383 research outputs found

    Three questions to the human brain

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    An approximately 20% increase in cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen manifest during whole body exercise with determination of brain tissue flow and arterial inflow to the brain. Yet, during intense exercise CBF approaches the resting level in response to the decrease in arterial carbon dioxide tension with the exponential increase in ventilation. Here it is illustrated that the increase in CBF during exercise appears to depend to the ability to raise cardiac output and it is speculated whether there is a sympathetic restrain on CBF when the increase in cardiac output is small. Furthermore, it is considered whether the restrain in CBF during intense exercise affects cerebral oxygenation to an extent that it provokes so-called central fatigue. Finally it is highlighted that the cerebral activation associated with exercise provokes uptake of carbohydrate, notably of lactate, that cannot be accounted for by the concomitant increase in the cerebral metabolic rate for oxygen and it is pointed out that it remains unknown why that apparently surplus carbohydrate uptake by the brain is in need

    Influence of intranasal and carotid cooling on cerebral temperature balance and oxygenation

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    The present study evaluated the influence of intranasal cooling with balloon catheters, increased nasal ventilation, or percutaneous cooling of the carotid arteries on cerebral temperature balance and oxygenation in six healthy male subjects. Aortic arch and internal jugular venous blood temperatures were measured to assess the cerebral heat balance and corresponding paired blood samples were obtained to evaluate cerebral metabolism and oxygenation at rest, following 60 min of intranasal cooling, 5 min of nasal ventilation, and 15 min with carotid cooling. Intranasal cooling induced a parallel drop in jugular venous and arterial blood temperatures by 0.30 ± 0.08°C (mean ± SD), whereas nasal ventilation and carotid cooling failed to lower the jugular venous blood temperature. The magnitude of the arterio-venous temperature difference across the brain remained unchanged at −0.33 ± 0.05°C following intranasal and carotid cooling, but increased to −0.44 ± 0.11°C (P < 0.05) following nasal ventilation. Calculated cerebral capillary oxygen tension was 43 ± 3 mmHg at rest and remained unchanged during intranasal and carotid cooling, but decreased to 38 ± 2 mmHg (P < 0.05) following increased nasal ventilation. In conclusion, percutaneous cooling of the carotid arteries and intranasal cooling with balloon catheters are insufficient to influence cerebral oxygenation in normothermic subjects as the cooling rate is only 0.3°C per hour and neither intranasal nor carotid cooling is capable of inducing selective brain cooling

    Dose of Bicarbonate to Maintain Plasma pH During Maximal Ergometer Rowing and Consequence for Plasma Volume

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    Rowing performance may be enhanced by attenuated metabolic acidosis following bicarbonate (BIC) supplementation. This study evaluated the dose of BIC needed to eliminate the decrease in plasma pH during maximal ergometer rowing and assessed the consequence for change in plasma volume. Six oarsmen performed “2,000-m” maximal ergometer rowing trials with BIC (1 M; 100–325 ml) and control (CON; the same volume of isotonic saline). During CON, pH decreased from 7.42 ± 0.01 to 7.17 ± 0.04 (mean and SD; p < 0.05), while during BIC, pH was maintained until the sixth minute where it dropped to 7.32 ± 0.08 and was thus higher than during CON (p < 0.05). The buffering effect of BIC on metabolic acidosis was dose dependent and 300–325 mmol required to maintain plasma pH. Compared to CON, BIC increased plasma sodium by 4 mmol/L, bicarbonate was maintained, and lactate increased to 25 ± 7 vs. 18 ± 3 mmol/L (p < 0.05). Plasma volume was estimated to decrease by 24 ± 4% in CON, while with BIC the estimate was by only 7 ± 6% (p < 0.05) and yet BIC had no significant effect on performance [median 6 min 27 s (range 6 min 09 s to 6 min 57 s) vs. 6 min 33 s (6 min 14 s to 6 min 55 s)]. Bicarbonate administration attenuates acidosis during maximal rowing in a dose-dependent manner and the reduction in plasma volume is attenuated with little consequence for performance

    Dehydration accelerates reductions in cerebral blood flow during prolonged exercise in the heat without compromising brain metabolism

