: The effect of PEEP on pulmonary circulation, at four different levels (0, 5, 10, and 15 cm H2O), was analyzed in 20 patients. MEASUREMENTS AND MAIN RESULTS: Mean pulmonary arterial pressure, left atrial pressure, pulmonary artery occlusion pressure, and pulmonary capillary pressure were measured at each PEEP level. A model consisting of two resistances in series was used to analyze the effect of PEEP on the pulmonary circulation. The pulmonary vascular resistance for each area (arterial and venous) of the circulation was calculated. Pulmonary vascular resistance increased from 216 +/- 70 dyne.sec/cm5 at a PEEP of 0 cm H2O to 308 +/- 125 dyne.sec/cm5 at a PEEP of 15 cm H2O (p < .001). This increase, however, resulted solely from an increase in the resistance of the venous part of the pulmonary circulation from 66 +/- 29 to 134 +/- 69 dyne.sec/cm5 (p < .001), without any change in pulmonary arterial resistance. CONCLUSIONS: PEEP increases pulmonary vascular resistance solely by increasing pulmonary venous resistance. When applying PEEP, changes in pulmonary vascular resistance may impede the resorption of pulmonary edema fluid.

Aged↗

PubMed1992

Effects of aortic pressure and vasoactive agents on the vascular resistance of the vasa vasorum in canine isolated thoracic aorta.

1. We have developed a new preparation for continuously measuring changes in vascular resistance of the vasa vasorum of the canine isolated thoracic aorta perfused at a constant flow rate with Krebs-bicarbonate solution. 2. An increase of more than 150 mmHg in aortic pressure caused a significant increase in the vascular resistance of the vasa vasorum. 3. 5-Hydroxytryptamine (5-HT), noradrenaline (NA), adrenaline and dopamine caused dose-dependent increases in the vascular resistance of the vasa vasorum. The decreasing order of potency in the vasoconstrictor responses was as follows: 5-HT >> NA = adrenaline >> dopamine. The 5-HT- and adrenaline-induced vasoconstrictor responses were inhibited by methysergide and by phentolamine plus propranolol, respectively. 4. Acetylcholine (ACh), isoprenaline (ISP), histamine (His), ATP, ADP and adenosine produced dose-related decreases in the vascular resistance of aortic vasa vasorum perfused with the Krebs solution containing 10(-5) M-NA. The decreasing order of potency in the response was as follows: ACh = ISP > His >> adenosine = ATP = ADP. The ACh-, ISP- and His-induced vasodilator responses were antagonized by atropine, propranolol and famotidine, respectively. 5. The results suggest that the preparation described is useful for studying the regulation of vascular resistance of aortic vasa vasorum and that aortic pressure and vasoactive compounds may directly regulate the vascular resistance of the vasa vasorum in canine isolated thoracic aorta.

Animals↗

PubMed1984

Blockade of central nervous system GABAergic tone causes sympathetic-mediated increases in coronary vascular resistance in cats.

Picrotoxin, an antagonist of gamma-aminobutyric acid, produces an increase in coronary vascular resistance, S-T segment elevation, and ventricular arrhythmias after an intravenous injection of 2 mg/kg in chloralose-anesthetized cats. To determine whether these responses were due to blockade of central nervous system GABAergic mechanisms leading to an increase in sympathetic outflow to the coronary vasculature, several types of experiments were performed. First, picrotoxin was injected directly into the brain in a dose of 600 micrograms while coronary blood flow and S-T segment changes were monitored. Central nervous system administration of this agent resulted in a significant increase in coronary vascular resistance, S-T segment elevation, and arrhythmias. Second, animals were pretreated with the gamma-aminobutyric acid receptor agonist drug, muscimol, prior to central administration of picrotoxin. Pretreatment prevented the usual increase in coronary vascular resistance, S-T segment elevation, and arrhythmias. Third, animals were subjected to acute bilateral cardiac sympathetic denervation prior to picrotoxin administration. Denervation attenuated the picrotoxin-induced increase in coronary vascular resistance (mean = 11.6 +/- 2.1% vs. 26.1 +/- 7.1%, P less than 0.05) and elevation in S-T segment (mean = 0.09 +/- 0.03 mV vs. 0.29 +/- 0.04 mV, P less than 0.05), and prevented arrhythmias. Pretreatment with the alpha-receptor blocking agent, phentolamine, produced even more pronounced antagonistic effects. These results suggest that blockade of central nervous system GABAergic tone leads to enhanced sympathetic outflow to the coronary vasculature, resulting in an increase in coronary vascular resistance of sufficient intensity to cause S-T segment elevation and arrhythmias.

