Some lessons learned from the COVID-19 pandemic: Subjective well-being before and during the pandemic among Brazilian adults.

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Effect of volume replacement during combined experimental hemorrhagic shock and traumatic brain injury in prostanoids, brain pathology and pupil status.

Traumatic brain injury (TBI) is the main cause of trauma-related deaths. Systemic hypotension and intracranial hypertension causes cerebral ischemia by altering metabolism of prostanoids. We describe prostanoid, pupilar and pathological response during resuscitation with hypertonic saline solution (HSS) in TBI. Method Fifteen dogs were randomized in three groups according to resuscitation after TBI (control group; lactated Ringer's (LR) group and HSS group), with measurement of thromboxane, prostaglandin, macroscopic and microscopic pathological evaluation and pupil evaluation.Result Concentration of prostaglandin is greater in the cerebral venous blood than in plasma and the opposite happens with concentration of thromboxane. Pathology revealed edema in groups with the exception of group treated with HSS.Discussion and conclusion There is a balance between the concentrations of prostaglandin and thromboxane. HSS prevented the formation of cerebral edema macroscopically detectable. Pupillary reversal occurred earlier in HSS group than in LR group.

Effect of volume replacement during combined experimental hemorrhagic shock and traumatic brain injury in prostanoids, brain pathology and pupil status / Efeito da reposição volêmica durante o choque hemorrágico combinado com traumatismo craniencefálico sobre prostanóides, patologia cerebral e status pupilar

Traumatic brain injury (TBI) is the main cause of trauma-related deaths. Systemic hypotension and intracranial hypertension causes cerebral ischemia by altering metabolism of prostanoids. We describe prostanoid, pupilar and pathological response during resuscitation with hypertonic saline solution (HSS) in TBI. Method Fifteen dogs were randomized in three groups according to resuscitation after TBI (control group; lactated Ringer’s (LR) group and HSS group), with measurement of thromboxane, prostaglandin, macroscopic and microscopic pathological evaluation and pupil evaluation.Result Concentration of prostaglandin is greater in the cerebral venous blood than in plasma and the opposite happens with concentration of thromboxane. Pathology revealed edema in groups with the exception of group treated with HSS.Discussion and conclusion There is a balance between the concentrations of prostaglandin and thromboxane. HSS prevented the formation of cerebral edema macroscopically detectable. Pupillary reversal occurred earlier in HSS group than in LR group.

O traumatismo cranioencefálico (TCE) é a principal causa de morte relacionada ao trauma. O choque hemorrágico e hipertensão intracraniana causam isquemia cerebral alterando o metabolismo de prostanóides. Neste estudo, relatamos o comportamento dos prostanóides, resposta pupilar e patologia durante a reposição volêmica com solução salina hipertônica (SSH) no TCE. Método Quinze cachorros foram randomizados em três grupos (controle, grupo de Ringer lactato e grupo de SSH) e foram avaliados tromboxane, prostaglandina, avaliação patológica macroscópica e microscópica e status pupilar.Resultado A concentração de prostaglandina é maior no sangue cerebral em comparação ao plasma, e o inverso ocorre com o tromboxane. A patologia revelou edema em todos os grupos, com exceção do grupo tratado com SSH.Discussão e conclusão Existe um equilíbrio entre concentrações cerebrais e plasmáticas de prostaglandina e tromboxane. A SSH protegeu o cérebro da formação de edema pós traumático.

Size and spatial distribution of stray dog population in the University of São Paulo campus, Brazil.

A longitudinal study was carried out to describe the size and spatial distribution of the stray dog population in the University of São Paulo campus, Brazil from November 2010 to November 2011. The campus is located within the urban area of São Paulo, the largest city of Brazil, with a population over 11 million. The 4.2 km(2) that comprise the university grounds are walled, with 10 access gates, allowing stray dogs to move in and out freely. Over 100,000 people and 50,000 vehicles circulate in the campus daily. Five observations were made during the study period, using a mark-resight method. The same route was performed in all observations, being traveled twice on each observation day. Observed animals were photographed and the sight coordinates were obtained using a GPS device. The estimated size of the stray dog population varied from 32 (CI 95% 23-56) to 56 (CI 95% 45-77) individuals. Differences between in- and outward dog movements influenced dog population estimates. Overlapping home ranges of docile dogs were observed in areas where most people circulate. An elusive group was observed close to a protected rain forest area and the estimated home range for this group did not overlap with the home ranges for other dogs within the campus. A kernel density map showed that higher densities of stray dog sighting is associated with large organic matter generators, such as university restaurants. We conclude that the preferred source of food of the stray dogs on the University of São Paulo campus was leftover food deliberately offered by restaurant users. The population was stable during the study period and the constant source of food was the main reason to retain this population within the campus.

Short-term effects of hydroxyethylstarch resuscitation on systemic and regional hemodynamics and metabolism in a brain-dead canine model.

BACKGROUND: Hydroxyethylstarch (HES) is a synthetic polymer of glucose that has been suggested for therapeutic use in long-term plasma expansion. The aim of this study was to test the hypothesis that the infusion of a small volume of HES may provide benefits in systemic and regional hemodynamics and metabolism in a brain-dead canine model compared with large volume crystalloid resuscitation. METHODS: Fourteen mongrel dogs were subjected to a brain-death protocol by consecutive insufflations of a balloon catheter in the epidural space. One hour after induction of brain-death, the animals were randomly assigned to two groups: NS (0.9% NaCl, 33 mL/kg), and HES (6%HES 450/0.7, 17 mL/Kg). Systemic and regional hemodynamics were evaluated using Swan-Ganz, ultrasonic flowprobes, and arterial catheters. Serial blood samples were collected for blood gas, electrolyte, and serum chemistry analysis. Systemic, hepatic, and splanchnic O(2)-derived variables were also calculated. RESULTS: Epidural balloon insufflations induced a significant increase in mean arterial pressure, cardiac output (MAP and CO, respectively), regional blood flow, and systemic vascular resistance. Following the hyperdynamic phase, severe hypotension with normalization of systemic and regional blood flow was observed. Fluid resuscitation induced a prompt increase in MAP, CO, and portal vein blood flow, and a significant reduction in systemic and pulmonary vascular resistance. There were no differences between groups in metabolic indices, liver function tests (LFTs), or renal function tests. HES was more effective than NS in restoring cardiac performance in the first 2h after fluid resuscitation (P < 0.05). Both tested solutions partially and temporarily restored systemic and regional oxygen delivery. CONCLUSION: Small volumes of 6% HES 450/0.7 improved cardiovascular performance and provided the same regional hemodynamic and metabolic benefits of large volumes of isotonic crystalloid solutions.

Fluid resuscitation with isotonic or hypertonic saline solution avoids intraneural calcium influx after traumatic brain injury associated with hemorrhagic shock.

BACKGROUND: Calcium is one of the triggers involved in ischemic neuronal death. Because hypotension is a strong predictor of outcome in traumatic brain injury (TBI), we tested the hypothesis that early fluid resuscitation blunts calcium influx in hemorrhagic shock associated to TBI. METHODS: Fifteen ketamine-halothane anesthetized mongrel dogs (18.7 kg +/- 1.4 kg) underwent unilateral cryogenic brain injury. Blood was shed in 5 minutes to a target mean arterial pressure of 40 mm Hg to 45 mm Hg and maintained at these levels for 20 minutes (shed blood volume = 26 mL/kg +/- 7 mL/kg). Animals were then randomized into three groups: CT (controls, no fluid resuscitation), HS (7.5% NaCl, 4 mL/kg, in 5 minutes), and LR (lactate Ringer's, 33 mL/kg, in 15 minutes). Twenty minutes later, a craniotomy was performed and cerebral biopsies were obtained next to the lesion ("clinical penumbra") and from the corresponding contralateral side ("lesion's mirror") to determine intracellular calcium by fluorescence signals of Fura-2-loaded cells. RESULTS: Controls remained hypotensive and in a low-flow state, whereas fluid resuscitation improved hemodynamic profile. There was a significant increase in intracellular calcium in the injured hemisphere in CT (1035 nM +/- 782 nM), compared with both HS (457 nM +/- 149 nM, p = 0.028) and LR (392 nM +/- 178 nM, p = 0.017), with no differences between HS and LR (p = 0.38). Intracellular calcium at the contralateral, uninjured hemisphere was 438 nM +/- 192 nM in CT, 510 nM +/- 196 nM in HS, and 311 nM +/- 51 nM in LR, with no significant differences between them. CONCLUSION: Both small volume hypertonic saline and large volume lactated Ringer's blunts calcium influx in early stages of TBI associated to hemorrhagic shock. No fluid resuscitation strategy promotes calcium influx and further neural damage.