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    Dehydration hastens the decline in cerebral blood flow (CBF) during incremental exercise, while the cerebral metabolic rate for oxygen (CMRO2) is preserved. It remains unknown whether CMRO2 is also maintained during prolonged exercise in the heat and whether an eventual decline in CBF is coupled to fatigue. Two studies were undertaken. In study 1, ten male cyclists cycled in the heat for ~2 h with (control) and without fluid replacement (dehydration) while internal (ICA) and external (ECA) carotid artery blood flow and core and blood temperature were obtained. Arterial and internal jugular venous blood samples were assessed with dehydration to evaluate the CMRO2. In study 2 (8 males), middle cerebral artery blood velocity (MCA Vmean) was measured during prolonged exercise to exhaustion in both dehydrated and euhydrated states. After a rise at the onset of exercise, ICA flow declined to baseline with progressive dehydration (P < 0.05). However, cerebral metabolism remained stable through enhanced oxygen and glucose extraction (P < 0.05). ECA flow increased for one hour but declined prior to exhaustion. Fluid ingestion maintained cerebral and extra-cranial perfusion throughout non-fatiguing exercise. During exhaustive exercise, however, euhydration delayed but did not prevent the decline in cerebral perfusion. In conclusion, during prolonged exercise in the heat dehydration accelerates the decline in CBF without affecting CMRO2 and also restricts extra-cranial perfusion. Thus fatigue is related to reduction in CBF and extra-cranial perfusion rather than in CMRO2.The study was supported by a grant from the Gatorade Sports Science Institute, PepsiCo Inc, USA

    Pulmonary perfusion with oxygenated blood or custodiol HTK solution during cardiac surgery for postoperative pulmonary function in COPD patients: a trial protocol for the randomized, clinical, parallel group, assessor and data analyst blinded Pulmonary Protection Trial

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    BACKGROUND: Five to thirty percent of patients undergoing cardiac surgery present with chronic obstructive pulmonary disease (COPD) and have a 2- to 10-fold higher 30-day mortality risk. Cardiopulmonary bypass (CPB) creates a whole body systemic inflammatory response syndrome (SIRS) that could impair pulmonary function. Impaired pulmonary function can, however, be attenuated by pulmonary perfusion with oxygenated blood or custodiol HTK (histidine-tryptophan-ketoglutarate) solution. METHODS/DESIGN: The Pulmonary Protection Trial (PP-Trial) randomizes 90 patients undergoing CPB-dependent cardiac surgery to evaluate whether pulmonary perfusion with oxygenated blood or custodiol HTK solution reduces postoperative pulmonary dysfunction in COPD patients. Further, we aim for a non-randomized evaluation of postoperative pulmonary function after transcatheter aortic-valve implantation (TAVI). The primary outcome measure is the oxygenation index measured from anesthesia induction to the end of surgery and until 24 hours after anesthesia induction for a total of six evaluations. DISCUSSION: Patients with COPD may be impaired by hypoxemia and SIRS. Thus, prolonged recovery and even postoperative complications and death may be reflected by the degree of hypoxemia and SIRS. The limited sample size does not aim for confirmatory conclusions on mortality, cardiovascular complications or risk of pneumonia and sepsis, but the PP-Trial is considered an important feasibility trial paving the road for a multicenter confirmatory trial. TRIAL REGISTRATION: ClinicalTrials.gov: NCT01614951

    Plasma pro-atrial natriuretic peptide to estimate fluid balance during open and robot-assisted esophagectomy:a prospective observational study

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    Abstract Background It remains debated how much fluid should be administered during surgery. The atrial natriuretic peptide precursor proANP is released by atrial distension and deviations in plasma proANP are reported associated with perioperative fluid balance. We hypothesized that plasma proANP would decrease when the central blood volume is compromised during the abdominal part of robot-assisted hybrid (RE) esophagectomy and that a positive fluid balance would be required to maintain plasma proANP. Methods Patients undergoing RE ( n \u2009=\u200925) or open (OE; n \u2009=\u200925) esophagectomy for gastroesophageal cancer were included consecutively in this prospective observational study. Plasma proANP was determined repetitively during esophagectomy to allow for distinction between the abdominal and thoracic part of the procedure. The RE group was 15\ub0 head up tilted during the abdominal procedure. Results The blood loss was 250 (150\u2013375) (RE) and 600\ua0ml (390\u2013855) (OE) ( p \u2009=\u20090.01), but the two groups of patients were provided with a similar positive fluid balance: 1705 (1390\u20131983) vs. 1528\ua0ml (1316\u20131834) ( p \u2009=\u20090.4). However, plasma proANP decreased by 21% ( p \u2009<\u20090.01) during the abdominal part of RE carried out during moderate head-up tilt, but only by 11% ( p \u2009=\u20090.01) during OE where the patients were supine. Plasma proANP and fluid balance were correlated in the RE-group ( r \u2009=\u20090.5 (0.073\u20130.840), p \u2009=\u20090.02) and tended to correlate in the OE group ( r \u2009=\u20090.4 (\u22120.045\u20130.833), p \u2009=\u20090.08). Conclusion The results support that plasma proANP decreases when the central blood volume is compromised and suggest that an about 2200\ua0ml surplus administration of crystalloid is required to maintain plasma proANP during esophagectomy. Trial registration Clinicaltrials.gov ( NCT02077673 ). Registered retrospectively February 12 th 2014
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