17 research outputs found
Maintaining intravenous volume mitigates hypothermia-induced myocardial dysfunction and accumulation of intracellular Ca2+
Previous research exploring pathophysiological mechanisms underlying circulatory collapse after rewarming victims of severe accidental hypothermia has documented post-hypothermic cardiac dysfunction and hypothermia-induced elevation of intracellular Ca2+ concentration ([Ca2+]i) in myocardial cells. The aim of the present study was to examine if maintaining euvolaemia during rewarming mitigates cardiac dysfunction and/or normalizes elevated myocardial [Ca2+]i. A total of 21 male Wistar rats (300 g) were surface cooled to 15âŚC, then maintained at 15âŚC for 4 h, and subsequently rewarmed to 37âŚC. The rats were randomly assigned to one of three groups: (1) non-intervention control (n = 7), (2) dextran treated (i.v. 12 ml/kg dextran 70; n = 7), or (3) crystalloid treated (24 ml/kg 0.9% i.v. saline; n = 7). Infusions occurred during the first 30 min of rewarming. Arterial blood pressure, stroke volume (SV), cardiac output (CO), contractility (dP/dtmax) and blood gas changes were measured. Post-hypothermic changes in [Ca2+]i were measured using the method of radiolabelled Ca2+ ( 45Ca2+). Untreated controls displayed post-hypothermic cardiac dysfunction with significantly reduced CO, SV and dP/dtmax. In contrast, rats receiving crystalloid or dextran treatment showed a return to pre-hypothermic control levels of CO and SV after rewarming, with the dextran group displaying significantly better amelioration of post-hypothermic cardiac dysfunction than the crystalloid group. Compared to the post-hypothermic increase in myocardial [Ca2+]i in non-treated controls, [Ca2+]i values with crystalloid and dextran did not increase to the same extent after rewarming. Volume replacement with crystalloid or dextran during rewarming abolishes posthypothermic cardiac dysfunction, and partially mitigates the hypothermia-induced elevation of [Ca2+]i
Family membersâ experiences of âwait and seeâ as a communication strategy in end-of-life decisions
The aim of this study is to examine family membersâ experiences of end-of-life decision-making processes in Norwegian intensive care units (ICUs) to ascertain the degree to which they felt included in the decision-making process and whether they received necessary information. Were they asked about the patientâs preferences, and how did they view their role as family members in the decision-making process? A constructivist interpretive approach to the grounded theory method of qualitative research was employed with interviews of 27 bereaved family members of former ICU patients 3â12 months after the patientâs death. The core finding is that relatives want a more active role in end-of-life decision-making in order to communicate the patientâs wishes. However, many consider their role to be unclear, and few study participants experienced shared decision-making. The clinicianâs expression âwait and seeâ hides and delays the communication of honest and clear information. When physicians finally address their decision, there is no time for family participation. Our results also indicate that nurses should be more involved in familyâphysician communication. Families are uncertain whether or how they can participate in the decision-making process. They need unambiguous communication and honest information to be able to take part in the decision-making process. We suggest that clinicians in Norwegian ICUs need more training in the knowledge and skills of effective communication with families of dying patients
Controversial treatment of a victim of severe head injury complicated by septic shock and acute respiratory distress syndrome
Pneumonia, severe sepsis, and acute respiratory distress syndrome (ARDS) are frequent complications after head trauma. Recombinant human activated protein C (APC) reportedly improves circulation and respiration in severe sepsis, but is contraindicated after head injury because of increased risk of intracranial bleeding. A 21-year-old man with severe head injury after a car accident was endotracheally intubated, mechanically ventilated, and hemodynamically stabilized before transfer to our university hospital. His condition became complicated with pneumonia, septic shock, ARDS, coagulation dysfunction, and renal failure. In spite of intensive therapy, oxygenation and arterial blood pressure fell to critically low values. Simultaneously, his intracranial pressure peaked and his pupils dilated, displaying no reflexes to light. His antibiotic regimen was changed and ventilation was altered to high frequency oscillations, and despite being ethically problematic, we added APC to his treatment. The patient recovered with modest neurological sequelae
Lens GSH metabolism.
<p>Relative levels of metabolites related to GSH metabolism in lenses from Atlantic salmon and rainbow trout reared at 13 or 19°C at the end of the 35d experiment: (A) 5-oxoproline, (B) cystathionine, (C) glutamate, (D) 2-aminobutyrate, (E) ophtalmate, (F) oxidized glutathione (GSSG), (G) reduced glutathione (GSH). Significant differences between species are denoted by an asterisk (*), significant differences between temperatures and interaction effects are denoted by lower case letters (a, b) (p<0.05).</p
Lens metabolomic profiling as a tool to understand cataractogenesis in Atlantic salmon and rainbow trout reared at optimum and high temperature
<div><p>Periods of high or fluctuating seawater temperatures result in several physiological challenges for farmed salmonids, including an increased prevalence and severity of cataracts. The aim of the present study was to compare cataractogenesis in Atlantic salmon (<i>Salmo salar</i> L.<i>)</i> and rainbow trout (<i>Oncorhynchus mykiss</i>) reared at two temperatures, and investigate whether temperature influences lens metabolism and cataract development. Atlantic salmon (101¹2 g) and rainbow trout (125¹3 g) were reared in seawater at either 13°C (optimum for growth) or 19°C during the 35 days experiment (n = 4 tanks for each treatment). At the end of the experiment, the prevalence of cataracts was nearly 100% for Atlantic salmon compared to ~50% for rainbow trout, irrespective of temperature. The severity of the cataracts, as evaluated by slit-lamp inspection of the lens, was almost three fold higher in Atlantic salmon compared to rainbow trout. The global metabolic profile revealed differences in lens composition and metabolism between the two species, which may explain the observed differences in cataract susceptibility between the species. The largest differences were seen in the metabolism of amino acids, especially the histidine metabolism, and this was confirmed by a separate quantitative analysis. The global metabolic profile showed temperature dependent differences in the lens carbohydrate metabolism, osmoregulation and redox homeostasis. The results from the present study give new insight in cataractogenesis in Atlantic salmon and rainbow trout reared at high temperature, in addition to identifying metabolic markers for cataract development.</p></div
Lens histidine and N-Acetylhistidine (NAH) concentrations.
<p>(A) Lens histidine and (B) NAH concentrations in lenses from Atlantic salmon and rainbow trout reared at 13 or 19°C at the end of the 35d experiment, as mean ¹ SEM (n = 4). Significant differences between the species are denoted by an asterisk (*), significant differences between temperatures and interaction effects are denoted by lower case letters (a, b) (p<0.05).</p
Lens histidine and N-Acetylhistidine (NAH) levels.
<p>(A) Relative levels of histidine and (B) NAH in lenses from Atlantic salmon and rainbow trout reared at 13 or 19°C at the end of the 35d experiment. Significant differences between the species are denoted by an asterisk (*), significant differences between temperatures and interaction effects are denoted by lower case letters (a, b) (p<0.05).</p
Lens lipid metabolism.
<p>Relative levels of metabolites related to the lipid metabolism in lenses from Atlantic salmon and rainbow trout reared at 13 or 19°C at the end of the 35d experiment: (A) prostaglandin E<sub>2</sub>, (B) arachidonate (20:4n-6), (C) carnitine, (D) acetylcarnitine, (E) sphingosine. Significant differences between species are denoted by an asterisk (*), significant differences between temperatures are denoted by lower case letters (a, b) (p<0.05).</p