Initial hepatosplanchnic blood flow distribution and oxygen metabolism in experimental model of hypotensive brain death.

BACKGROUND: Organs from the so-called marginal donors have been used with a significant higher risk of primary non function than organs retrieved from the optimal donors. We investigated the early metabolic changes and blood flow redistribution in splanchnic territory in an experimental model that mimics marginal brain-dead (BD) donor. MATERIAL/METHODS: Ten dogs (21.3+/-0.9 kg), were subjected to a brain death protocol induced by subdural balloon inflation and observed for 30 min thereafter without any additional interventions. Mean arterial and intracranial pressures, heart rate, cardiac output (CO), portal vein and hepatic artery blood flows (PVBF and HABF, ultrasonic flowprobe), and O(2)-derived variables were evaluated. RESULTS: An increase in arterial pressure, CO, PVBF and HABF was observed after BD induction. At the end, an intense hypotension with normalization in CO (3.0+/-0.2 vs. 2.8+/-2.8 L/min) and PVBF (687+/-114 vs. 623+/-130 ml/min) was observed, whereas HABF (277+/-33 vs. 134+/-28 ml/min, p<0.005) remained lower than baseline values. CONCLUSIONS: Despite severe hypotension induced by sudden increase of intracranial pressure, the systemic and splanchnic blood flows were partially preserved without signs of severe hypoperfusion (i.e. hyperlactatemia). Additionally, the HABF was mostly negatively affected in this model of marginal BD donor. Our data suggest that not only the cardiac output, but the intrinsic hepatic microcirculatory mechanism plays a role in the hepatic blood flow control after BD.

Indução anestésica após o tratamento do choque hemorrágico: estudo experimental comparando a cetamina e o etomidato / Anesthetic induction after treated hemorrhagic shock: experimental study comparing ketamine and etomidate

JUSTIFICATIVA E OBJETIVOS: O sangramento que leva ao choque hemorrágico geralmente necessita tratamento cirúrgico sob anestesia geral. Por sua vez, os anestésicos podem comprometer ainda mais as condições hemodinâmicas. O objetivo deste estudo foi o de comparar os efeitos hemodinâmicos da cetamina e do etomidato durante a indução anestésica em cães submetidos a um modelo experimental de choque hemorrágico e reanimação. MÉTODO: Trinta e dois cães mestiços foram submetidos ao choque hemorrágico pressão-controlado, reanimação e indução anestésica. Após atingir a pressão alvo de 40 mmHg eles foram divididos aleatoriamente em dois grupos de acordo com a solução usada na reanimação: NaCl a 0.9 por cento (32 ml.kg-1) e NaCl a 7,5 por cento (4 mL.kg-1). Após a infusão de volume, esses grupos foram divididos novamente de acordo com o anestésico utilizado: GI) NaCl a 0.9 por cento e cetamina; GII) NaCl a 7.5 por cento e cetamina; GIII) NaCl a 0.9 por cento e etomidato; e GIV) NaCl a 7.5 por cento e etomidato. Medições hemodinâmicas foram obtidas em cinco momentos: (M0) inicial; (M1) após o desenvolvimento do choque hemorrágico; (M2) após a administração de fluidos; (M3) 5 minutos após a indução anestésica; (M4) 15 minutos após a indução anestésica. Foi feita a análise estatística usando o teste t de Student e two-way ANOVA. Foram considerados significativos valores de p menores do que 0,05. RESULTADOS: Após a instalação do choque, ambas as soluções restabeleceram os padrões hemodinâmicos aos valores iniciais. Independente do anestésico ou da solução utilizados, após a indução anestésica a pressão arterial média permaneceu inalterada em todos os grupos. A pressão venosa central, freqüência cardíaca, pressão capilar pulmonar e o índice de resistência pulmonar vascular aumentaram significativamente após a administração de cetamina. O índice cardíaco, o índice de resistência vascular sistêmica e o transporte de oxigênio permaneceram estáveis em todos os grupos. CONCLUSÕES: O etomidato ou a cetamina foram capazes de manter a estabilidade hemodinâmica nos cães que sofreram choque hemorrágico intenso e que foram tratados com NaCl a 0,9 por cento ou NaCl a 7,5 por cento.

