Pulmonary Arterial, Capillary and Venous Resistances From Arterial Occlusion

Yamada, Yoshio; Suzukawa, Masayuki; Chinzei, Mieko; Suwa, Kunio; Numata, K

doi:10.1097/00000542-198909001-00172

Cited by 2 publications

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“…While the previous studies [15,[17][18][19] indicate, that drug induced changes of the longitudinal distribution of pulmonary vascular resistance have only little effect on the middle resistance, these changes nevertheless constitute an unavoidable source of error in Pc determination. A further source of error when analyzing wedge pressure curves, is the point of time during the cardiac cycle at which pulmonary arterial occlusion occurs [20].…”

Section: Discussionmentioning

confidence: 89%

Pulmonary capillary pressure and gas exchange after E. coli bacteremia in pigs

et al. 1990

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In 9 Goettingen minipigs we studied the effect of E. coli bacteremia on effective pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance. Precapillary pressure gradient (dPa) was calculated as the difference between mean pulmonary artery pressure (MPP) and effective pulmonary capillary pressure (Pc) (dPa = MPP-Pc), postcapillary pressure gradient (dPv) as the difference between Pc and left atrial pressure (dPv = Pc-LAP). The disturbance of pulmonary gas exchange was quantified by the AaDO2 quotient 1-PaO2/PAO2. Live E. coli infusion resulted in hypodynamic circulatory failure. Cardiac index fell from 3.7 +/- 0.81 . min-1.m-2 to 2.2 +/- 0.71 .min-1.m-2 after bacteremia lasting for 3.5 h. Simultaneously venous pulmonary vascular resistance rose from 25% of total pulmonary vascular resistance before to 32% after 3.5 h bacteremia, thus raising Pc from 11 mmHg to 16 mmHg. The degree of respiratory insufficiency was correlated with changes of MPP, dPa and dPv: 1-PaO2/PAO2 = 0.2 + 0.035.dPv (r = 0.829). Our results show, that the longitudinal distribution of pulmonary vascular resistance changes during septicemia, thus raising Pc. This may be an important factor in the genesis of septic pulmonary failure.

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Section: Discussionmentioning

confidence: 89%

Pulmonary capillary pressure and gas exchange after E. coli bacteremia in pigs

et al. 1990

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Up-regulation of nitric oxide synthase and modulation of the guanylate cyclase activity by corticotropin-releasing hormone but not urocortin II or urocortin III in cultured human pregnant myometrial cells

Aggelidou

Hillhouse

Grammatopoulos

2002

Proc. Natl. Acad. Sci. U.S.A.

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The biological actions of corticotropin-releasing hormone (CRH) in the human myometrium during pregnancy and labor are unknown. We hypothesized that CRH may modulate the nitric oxide system, and influence myometrial relaxation͞contractility. Incubation of myometrial cells with CRH, but not urocortin II or urocortin III, for 8 -16 h significantly induced mRNA and protein expression of endothelial and brain but not inducible nitric oxide synthase (NOS) isoforms. This action resulted in increased activity of soluble guanylate cyclase (GC s), demonstrated by the enhanced cGMP-producing capacity of the NO donor, sodium nitroprusside. CRH also caused acute activation of the membrane-bound GC, shown by increased basal or atrial natriuretic peptide (ANP)-stimulated cGMP production. These effects appeared to be mediated via the R1 receptors because the CRH receptor antagonists, astressin and antalarmin but not anti-sauvagine 30, could block them. The acute effects of CRH were significantly reduced by inhibition of protein kinase A (PKA) activity, suggesting it is partially PKA dependant. Activation of protein kinase C (PKC) resulted in significant inhibition of both ANP-and CRH-stimulated cGMP production, suggesting a direct effect of PKC on membrane-bound GC. In conclusion, CRH appears to have a dual effect on myometrial NOS͞GC pathway, a short term effect predominantly mediated by PKA, and a long-term effect increasing constitutive NOS expression, mediated by a PKA-independent mechanism. This mechanism could potentially be active during human pregnancy, and, because cGMP stimulates myometrial relaxation, these findings further suggest that during pregnancy CRH primarily activates intracellular signals that contribute to the maintenance of myometrial quiescence.

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Pulmonary Arterial, Capillary and Venous Resistances From Arterial Occlusion

Cited by 2 publications

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Pulmonary capillary pressure and gas exchange after E. coli bacteremia in pigs

Pulmonary capillary pressure and gas exchange after E. coli bacteremia in pigs

Up-regulation of nitric oxide synthase and modulation of the guanylate cyclase activity by corticotropin-releasing hormone but not urocortin II or urocortin III in cultured human pregnant myometrial cells

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