Key result
ANP-receptor blockade increases lung lymph flow ~64% without altering protein permeability in septic sheep.
Why the study?
Atrial natriuretic peptide is considered an important regulator of pulmonary vasomotor tone and permeability, motivating investigation into its role in sepsis-associated pulmonary pathophysiology.
Does blockade of atrial natriuretic peptide receptors with HS-142-1 alter pulmonary transvascular fluid flux and vasoregulation in sheep with chronic Pseudomonas aeruginosa sepsis?
Does blockade of atrial natriuretic peptide receptors with HS-142-1 alter pulmonary transvascular fluid flux and vasoregulation in sheep with chronic Pseudomonas aeruginosa sepsis?
Atrial natriuretic peptide receptor blockade increases pulmonary transvascular fluid flux without altering protein permeability in ovine sepsis, suggesting ANP plays a protective role for the alveolar-capillary barrier during sepsis.
Answers are grounded in this paper and cite their sources.
ANP-receptor blockade may increase pulmonary fluid flux in ovine sepsis; hypothesis-generating for barrier protection, no clinical implications yet.
Objective Atrial natriuretic peptide is regarded as an important regulator of pulmonary vasomotor tone and permeability. This study investigated the role of atrial natriuretic peptide in sepsis-associated pulmonary pathophysiology. Design Prospective experimental investigation. Setting Laboratory at a university hospital. Subjects Twelve awake, chronically instrumented sheep. Interventions The sheep were instrumented with lung lymph fistulas and received a continuous infusion with live Pseudomonas aeruginosa for 48 hrs. After 40 hrs, the atrial natriuretic peptide-receptor antagonist HS-142-1 was continuously infused in the HS-124-1 group (3 mg/kg/hr, n = 6) for 8 hrs, whereas the control group received the carrier (n = 6). Measurements and main results Lung lymph flow was markedly elevated in response to sepsis after 40 hrs in both groups. Atrial natriuretic peptide-receptor blockade further increased lymph flows by 41 +/- 17% (41 hrs) up to 64 +/- 20% (44 hrs, p < .05) in the presence of normal permeability to protein. Although mean pulmonary artery pressure increased (p < .05 vs. 40 hrs), capillary pressure remained unaffected. Despite identical fluid balances in both groups, cardiovascular filling variables significantly increased in the HS-142-1 group. This was associated with increasing cardiac index and mean arterial pressure (p < .05 vs. 40 hrs). In the control group, all variables remained constant between 41 and 48 hrs. Conclusion Blockade of atrial natriuretic peptide receptors increases pulmonary transvascular fluid flux independent of changes in permeability to protein in chronic ovine sepsis. Atrial natriuretic peptide may therefore play a protective role for the alveolar-capillary barrier during sepsis.
No takes yet. Share an insight, caveat, or question.
Stubbe et al. (2004) studied Ovine sepsis (induced by continuous infusion of live Pseudomonas aeruginosa) (n=12). HS-142-1 (atrial natriuretic peptide-receptor antagonist) vs. Carrier infusion was evaluated on Lung lymph flow (pulmonary transvascular fluid flux) (p=<0.05). Atrial natriuretic peptide-receptor blockade with HS-142-1 increased lung lymph flows by up to 64 ± 20% (p < 0.05) without altering protein permeability in septic sheep.
Synapse has enriched 10 related papers. Consider them for comparative context: