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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies suggest that pulmonary capillary distensibility and recruitment may differ in lambs and sheep. To study the effect of pulmonary blood flow (PBF) and vascular pressure on capillary hemodynamics in lambs and sheep we measured the diffusing capacity for carbon monoxide (DLCO) as an index of pulmonary capillary blood volume during a baseline period, after increasing PBF, and during left atrial hypertension. In the lamb, DLCO did not change significantly either with a 65% increase in PBF or with an increase in left atrial pressure (Pla) of 1.33 kPa at constant PBF. In the sheep on the other hand, doubling PBF led to a 28% increase in DLCO (P less than 0.02), and an increase in Pla of 1.87 kPa at constant PBF led to a 19% increase in DLCO (P less than 0.01). These results suggest that the neonatal lamb has a nearly fully recruited and relatively non-compliant pulmonary capillary bed at rest, unlike the adult sheep which can respond to hemodynamic changes with distension and recruitment of the pulmonary capillary bed.
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PMID:The effect of blood flow and left atrial pressure on the DLCO in lambs and sheep. 161 30

To study the relationship between lung weight and lymph flow, we used an in situ, isolated sheep lung preparation that allowed these two variables to be measured simultaneously. All lungs were perfused for 4.5 h at a constant rate of 100 ml X min-1 X kg-1. In control lungs, the left atrial pressure (Pla) was kept at atmospheric pressure. In experimental lungs, Pla was kept atmospheric except for a 50-min elevation to 18 mmHg midway through the perfusion. During this period of left atrial hypertension, pulmonary arterial pressure rose from 18 to 31 mmHg, lymph flow rose from 3 to 12 ml/h, and the lymph-to-plasma oncotic pressure ratio (pi L/pi P) fell from 0.7 to 0.48. After left atrial pressure was returned to control, pulmonary arterial pressure, lymph flow, and pi L/pi P all returned to control levels. The rate of weight gain after the return of left atrial pressure to control was also the same as that in the control group. However, during the period of left atrial hypertension 135 ml of fluid were filtered into the lung, and this large increase in lung weight remained after the pressure was lowered. The presence of this substantial excess lung water despite control values for vascular pressures, lymph flow, rate of weight gain, and pi L/pi P suggests that the absolute amount of lung water has little influence on the dynamic aspects of lung fluid balance. These results are consistent with a two-compartment model of the interstitial space, where only one of the compartments is readily drained by the lymphatics.
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PMID:Lymph flow and lung weight in isolated sheep lungs. 378 91

We examined the effect of complement depletion on lung fluid and protein exchange after thrombin-induced pulmonary thromboembolization. Sheep were prepared with lung lymph fistulas to assess pulmonary transvascular fluid and protein dynamics. Studies were made in three groups: in group I (n = 5) pulmonary thromboembolization (PT) was induced by an iv infusion of thrombin (55.0 +/- 12.9 NIH U/kg); in group II (n = 6) cobra venom factor (CVF) was given ip (94.5 +/- 18.8 U/kg/day) for 2 days to deplete complement, and then thrombin (66.4 +/- 37.0 NIH U/kg) was infused to raise pulmonary vascular resistance to the same level as in group I; in group III (n = 10) left atrial pressure (Pla) was increased by 10-15 Torr in normal animals by inflation of a Foley balloon catheter. In group I, thrombin infusion caused an increase in pulmonary lymph flow (Qlym) with a gradual increase in the lymph-to-plasma protein concentration ratio (L/P). In complement-depleted sheep, thrombin caused a transient increase in Qlym, which was associated with a decrease in L/P. In group I an increase in Pla further increased Qlym but without a change in L/P, indicating an increase in lung vascular permeability to proteins; whereas in the decomplemented-thrombin sheep raising Pla increased Qlym but decreased L/P. Results in the latter group were similar to those obtained in normal animals after left atrial hypertension (group III). Therefore the complement system participates in the increase in lung vascular permeability following thrombin-induced microembolization.
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PMID:Effect of complement depletion on lung fluid balance after thrombin. 664 85

Elevation of intracranial pressure (ICP; 50-150 Torr) in sheep produces an increase in protein-rich lymph flow (QL) from the lung. This may be attributed to either microvascular permeability changes or increases in filtration surface area through recruitment. To eliminate increases in surface area, we recruited potential filtration beds by increasing left atrial pressure (Pla; 27-35 Torr) prior to elevating ICP in sheep anesthetized with pentobarbital sodium or halothane. Under these conditions, increased pulmonary microvascular permeability would be expected to produce an increased QL, lymphatic protein flux (CL), and plasma clearance of protein (CP). The results of ICP elevation following a period of steady-state Pla hypertension showed no such change in QL, CL or CP (n=8) compared with prior period of increased Pla. ICP elevation alone (n=6) produces a significant increase in CP manifested as an increase in QL (73%), with little change in the lymph-to-plasma ratio of protein concentration. These results suggest that a change in pulmonary microvascular surface area (not permeability) is the primary mechanism underlying increases in protein-rich QL following the elevation of ICP alone.
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PMID:Effects of intracranial and left atrial hypertension on lung fluid balance in sheep. 709 55

