Blood redistribution preferentially protects vital organs under hypoxic stress in Pelteobagrus vachelli.

Blood redistribution occurs in mammals under hypoxia but has not been reported in fish. This study investigated the tissue damage, hypoxia-inducible factor (HIF) activation level, and blood flow changes in the brain, liver, and muscle of Pelteobagrus vachelli during the hypoxia process for normoxia-hypoxia-asphyxia. The results showed that P. vachelli has tissue specificity in response to hypoxic stress. Cerebral blood flow increased with less damage than in the liver and muscle, suggesting that P. vachelli may also have a blood redistribution mechanism in response to hypoxia. It is worth noting that severe hypoxia can lead to a sudden increase in the degree of brain tissue damage. In addition, higher dissolved oxygen levels activate HIF and may have contributed to the reduced damage observed in the brain. This study provides basic data for investigating hypoxic stress in fish.

The range of normative surface skin temperature changes in adolescents: prospective multicenter study.

AIM: We aimed to establish a normative range of surface skin temperature (SST) changes due to blood redistribution in adolescents and to register the time needed for complete postural change-related blood redistribution. METHODS: The healthy volunteers (age 15-18, n = 500, M 217, F 283) were recruited for this prospective multicenter study. The volunteers were asked to keep one extremity down and another extremity up in supine rest, sitting with straight legs, and upright rest. We obtained temperature readings being taken from the tips of the middle fingers and temperature readings from the tips of the first toes at the ambient temperature of 25 °C and 30 °C. The control group consisted of a 100 of adult volunteers. RESULTS: The resting temperature of the middle fingers for a sitting participant was 28.6 ± 0.8 °C. The physiological change of this temperature during body position changes was 4.5 ± 1.1 °C and for most of the participants remained within the 26.5-31.5 °C range at 25 °C. For the toe, physiological skin temperature range was 25.5-33 °C. At 30 °C, these ranges were 27-33 °C for the fingers and 27-34 °C for the toes. On average, 2-3 min were needed for such temperature changes. CONCLUSION: At normal room temperature, the SST of thermoneutral adolescents may vary within a range of approximately 5 °C only due to the blood redistribution in the body. This range is specific for each person due to individual peculiarities of the vasomotor activity. This normative range of SSTs should be taken into account during investigations of thermoregulation.

Normative surface skin temperature changes due to blood redistribution: A prospective study.

The continuing development and manufacture of infrared devices, together with improvements in thermal body mapping techniques have simplified surface skin thermography which is being used more extensively than ever before. Normative thermography data, however, remains incomplete. A normative blood redistribution range of skin temperatures was established for use as a reference for laboratory infrared thermography (IT), thermal body mapping, and mass fever screenings. 500 healthy volunteers participated in this prospective study. To determine the maximum range of the skin temperature changes due to the posture-related physiological blood redistribution, the volunteers were asked to keep one extremity up and another extremity down whilst lying, sitting, and standing. We obtained 6000 hand and 400 foot temperature readings. The normal temperature was 29.1 ±â€¯0.6 °C for the middle fingers and 27.8 ±â€¯0.7 °C for the toes. The physiological temperature change during body position changes ranged from 4 to 6 °C (fingers: 27-31 °C; toes: 26-32 °C). At normal room temperature, the surface skin temperature may vary within this range due to blood redistribution. These changes reflect the individual variability of vasomotor activity. This physiological range of temperatures should be taken into account during IT and other thermography-involved investigations.

Vasopressors induce passive pulmonary hypertension by blood redistribution from systemic to pulmonary circulation.

Vasopressors are widely used in resuscitation, ventricular failure, and sepsis, and often induce pulmonary hypertension with undefined mechanisms. We hypothesize that vasopressor-induced pulmonary hypertension is caused by increased pulmonary blood volume and tested this hypothesis in dogs under general anesthesia. In normal hearts (model 1), phenylephrine (2.5 µg/kg/min) transiently increased right but decreased left cardiac output, associated with increased pulmonary blood volume (63% ± 11.8, P = 0.007) and pressures in the left atrium, pulmonary capillary, and pulmonary artery. However, the trans-pulmonary gradient and pulmonary vascular resistance remained stable. These changes were absent after decreasing blood volume or during right cardiac dysfunction to reduce pulmonary blood volume (model 2). During double-ventricle bypass (model 3), phenylephrine (1, 2.5 and 10 µg/kg/min) only slightly induced pulmonary vasoconstriction. Vasopressin (1U and 2U) dose-dependently increased pulmonary artery pressure (52 ± 8.4 and 71 ± 10.3%), but did not cause pulmonary vasoconstriction in normally beating hearts (model 1). Pulmonary artery and left atrial pressures increased during left ventricle dysfunction (model 4), and further increased after phenylephrine injection by 31 ± 5.6 and 43 ± 7.5%, respectively. In conclusion, vasopressors increased blood volume in the lung with minimal pulmonary vasoconstriction. Thus, this pulmonary hypertension is similar to the hemodynamic pattern observed in left heart diseases and is passive, due to redistribution of blood from systemic to pulmonary circulation. Understanding the underlying mechanisms may improve clinical management of patients who are taking vasopressors, especially those with coexisting heart disease.