Etiologic factors and sites of origin of pulmonary vascular resistance hysteresis

Kevin M. Creamer, Laryssa L. McCloud, Lyle E Fisher, Ina C. Ehrhart

Research output: Contribution to journalArticle

Abstract

Introduction: Previously we have shown that there is pulmonary vascular resistance hysteresis (PVRH) with lower PVR on deflation when lungs are inflated and deflated from complete collapse. We performed a series of studies using isolated blood perfused canine lung lobes to determine both, where in the vascular bed this occurred and the etiology of this hysteresis. Methods: The isolated lobes had constant blood flow and a set pulmonary vein pressure (5cm H2O). PVR was measured during stepwise inflation and deflation (I+D). Vascular clamping techniques and first pass metabolism of a tritiated angiotensin converting enzyme substrate were used to measure segmental resistances and perfused capillary surface area respectively. Some lobes were I+D with saline to determine surface tension s effect on PVRH. Intralobar PVR means for I+D and intergroup results were compared with t-Tests. An * represents P<0.05 inflation vs. deflation and an @ is P<0.05 compared to the normal flow group. Results: The 18 lobes tested at normal flow (600ml/min) had mean PVRH of 9.8%*. A subgroup of 7 lobes underwent double occlusion of both the pulmonary artery and vein during I+D to see the segmental resistance changes. Downstream from the midpoint of the capillary demonstrated 62.5%* of the PVRH. A separate arterial and venous occlusion technique in a subgroup of 5 lobes showed significant downstream PVRH and trends toward PVRH in the middle vessels but not in the upstream vessels. Measures of perfused capillary surface area in the other 6 normal flow lobes demonstrated no change despite a 15%* drop in PVR at the deflation volume tested. Saline I+D of 5 lobes reduced PVRH to 2.8% Six high flow lobes (1200ml/min) and 6 high pulmonary vein pressure lobes (10cm H2O) had PVRH reduced to 5.3%*@ and 5.4%*@ respectively, while 6 low flow lobes (300ml/min) had accentuated PVRH to 18.1%* Conclusion: Surface tension not capillary recruitment acts as a major source of PVRH. Hydrostatic pressure by either venous stasis or high flow can reduce this effect. Surprisingly, the majority of these effects occur on the downstream side of the pulmonary capillary and in the pulmonary veins.

Original languageEnglish (US)
JournalCritical Care Medicine
Volume27
Issue number12 SUPPL.
StatePublished - Dec 1 1999

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Vascular Resistance
Pulmonary Veins
Surface Tension
Economic Inflation
Lung
Blood Vessels
Capillary Resistance
Pressure
Hydrostatic Pressure
Peptidyl-Dipeptidase A
Constriction
Pulmonary Artery
Canidae

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Etiologic factors and sites of origin of pulmonary vascular resistance hysteresis. / Creamer, Kevin M.; McCloud, Laryssa L.; Fisher, Lyle E; Ehrhart, Ina C.

In: Critical Care Medicine, Vol. 27, No. 12 SUPPL., 01.12.1999.

Research output: Contribution to journalArticle

Creamer, Kevin M. ; McCloud, Laryssa L. ; Fisher, Lyle E ; Ehrhart, Ina C. / Etiologic factors and sites of origin of pulmonary vascular resistance hysteresis. In: Critical Care Medicine. 1999 ; Vol. 27, No. 12 SUPPL.
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T1 - Etiologic factors and sites of origin of pulmonary vascular resistance hysteresis

AU - Creamer, Kevin M.

AU - McCloud, Laryssa L.

AU - Fisher, Lyle E

AU - Ehrhart, Ina C.

