Haemodynamic alterations in anaesthetized and acutely intoxicated newborn piglets

Chandler, Cara J.; Ong, B. Y.; Sitar, Daniel S.

doi:10.1111/j.1476-5381.1990.tb12118.x

Cited by 4 publications

(3 citation statements)

References 26 publications

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“…All measured parameters in experimental piglet (exposed to isoflurane, 0.55‐vol%, + N 2 O, 75‐vol%, + midazolam, 1 mg/kg, i.m.) and sham control piglet (exposed to a continuous fentanyl infusion, 15 μg/kg/h) were within physiologically acceptable ranges ( dashed lines ) 23,24 . Arterial blood gas analysis was done every hour during anesthesia exposure (B).…”

Section: Pigletsmentioning

confidence: 99%

“…) and sham control piglet (exposed to a continuous fentanyl infusion, 15 g/kg/h) were within physiologically acceptable ranges (dashed lines). 23,24 Arterial blood gas analysis was done every hour during anesthesia exposure (B). All measured parameters in piglets (exposed to isoflurane, 0.55-vol%, + N 2 O, 75-vol%, + midazolam, 1 mg/kg, i.m.)…”

Section: Histopathological Studiesmentioning

confidence: 99%

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Timing versus duration

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Jevtović-Todorović

2010

Annals of the New York Academy of Sciences

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Rapidly accumulating evidence indicates that clinically used general anesthesia causes massive, widespread neuroapoptotic degeneration in the developing mammalian brain. Susceptibility to anesthesia-induced neurotoxicity has been documented in rats, mice, guinea pigs, primates, and in this study, piglets; in short, anesthesia-induced developmental neuroapoptosis is not species-dependent. Our findings with piglets, like those in other immature mammals, demonstrate that relatively short exposure to anesthesia is just as detrimental to species with long periods of synaptogenesis as it is to those with short periods of synaptogenesis. However, the highly reproducible findings in different species also indicate that the timing of exposure to anesthesia is critically important; that is, brain regions that are at the peak of synaptogenesis are most vulnerable even when the exposure to anesthesia is relatively brief. Because the peak of synaptogenesis is characterized by intense, highly programmed neuronal communication that is vital for the survival and proper function of immature neurons, we conclude that anesthesia causes severe disturbances in the fine equilibrium between excitatory and inhibitory neurotransmission in the developing mammalian brain, ultimately leading to neuronal redundancy and death.

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Section: Pigletsmentioning

confidence: 99%

Section: Histopathological Studiesmentioning

confidence: 99%

Timing versus duration

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Ori

Jevtović-Todorović

2010

Annals of the New York Academy of Sciences

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“…Of particular importance to the field of cardiopulmonary science is that despite some anatomic differences, the haemodynamics, respiratory and associated metabolic processes are similar in humans and pigs (Chandler et al 1990;Phillips et al 2006 Kuntscher et al 2007). Studies in newborn animals have similar goals (Gavianes et al 2001, Juvik et al 2007.…”

Section: Discussionmentioning

confidence: 99%

Ventilation and Haemodynamic Indicators in Spontaneously Breathing Pigs under General Anaesthesia

et al. 2010

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The aim of this study was to obtain ventilation and haemodynamic data of healthy piglets under general anaesthesia for future patho-physiological experimental studies. A total of 34 domestic piglets of the Czech Black Pied (Přeštice) breed were used in the study. The animals (male to female ratio 8 : 9) were six weeks old and their average body mass was 22 kg.A general anaesthetic (fentanyl and azaperon) was introduced via a pulmonary artery catheter and the spontaneously breathing animals were monitored for 60 min. Cardiac output and haemodynamic indicators were established using intermittent pulmonary artery thermodilution. Blood gas data were deduced using fan dynamic parameters of ventilation and ventilation indices.The study yielded reliable data of dynamic lung indicators (p < 0.05); e.g. the tidal volume 6.00 ± 0.82 ml/kg, hypoxemic index 350.47 ± 42.50 mmHg, lung compliance 0.63 ± 0.12 ml/cmH 2 O/kg, and haemodynamic indicators (p < 0.01) such as cardiac output 2.12 ± 0.75 l/min, pulmonary vascular resistance 3.92 ± 0.52 and systemic vascular resistance 15.8 ± 6.81 Woods units.Reliable data regarding lung dynamics, cardiac output, preload and afterload of both heart ventricles in spontaneously breathing healthy piglets under general anaesthesia were achieved.

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Ethanol‐induced inhibition of ventricular protein synthesis in vivo and the possible role of acetaldehyde

Siddiq

Richardson

Mitchell

et al. 1993

Cell Biochemistry & Function

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We have determined the extent to which acute ethanol administration perturbs the synthesis of ventricular contractile and non-contractile proteins in vivo. Male Wistar rats were treated with a standard dose of ethanol (75 mmol kg-1 body weight; i.p.). Controls were treated with isovolumetric amounts of saline (0.15 mol l-1 NaCl). Two metabolic inhibitors of ethanol metabolism were also used namely 4-methylpyrazole (alcohol dehydrogenase inhibitor) and cyanamide (acetaldehyde dehydrogenase inhibitor) which in ethanol-dosed rats have been shown to either decrease or increase acetaldehyde formation, respectively. After 2.5 h, fractional rates of protein synthesis (i.e. the percentage of tissue protein renewed each day) were measured with a large (i.e. 'flooding') dose of L-[4-3H]phenylalanine (150 mumol (100 g)-1 body weight into a lateral vein). This dose of phenylalanine effectively floods all endogenous free amino acid pools so that the specific radioactivity of the free amino acid at the site of protein synthesis (i.e. the amino acyl tRNA) is reflected by the specific radioactivity of the free amino acid in acid-soluble portions of cardiac homogenates. The results showed that ethanol alone and ethanol plus 4-methylpyrazole decreased the fractional rates of mixed, myofibrillar (contractile) and sarcoplasmic (non-contractile) protein synthesis to the same extent (by approx. 25 per cent). Profound inhibition (i.e. 80 per cent) in the fractional rates of mixed, myofibrillar and sarcoplasmic protein synthesis occurred when cyanamide was used to increase acetaldehyde formation. There was also a significant decrease in cardiac DNA content. The results suggest that acute ethanol-induced cardiac injury in the rat may be mediated by both acetaldehyde and ethanol.

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Haemodynamic alterations in anaesthetized and acutely intoxicated newborn piglets

Cited by 4 publications

References 26 publications

Timing versus duration

Timing versus duration

Ventilation and Haemodynamic Indicators in Spontaneously Breathing Pigs under General Anaesthesia

Ethanol‐induced inhibition of ventricular protein synthesis in vivo and the possible role of acetaldehyde

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