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Hemoglobin-based oxygen-carrying solutions (HBOC) provide emergency alternatives to blood transfusion to carry oxygen to tissues without the risks of disease transmission or transfusion reaction. Two ...primary concerns hampering the clinical acceptance of acellular HBOC are the occurrence of systemic and pulmonary vasoconstriction and the maintenance of the heme-iron in the reduced state (Fe2+). We recently demonstrated that pretreatment with inhaled nitric oxide prevents the systemic hypertension induced by HBOC-201 (polymerized bovine hemoglobin) infusion in awake mice and sheep without causing methemoglobinemia. However, the impact of HBOC-201 infusion with or without inhaled nitric oxide on pulmonary vascular tone has not yet been examined.
The pulmonary and systemic hemodynamic effects of breathing nitric oxide both before and after the administration of HBOC-201 were determined in healthy, awake lambs.
Intravenous administration of HBOC-201 (12 ml/kg) induced prolonged systemic and pulmonary vasoconstriction. Pretreatment with inhaled nitric oxide (80 parts per million ppm for 1 h) prevented the HBOC-201--induced increase in mean arterial pressure but not the increase of pulmonary arterial pressure, systemic vascular resistance, or pulmonary vascular resistance. Pretreatment with inhaled nitric oxide (80 ppm for 1 h) followed by breathing a lower concentration of nitric oxide (5 ppm) during and after HBOC-201 infusion prevented systemic and pulmonary vasoconstriction without increasing methemoglobin levels.
These findings demonstrate that pretreatment with inhaled nitric oxide followed by breathing a lower concentration of the gas during and after administration of HBOC-201 may enable administration of an acellular hemoglobin substitute without vasoconstriction while preserving its oxygen-carrying capacity.
One of the major obstacles hindering the clinical development of a cell-free, hemoglobin-based oxygen carrier (HBOC) is systemic vasoconstriction.
Experiments were performed in healthy mice and lambs ...by infusion of either murine tetrameric hemoglobin (0.48 g/kg) or glutaraldehyde-polymerized bovine hemoglobin (HBOC-201, 1.44 g/kg). We observed that intravenous infusion of either murine tetrameric hemoglobin or HBOC-201 induced prolonged systemic vasoconstriction in wild-type mice but not in mice congenitally deficient in endothelial nitric oxide (NO) synthase (NOS3). Treatment of wild-type mice by breathing NO at 80 ppm in air for 15 or 60 minutes or with 200 ppm NO for 7 minutes prevented the systemic hypertension induced by subsequent intravenous administration of murine tetrameric hemoglobin or HBOC-201 and did not result in conversion of plasma hemoglobin to methemoglobin. Intravenous administration of sodium nitrite (48 nmol) 5 minutes before infusion of murine tetrameric hemoglobin also prevented the development of systemic hypertension. In awake lambs, breathing NO at 80 ppm for 1 hour prevented the systemic hypertension caused by subsequent infusion of HBOC-201.
These findings demonstrate that HBOC can cause systemic vasoconstriction by scavenging NO produced by NOS3. Moreover, in 2 species, inhaled NO administered before the intravenous infusion of HBOC can prevent systemic vasoconstriction without causing methemoglobinemia.
Breathing hydrogen sulfide (H2S) has been reported to induce a suspended animation-like state with hypothermia and a concomitant metabolic reduction in rodents. However, the impact of H2S breathing ...on cardiovascular function remains incompletely understood. In this study, the authors investigated the cardiovascular and metabolic effects of inhaled H2S in a murine model.
The impact of breathing H2S on cardiovascular function was examined using telemetry and echocardiography in awake mice. The effects of breathing H2S on carbon dioxide production and oxygen consumption were measured at room temperature and in a warmed environment.
Breathing H2S at 80 parts per million by volume at 27 degrees C ambient temperature for 6 h markedly reduced heart rate, core body temperature, respiratory rate, and physical activity, whereas blood pressure remained unchanged. Echocardiography demonstrated that H2S exposure decreased both heart rate and cardiac output but preserved stroke volume. Breathing H2S for 6 h at 35 degrees C ambient temperature (to prevent hypothermia) decreased heart rate, physical activity, respiratory rate, and cardiac output without altering stroke volume or body temperature. H2S breathing seems to induce bradycardia by depressing sinus node activity. Breathing H2S for 30 min decreased whole body oxygen consumption and carbon dioxide production at either 27 degrees or 35 degrees C ambient temperature. Both parameters returned to baseline levels within 10 min after the cessation of H2S breathing.
Inhalation of H2S at either 27 degrees or 35 degrees C reversibly depresses cardiovascular function without changing blood pressure in mice. Breathing H2S also induces a rapidly reversible reduction of metabolic rate at either body temperature.
Induction of a reversible “suspended animation” state by H2S breathing may preserve organ function in very ill patients. In this study, we measured the cardiovascular and metabolic effects of ...breathing H2S in mice.
In C57BL6 mice with telemeters, breathing H2S (80 ppm) at 27°C ambient temperature (Ta) for 6 h, markedly reduced heart rate (HR) (520±20 to 258±34bpm, mean±SE, P<0.05), core body temperature (Tb) (from 37.3±0.4 to 29.2±0.5, P<0.05), activity and respiratory rate (RR), but not mean arterial pressure (MAP). Values returned to control after breathing air for 3 h. Echocardiography demonstrated H2S reduced HR (from 690±19 to 233±23 bpm, P<0.05) and cardiac output (CO, from 19±1 to 7±1 ml/min P<0.05) but preserved stroke volume (SV). To determine if the inhibitory effects of H2S on metabolism were due to hypothermia, we studied the response to breathing H2S in a warm chamber. Inhaling H2S for 6h with Tb of 35°C decreased HR, activity, RR and CO (from 19±1 to 10±1 ml/min P<0.05), preserved SV, and increased MAP compared to 27°C H2S breathing (P<0.05).
Exhaled CO2 production was measured in mice breathing H2S for 30 min at either 27 or 35°C. Breathing H2S for 5 min decreased CO2 production in both groups (from 50±6 to 28±2 and from 59±1 to 44±1 μM/min respectively, both P<0.05 vs. baseline). These results suggest breathing 80ppm H2S reversibly decreases murine metabolic rate.
Supported by NIH grants HL 42397and 71987.
People with chronic obstructive pulmonary disease (COPD) may suffer from anxiety, depression, low quality of life, and cognitive deficits that could play a role in their clinical conditions. These ...situations could be worsened during the adaptation process to a new treatment such as noninvasive ventilation (NIV), which is often rejected or inappropriately used. The study aimed to analyze the impact of a brief psychological support intervention on adherence to NIV among patients with COPD.
A two-branch randomized controlled trial was conducted on 90 patients with COPD who had an indication for NIV. The experimental group received cognitive behavioral therapy support, including counseling, relaxation, and mindfulness-based exercises. Controls received standard care and watched educational videos. The course had been structured for four to eight meetings at the hospital, at home, and/or via telemedicine.
The psychological intervention was related to improvements in both adherence to NIV (F(304) = 19.054, p < .001) and quality of life (F(156) = 10.264, p = .002) after eight meetings from baseline compared with the control group. Results indicated a significant change in the quality of life also over time (F(71.480) = 8.114, p = .006).
The findings suggest that the psychological intervention is an appropriate treatment for acceptance of and adherence to NIV in COPD in clinical practice and highlight the importance of determining the underlying reasons for NIV use.Trial Registration:ClinicalTrials.gov identifier NCT02499653.
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