Animals↗

PubMed2002

Short-term cortisol infusion in the brachial artery, with and without inhibiting 11 beta-hydroxysteroid dehydrogenase, does not alter forearm vascular resistance in normotensive and hypertensive subjects.

BACKGROUND: Vascular tone is increased in primary hypertension, and glucocorticoids affect vascular tone. Local cortisol availability is modulated by activity of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD). As this activity may be decreased in patients with primary hypertension, vascular sensitivity to cortisol may be increased in these patients. We studied the acute effect of cortisol on forearm vascular resistance (FVR) by infusing cortisol directly into the brachial artery, both with and without inhibition of 11 beta-HSD, in normotensive and hypertensive subjects. DESIGN: Twenty normotensive volunteers and 20 patients with primary hypertension participated in the study. After a 10-min infusion of vehicle (glucose 5%), cortisol was infused into the brachial artery in three stepwise increasing doses (3.5, 10.5 and 35 microg per 100 mL of forearm volume), each for 10 min. Next, the participants received placebo or 500 mg glycyrrhetinic acid (GA) orally, and 150 min later the same infusion schedule was repeated. Forearm vascular resistance was measured during the last 5 min of the infused vehicle and of each dose. Arterial and forearm venous plasma samples for measurement of cortisol and cortisone were taken at the end of the infusions of glucose 5% and the highest cortisol dose. RESULTS: In both normotensive and hypertensive subjects, neither the infusion of cortisol nor the administration of GA changed FVR. Also 2 h after the cortisol infusion there remained no change in FVR in both the normotensive and hypertensive groups who received placebo. Following the infusion of the highest cortisol dose, total plasma cortisone levels in the venous plasma were decreased compared with levels in the arterial plasma (36 +/- 3 and 49 +/- 4 nmol L-1, respectively, P < 0.05). The protein-bound venous cortisone was 37.1 +/- 4.8 nmol L-1 during the vehicle compared with 23.9 +/- 3.7 nmol L-1 during the cortisol infusion (P < 0.01), whereas the free cortisone level was not altered by the cortisol infusion. CONCLUSIONS: In both normotensive and hypertensive subjects, high-dose cortisol infusion both with and without 11 beta-HSD inhibition did not change FVR either immediately or after 2 h. We could not demonstrate in vivo 11 beta-HSD activity in the forearm vascular tissues. When binding of cortisone to CBG is changed, e.g. during cortisol infusion, arterio-venous changes in cortisone cannot reliably be used to assess (alterations in) local 11 beta-HSD activity.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed1975

Correlation between pulmonary vascular resistance and pulmonary arterial diastolic pressure in congenital heart diseases with left to right shunt.

Our studies recently conducted on the correlation between pulmonary vascular resistance and pulmonary arterial diastolic pressure in 467 cases, identified an extremely high correlation between the two. The correlation coefficient between pulmonary arterial diastolic pressure (PAdp) and pulmonary to systemic resistance ratio (Rp/Rs) was 0.799 and that between pulmonary vascular resistance index (RP-index) and PAdp was found to be 0.791. And a still higher correlation was observed between pulmonary vascular resistance and pressure gradient between PAdp and left atrial mean pressure (LAmp), where the correlation coefficient between Rp/Rs and (PAdp-LAmp) was 0.851 and that between Rp-index and (PAdp-LAmp) was 0.813. Those correlations are found to be higher in degree than the correlations between pulmonary arterial mean pressure or pulmonary arterial systolic pressure and pulmonary vascular resistance, leading to the conclusion that the pulmonary arterial diastolic pressure is of extremely high clinical importance as an index for increase in pulmonary vascular resistance.

Adolescent↗

PubMed1994

Regulation of pulmonary vascular resistance by endogenous and exogenous nitric oxide.

Inhaled nitric oxide (NO) causes selective pulmonary vasodilation under conditions of hypoxia or pulmonary vascular dysfunction. We have observed that NO affects canine pulmonary vascular resistance minimally under normal conditions. We hypothesized that endogenous NO is partly responsible for pulmonary vasomotor regulation in normoxic and hypoxic states. Dogs were studied before and after pulmonary endothelial injury with monocrotaline and N-omega-nitro-L-arginine (LNNA). Systemic vascular resistance was unaffected by NO. Under normal conditions, exogenous NO had little effect on pulmonary vascular resistance. After monocrotaline administration, baseline pulmonary vascular resistance was unchanged but decreased further in response to NO. After LNNA administration, pulmonary vascular resistance increased and there was an exaggerated increase with hypoxia that was reduced by NO. The effect of monocrotaline on in vitro endothelial function was evaluated with isolated pulmonary arteries, which showed a decreased relaxation response to bradykinin (an endothelial-dependent vasodilator) and a normal response to nitroprusside (an endothelial-independent vasodilator). These results support the hypothesis that endogenous NO is an important regulator of pulmonary vasomotor tone and is of even greater importance during hypoxia.

Animals↗

PubMed1977

Reflex changes in hindlimb and renal vascular resistance in response to distention of the isolated pulmonary arteries of the dog.

We describe a preparation that uses a constant flow, right heart bypass for perfusion of an isolated pouch of the main pulmonary arteries at controlled pressures, and show that increments in pressure in the pulmonary arterial pouch are accompanied by increases in systemic vascular resistance and in hindlimb vascular resistance. These changes are demonstrated over the whole range of 5-120 cm H2O pressure in the pulmonary arterial pouch. In contrast there are no significant changes in renal vascular resistance or heart rate. We find that changing the temperature of the perfusate in the pulmonary arterial pouch from 37 degrees C to 30 degress C is associated with a decrease in systemic vascular resistance. Furthermore, the effects of raising the pulmonary arterial pouch pressure and of cooling are abolished by cervical vagotomy. These findings suggest that there is a tonic reflex vasoconstrictor tone generated by the activity of receptors lying in or close to the walls of the pulmonary artery. These findings also suggest that the differential effects on systemic vascular resistance and renal resistance may provide one mechanism by which changes in blood volume may lead to appropriate changes in renal solute excretion.

Animals↗

PubMed1999

Capillary filtration coefficient, vascular resistance, and compliance in isolated mouse lungs.

Although many recently produced transgenic mice possess gene alterations affecting pulmonary vascular function, there are few baseline measurements of vascular resistance and permeability. Therefore, we excised the lungs of C57/BL6 mice and perfused them with 5% bovine serum albumin in RPMI-1640 culture medium at a nominal flow of 0.5 ml/min and ventilated them with 20% O(2)-5% CO(2)-75% N(2). The capillary filtration coefficient, a sensitive measurement of hydraulic conductivity, was unchanged over 2 h (0.33 +/- 0.03 ml. min(-1). cmH(2)O(-1). 100 g(-1)) in a control group ventilated with low peak inflation pressures (PIP) but increased 4. 3-fold after high PIP injury. Baseline pulmonary vascular resistance was 6.1 +/- 0.4 cmH(2)O. ml(-1). min. 100 g(-1) and was distributed 34% in large arteries, 18% in small arteries, 14% in small veins, and 34% in large veins on the basis of vascular occlusion pressures. Baseline vascular compliance was 5.4 +/- 0.3 ml. cmH(2)O(-1). 100 g(-1) and decreased significantly with increased vascular pressures. Baseline pulmonary vascular resistance was inversely related to both perfusate flow and microvascular pressure and increased to 202% of baseline after infusion of 10(-4) M phenylephrine due to constriction of large arterial and venous segments. Thus isolated mouse lung vascular permeability, vascular resistance, and the longitudinal distribution of vascular resistance are similar to those in other species and respond in a predictable manner to microvascular injury and a vasoconstrictor agent.

Animals↗

PubMed1975

Reduced myocardial reflow and increased coronary vascular resistance following prolonged myocardial ischemia in the dog.

Studies were performed to determine whether an alteration in coronary vascular resistance and a reduction in the reflow phenomenon occurred in the blood-perfused, heparinized canine heart after various periods of myocaridal ischemia. Regional myocardial blood flow was measured with radioactive microspheres. Proximal left anterior descending coronary artery blood flow was measured with a periarterial flow transducer. Reduced reflow to the ischemic portion of the left ventricle and increased resistance in the left anterior descending coronary artery were present after 120 minutes of myocardial ischemia. The reduction in reflow was specific to the subendocardium of the ischemic area. Saline and isosorbide dinitrate (Isordi) did not prevent the increase in coronary vascular resistance or the significant reduction in reflow to the subendocardial portion of the ischemic area. Hypertonic mannitol given so as to increase serum osmolality 40 mosmoles/kg prevented the increase in coronary vascular resistance and modified the reduction in the reflow phenomenon to the subendocardial portion of the ischemic area. Thus, both an increase in coronary vascular resistance and a significant reduction in reflow to the subendocardial portion of the ischemic area occur in the canine heart after 120 minutes of myocardial ischemia. Moreover, the increase in coronary vascular resistance can be prevented and the reduction in reflow to the subendocardial portion of the ischemic area can be modified by the administration of hypertonic mannitol.

Animals↗

PubMed1988

Do beta-blockers really increase peripheral vascular resistance? Review of the literature and new observations under basal conditions.

Most antihypertensive drugs act by counteracting vasoconstrictor mechanisms and lower blood pressure by lowering vascular resistance. The beta-blockers, which have the unique feature of counteracting cardiac sympathetic drive, seem to be a major exception to this generalization. Moreover, their degree of cardiodepression is not only directly correlated with the initial sympathetic tone, but also with their degree of intrinsic sympathicomimetic activity (ISA). Cardiodepression initially evokes a proportional rise in vascular resistance. As indicated by review of the literature, the antihypertensive effect of beta-blockers always parallels a decline in vascular resistance. Minimizing cardiac sympathetic drive by strict bedrest and studying beta-blockers with different degrees of ISA in 50 hypertensive patients showed that initially the effect of the drugs is offset by a rise in vascular resistance proportional to the fall in cardiac output. After that, blood pressure always fell parallel with the decline in vascular resistance. In the long run blood pressure and vascular resistance were always positively correlated, whatever the level of cardiac output. Thus, like all other antihypertensive agents, beta-blockers also lower blood pressure through interference with a vasoconstrictor mechanism.

Adrenergic beta-Antagonists↗

PubMed1968

Longitudinal distribution of vascular resistance in the pulmonary arteries, capillaries, and veins.

A new method has been described for measuring the pressure and resistance to blood flow in the pulmonary arteries, capillaries, and veins. Studies were performed in dog isolated lung lobes perfused at constant flow with blood from a donor dog. Pulmonary artery and vein volume and total lobar blood volume were measured by the ether plethysmograph and dyedilution techniques. The longitudinal distribution of vascular resistance was determined by analyzing the decrease in perfusion pressure caused by a bolus of low viscosity liquid introduced into the vascular inflow of the lobe. The pulmonary arteries were responsible for 46% of total lobar vascular resistance, whereas the pulmonary capillaries and veins accounted for 34 and 20% of total lobar vascular resistance respectively. Vascular resistance was 322 dynes .sec.cm(-5)/ml of vessel in the lobar pulmonary arteries, 112 dynes.sec.cm(-5)/ml in the pulmonary capillaries, and 115 dynes.sec.cm(-5)/ml in the lobar pulmonary veins. Peak vascular resistivity (resistance per milliliter of volume) was in an area 2 ml proximal to the capillary bed, but resistivity was high throughout the pulmonary arterial tree. The pulmonary arteries accounted for approximately 50% of vascular resistance upstream from the sluice point when alveolar pressure exceeded venous pressure. The method described provides the first measurements of pulmonary capillary pressure. Mid-capillary pressure averaged 13.3 cm H(2)O, pulmonary artery pressure averaged 20.4 cm H(2)O, and pulmonary vein pressure averaged 9.2 cm H(2)O. These techniques also provide a way of analyzing arterial, capillary, and venous responses to various pharmacologic and physiologic stimuli.