Volume replacement with lactated Ringer's or 3% hypertonic saline solution during combined experimental hemorrhagic shock and traumatic brain injury.

BACKGROUND: The devastating effects of hypotension on head-trauma-related mortality are well known. This study evaluates the systemic and cerebral hemodynamic responses to volume replacement with 3% hypertonic saline (HSS) or lactated Ringer's solution (LR), during the acute phase of hemorrhagic shock (HS) associated with traumatic brain injury (TBI). METHODS: Fifteen dogs were assigned to one of three groups (n = 5, each) according to the volume replacement protocol, infused after TBI (brain fluid percussion, 4 atm) and epidural balloon to an intracranial pressure (ICP) higher than 20 mm Hg and HS, induced by blood removal to a mean arterial pressure (MAP) of 40 mm Hg in 5 minutes: Group HS+TBI+HSS (8 mL/kg of 3% HSS), HS+TBI+LR (16 mL/kg LR), and Group HS+TBI (controls, no fluids). We simulated treatment during prehospital and early hospital admission. Groups HS+ TBI and HS+TBI+LR received shed blood infusion to a target hematocrit of 30%. Measurements included shed blood volume, fluid volume infused to restore MAP, MAP, cardiac output, cerebral perfusion pressure, cerebral and systemic lactate, and oxygen extraction ratios. RESULTS: Fluid replacement with HSS 3% or LR promoted major hemodynamic benefits over control animals without luids. Cerebral perfusion pressure was higher than controls and similar between treated groups; however, HSS 3% infusion was associated with lower ICP during the "early hospital phase" and a higher serum sodium and osmolarity. CONCLUSION: In the event of severe head trauma and hemorrhagic shock, the use of HSS 3% and larger volumes of LR promote similar systemic and cerebral hemodynamic benefits. However, a lower ICP was observed after HSS 3% than after LR.

[Anesthetic induction after treated hemorrhagic shock: experimental study comparing ketamine and etomidate.]. / Indução anestésica após o tratamento do choque hemorrágico: estudo experimental comparando a cetamina e o etomidato.

BACKGROUND AND OBJECTIVES: Bleeding causing hemorrhagic shock usually requires surgical treatment under general anesthesia. Anesthetic drugs may further compromise hemodynamics. The objective was to compare the hemodynamic effects of ketamine and etomidate during anesthetic induction in dogs submitted to an experimental model of hemorrhagic shock and resuscitation. METHODS: Thirty-two mongrel dogs were submitted to a pressure-controlled hemorrhagic shock, resuscitation and anesthetic induction model. After achieving the target pressure of 40 mmHg, they were randomly assigned in two groups according to the resuscitation fluid to be used: NaCl 0.9% (32 mL.kg-1) and NaCl 7.5% (4 mL.kg-1). After volume infusion, these groups were reassigned according to anesthetic drug used: GI) NaCl 0.9% and ketamine; GII) NaCl 7.5% and ketamine; GIII) NaCl 0.9% and etomidate; and GIV) NaCl 7.5% and etomidate. Hemodynamic measurements were obtained at five moments: (M0) baseline; (M1) after bleeding to shock; (M2) after volume expansion; (M3) 5 minutes after anesthetic induction; (M4) 15 minutes after anesthetic induction. Statistical analysis was performed using Student t test and two way ANOVA. Value of p lower than 0.05, was considered significant. RESULTS: After shock, both solutions restored hemodynamics to baseline values. Independently of anesthetic agent or expansion solution used, mean arterial pressure remained unaltered for all groups after induction. Central venous pressure, heart rate, pulmonary capillary wedge pressure and pulmonary vascular resistance index increased significantly after ketamine infusion. Cardiac index, systemic vascular resistance index and oxygen transport variables remained stable in all groups. CONCLUSIONS: Etomidate or ketamine were able to maintain hemodynamic stability in dogs undergoing severe hemorrhagic shock treated with NaCl 0.9% or NaCl 7.5%.