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N2 - Introduction: Previously we have shown that there is pulmonary vascular resistance hysteresis (PVRH) with lower PVR on deflation when lungs are inflated and deflated from complete collapse. We performed a series of studies using isolated blood perfused canine lung lobes to determine both, where in the vascular bed this occurred and the etiology of this hysteresis. Methods: The isolated lobes had constant blood flow and a set pulmonary vein pressure (5cm H2O). PVR was measured during stepwise inflation and deflation (I+D). Vascular clamping techniques and first pass metabolism of a tritiated angiotensin converting enzyme substrate were used to measure segmental resistances and perfused capillary surface area respectively. Some lobes were I+D with saline to determine surface tension s effect on PVRH. Intralobar PVR means for I+D and intergroup results were compared with t-Tests. An * represents P<0.05 inflation vs. deflation and an @ is P<0.05 compared to the normal flow group. Results: The 18 lobes tested at normal flow (600ml/min) had mean PVRH of 9.8%*. A subgroup of 7 lobes underwent double occlusion of both the pulmonary artery and vein during I+D to see the segmental resistance changes. Downstream from the midpoint of the capillary demonstrated 62.5%* of the PVRH. A separate arterial and venous occlusion technique in a subgroup of 5 lobes showed significant downstream PVRH and trends toward PVRH in the middle vessels but not in the upstream vessels. Measures of perfused capillary surface area in the other 6 normal flow lobes demonstrated no change despite a 15%* drop in PVR at the deflation volume tested. Saline I+D of 5 lobes reduced PVRH to 2.8% Six high flow lobes (1200ml/min) and 6 high pulmonary vein pressure lobes (10cm H2O) had PVRH reduced to 5.3%*@ and 5.4%*@ respectively, while 6 low flow lobes (300ml/min) had accentuated PVRH to 18.1%* Conclusion: Surface tension not capillary recruitment acts as a major source of PVRH. Hydrostatic pressure by either venous stasis or high flow can reduce this effect. Surprisingly, the majority of these effects occur on the downstream side of the pulmonary capillary and in the pulmonary veins.

AB - Introduction: Previously we have shown that there is pulmonary vascular resistance hysteresis (PVRH) with lower PVR on deflation when lungs are inflated and deflated from complete collapse. We performed a series of studies using isolated blood perfused canine lung lobes to determine both, where in the vascular bed this occurred and the etiology of this hysteresis. Methods: The isolated lobes had constant blood flow and a set pulmonary vein pressure (5cm H2O). PVR was measured during stepwise inflation and deflation (I+D). Vascular clamping techniques and first pass metabolism of a tritiated angiotensin converting enzyme substrate were used to measure segmental resistances and perfused capillary surface area respectively. Some lobes were I+D with saline to determine surface tension s effect on PVRH. Intralobar PVR means for I+D and intergroup results were compared with t-Tests. An * represents P<0.05 inflation vs. deflation and an @ is P<0.05 compared to the normal flow group. Results: The 18 lobes tested at normal flow (600ml/min) had mean PVRH of 9.8%*. A subgroup of 7 lobes underwent double occlusion of both the pulmonary artery and vein during I+D to see the segmental resistance changes. Downstream from the midpoint of the capillary demonstrated 62.5%* of the PVRH. A separate arterial and venous occlusion technique in a subgroup of 5 lobes showed significant downstream PVRH and trends toward PVRH in the middle vessels but not in the upstream vessels. Measures of perfused capillary surface area in the other 6 normal flow lobes demonstrated no change despite a 15%* drop in PVR at the deflation volume tested. Saline I+D of 5 lobes reduced PVRH to 2.8% Six high flow lobes (1200ml/min) and 6 high pulmonary vein pressure lobes (10cm H2O) had PVRH reduced to 5.3%*@ and 5.4%*@ respectively, while 6 low flow lobes (300ml/min) had accentuated PVRH to 18.1%* Conclusion: Surface tension not capillary recruitment acts as a major source of PVRH. Hydrostatic pressure by either venous stasis or high flow can reduce this effect. Surprisingly, the majority of these effects occur on the downstream side of the pulmonary capillary and in the pulmonary veins.

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