Animals↗

PubMed2003

Pulmonary blood pressure, not flow, is associated with net endothelin-1 production in the lungs of patients with congenital heart disease and normal pulmonary vascular resistance.

OBJECTIVE: Endothelin-1 concentrations are increased in patients with increased mean pulmonary arterial pressure, pulmonary blood flow, and pulmonary vascular resistance. However, endothelin-1 concentrations have not been well characterized in patients with congenital heart disease and normal pulmonary vascular resistance. In particular, it is unclear whether pressure or flow is the key regulator of endothelin- 1 in this setting. We tested the hypothesis that pulmonary blood pressure and not flow is associated with net endothelin-1 production in patients with congenital heart disease and normal pulmonary vascular resistance. METHODS: With a commercially available immunoassay, we measured endothelin-1 concentrations in pulmonary arterial and pulmonary venous plasma of 56 consecutive patients with congenital heart disease and pulmonary vascular resistance less than 2 U. m(2) undergoing cardiac catheterization. We used multiple linear regression to analyze the effect of demographic and hemodynamic variables on pulmonary arterial and venous endothelin-1 concentrations and on the change of endothelin-1 concentration over the pulmonary vascular bed. RESULTS: Multiple linear regression revealed that of all the hemodynamic variables tested, mean pulmonary arterial pressure had the greatest effect on increasing the change of endothelin-1 concentration over the pulmonary vascular bed (P <.0001). Pulmonary blood flow did not have any effect on endothelin-1 concentrations or on the change of endothelin-1 concentration over the pulmonary vascular bed. CONCLUSIONS: This study shows that pulmonary blood pressure and not flow is associated with net endothelin-1 production in patients with congenital heart disease and normal pulmonary vascular resistance.

Blood Pressure↗

PubMed2006

Aprotinin attenuates the elevation of pulmonary vascular resistance after cardiopulmonary bypass.

Pulmonary vascular resistance (PVR) is generally believed to be elevated after cardiopulmonary bypass (CPB) due to whole body inflammation. Aprotinin has an antiinflammatory action, and it was hypothesized that aprotinin would attenuate the PVR increase induced by CPB. Ten mongrel dogs were placed under moderately hypothermic CPB for 2 hr. The experimental animals were divided into a control group (n=5, group I) and an aprotinin group (n=5, group II). In group II, aprotinin was administered during pre-bypass (50,000 KIU/kg) and post-bypass (10,000 KIU/kg) periods. Additional aprotinin (50,000 KIU/kg) was mixed in CPB priming solution. PVRs at pre-bypass and post-bypass 0, 1, 2, 3 hr were calculated, and lung tissue was obtained after the experiment. Post-bypass PVRs were significantly higher than prebypass levels in all animals (n=10, p<0.001). PVR elevation in group II was less than in group I at 3 hr post-bypass (p=0.0047). Water content of the lung was lower in group II (74+/-9.4%) compared to that of group I (83+/-9.5%), but the difference did not reach significance (p=0.076). Pathological examination showed a near normal lung structure in group II, whereas various inflammatory reactions were observed in group I. We concluded that aprotinin may attenuate CPB-induced PVR elevation through its anti-inflammatory effect.

Animals↗

PubMed1985

Metabolic control of renal vascular resistance and glomerulotubular balance.

Renal vascular resistance (RVR) and glomerulotubular balance were examined in isolated rat kidneys perfused at 100 mm Hg with 10 mM lactate (L) or 10 mM pyruvate (P) or 5 mM glucose (G) either alone or with a mixture of 20 amino acids (13.5 mM, AA); albumin oncotic pressure 24 +/- 1 mm Hg. RVR was L greater than P greater than G = AA. Vasodilation by G and AA was additive. Proximal tubular sodium-cotransport was evaluated from fractional reabsorption (FR) of phosphate (Pi), G, and L. FR Pi was 91% in AA, 86% in P, 72% in L, and 67% in G. Combining AA or P with L or G increased FR Pi to 89 to 90%. FRs of G and L by G and L perfused kidneys were 83 and 78%, respectively, and were increased to 97 to 99% by combining G or L with AA or P. P and AA also increased FR sodium and FR water when combined with L or G or when combined with each other. GFR correlated positively with FR sodium and FR water. AA combined synergistically with L to increase gluconeogenesis. These results indicate that, compared with pyruvate or AA, neither glucose nor lactate alone is a good energy source for proximal tubular reabsorption, that synergistic interactions between AA or pyruvate and lactate or glucose augment GFR by increasing proximal tubular reabsorption, and that the vasodilating effects of glucose and AA are not related directly to their effects on GFR.