The purpose of this study was to measure hemodynamic and transvascular filtration changes in the lung during strenuous exercise in sheep. The specific goals were (1) to determine the nature of the reduction in pulmonary arterial pressure (Ppa) after its initial peak rise with onset of exercise; (2) to use a pulmonary artery catheter distal wedge technique ("microwedge") to better assess longitudinal changes in resistance in the pulmonary circulation with exercise; and (3) to compare lung lymph flow and protein concentration changes at comparable estimated microvascular pressure (Pmv) (mean Ppa - mean left atrial pressure) (Pla) x 0.4 + mean Pla) during exercise versus passive left atrial hypertension to determine whether exercise causes a higher than expected lymph flow. We found that cardiac output rises quickly and thereafter remains constant with constant-rate exercise, and, thus, the secondary reduction in Ppa was due to vasodilation and/or recruitment. The microwedge pressure rose more than did Pla, suggesting that actual Pmv was probably higher than that estimated. With hypoxia, most of the change in pulmonary vascular resistance was in upstream vessels (arteries and capillaries), as was most of the exercise-induced vasodilation. Lymph flow rose more quickly and was much higher during brief exercise than during left atrial hypertension at a comparable calculated Pmv, and lymph protein content decreased more quickly. The data point to a Pmv with strenuous exercise that is higher than expected.
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PMID:Pressure and flow changes in the pulmonary circulation in exercising sheep: evidence for elevated microvascular pressure. 846 28

We hypothesized that left atrial hypertension results in pulmonary vasoconstriction, which is obscured by the expected passive decrease in pulmonary vascular resistance. The objectives of this study were to demonstrate and quantify the vasoconstrictive changes that occur in the pulmonary circulation during experimental left atrial hypertension, to determine the site of vasoconstriction, and to explore its mechanism. Sheep were instrumented for measurement of pulmonary arterial (Ppa), left atrial (Pla), and systemic arterial pressures (Psa) with a Foley balloon catheter to variably obstruct the mitral valve. Distal pulmonary arterial wedge pressure (Ppaw) was determined by using a 5-Fr Swan-Ganz catheter that was advanced until it wedged with the balloon deflated. Cardiac output (CO) was estimated by thermodilution; pulmonary vascular resistances (PVR) were calculated as mean (Ppa - Pla)/CO = total PVR, (Ppa - Ppaw)/CO = upstream PVR, and (Ppaw - Pla)/CO = downstream PVR. We studied 15 awake sheep at baseline and during increases in Pla of 10 and 20 cmH2O, with and without inhalation of approximately 36 parts per million of nitric oxide. Left atrial hypertension resulted in elevation of Ppa. CO decreased only slightly at both levels of Pla elevation. Nitric oxide inhalation caused a significant decrease in PVR, which was greater as Pla increased. This vasodilator effect was most striking in downstream vessels. Experiments with phentolamine, atropine, and ibuprofen failed to reveal the mechanism of the reactive pulmonary vasoconstriction.
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PMID:Pulmonary vasoconstriction induced by mitral valve obstruction in sheep. 980 66

Sildenafil has been shown to be an effective treatment of pulmonary arterial hypertension and is believed to present with pulmonary selectivity. This study was designed to determine the site of action of sildenafil compared with inhaled nitric oxide (NO) and intravenous sodium nitroprusside (SNP), known as selective and nonselective pulmonary vasodilators, respectively. Inhaled NO (40 ppm), and maximum tolerated doses of intravenous SNP and sildenafil, (5 microg x kg(-1) x min(-1) and 0.1 mg x kg(-1) x h(-1)), respectively, were administered to eight dogs ventilated in hypoxia. Pulmonary vascular resistance (PVR) was evaluated by pulmonary arterial pressure (Ppa) minus left atrial pressure (Pla) vs. flow curves, and partitioned into arterial and venous segments by the occlusion method. Right ventricular hydraulic load was defined by pulmonary arterial characteristic impedance (Zc) and elastance (Ea) calculations. Right ventricular arterial coupling was estimated by the ratio of end-systolic elastance (Ees) to Ea. Decreasing the inspired oxygen fraction from 0.4 to 0.1 increased Ppa - Pla at a standardized flow of 3 l x min(-1) x m(-2) from 6 +/- 1 to 18 +/- 1 mmHg (mean +/- SE). Ppa - Pla was decreased to 9 +/- 1 by inhaled NO, 14 +/- 1 by SNP, and 14 +/- 1 mmHg by sildenafil. The partition of PVR, Zc, Ea, and Ees/Ea was not affected by the three interventions. Inhaled NO did not affect systemic arterial pressure, which was similarly decreased by sildenafil and SNP, from 115 +/- 4 to 101 +/- 4 and 98 +/- 5 mmHg, respectively. We conclude that inhaled NO inhibits hypoxic pulmonary vasoconstriction more effectively than sildenafil or SNP, and sildenafil shows no more selectivity for the pulmonary circulation than SNP.
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PMID:Effects of sildenafil on hypoxic pulmonary vascular function in dogs. 1677 5