Amino Acids↗

PubMed1985

Calf blood flow and vascular resistance in middle-aged and elderly hypertensives.

Hypertension is associated with increased total peripheral vascular resistance. Calf blood flow and vascular resistance in two groups of hypertensives of different age has been evaluated: 85 middle-aged hypertensives (MH) and 25 elderly hypertensives (EH), and in two groups of 20 normotensive control subjects of similar age. Calf blood flow at rest (RF) and after ischaemia (PF) was determined by strain-gauge plethysmography. Basal (BVR) and minimal (MVR) vascular resistance were obtained by the mean blood pressure (MBP):RF and MBP:PF ratio. Blood flow at rest was reduced only in EH, while PF was significantly lower in MH and in EH in comparison with the respective controls. In parallel, BVR and MVR were higher in MH and in EH compared with controls. The increase of BVR and of MVR was more evident in EH. These results suggest that in EH there is an impairment of the calf maximal vasodilatation capacity, probably due to the long duration of hypertension.

Adolescent↗

PubMed1989

The longitudinal distribution of pulmonary vascular resistance during unilateral hypoxia.

Pulmonary capillary hydrostatic pressure and the longitudinal distribution of pulmonary vascular resistance (arterial and venous components) can be determined by analysis of pressure decay curves following pulmonary artery occlusion. To validate this technique in intact animals, pulmonary artery occlusion pressure decay curves were obtained from both lungs in six anesthetized sheep during control conditions (100% O2) and during unilateral hypoxic ventilation (100% O2 versus 100% N2). Analysis of pulmonary artery occlusion pressure curves indicated the following: 1) in the hypoxic lung, unilateral hypoxia increased the precapillary portion of pulmonary vascular resistance from 72% of the total resistance to 89% of the total resistance in that lung; 2) in the nonhypoxic lung, unilateral hypoxia did not significantly affect the distribution of pulmonary vascular resistance; and 3) unilateral hypoxia produced no significant change in pulmonary capillary pressure in the hypoxic lung compared with control; however, pulmonary capillary pressure was significantly greater in the nonhypoxic lung. These results are consistent with other evidence that hypoxic pulmonary vasoconstriction acts locally and primarily affects resistance at the arteriolar level. Pulmonary artery occlusion pressure decay curve analysis appears to be a valid technique for the measurement of pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance in intact anesthetized animals. These measurements pertain only to the vasculature distal to the site of pulmonary artery occlusion with the catheter, and, thus, caution must be used when applying this technique in a setting of nonhomogenous lung injury.

Animals↗

PubMed1994

Basis for the selective reduction of pulmonary vascular resistance in humans during infusion of adenosine.

The objective of this study was to demonstrate the basis for the selective reduction of pulmonary vascular resistance by intravenous infusion of adenosine. Secondary objectives of the study were to determine the rate of central infusion of adenosine at which the nucleoside appears in the systemic circulation and to relate this to hemodynamic events. Plasma concentrations of adenosine in the right and left atria were measured during peripheral (5 patients) and central (12 patients) infusions of adenosine in adults with normal pulmonary arterial pressures undergoing coronary artery bypass surgery. The hemodynamic effects of central (right ventricle) infusion of adenosine were also examined. The extraction of adenosine across the pulmonary vascular bed was found to be 73.6 +/- 4.8%. The mean maximal decrease in pulmonary vascular resistance index, 48.8 +/- 9.6%, occurred at an adenosine infusion rate of 30 micrograms.kg-1.min-1, whereas the systemic vascular resistance index remained unchanged. Thus, adenosine, administered centrally in anesthetized patients with normal pulmonary vascular resistances, selectively lower pulmonary vascular resistance. The basis for this selective effect is the substantial extraction of adenosine during passage through the pulmonary vascular bed.

Adenosine↗