Biomedical subjects
Publications and source records attributed to E Schrauwen.
A peripheral sensory neuropathy was diagnosed in two Border collie puppies. Neurological, electrophysiological and histopathological examinations suggested a purely sensory neuropathy with mainly distal involvement. Urinary incontinence was observed in one of the puppies and histological examination of the vagus nerve revealed degenerative changes. An inherited disorder was suspected.
Eight dogs suffered chronic defecation problems characterised by severe dyschezia, manifested by signs of fear and vocalisation on defecation. One or more depigmented, discrete erosions, easily bleeding on palpation, were found in the perineal region. Histopathological changes included interface dermatitis, apoptotic keratinocytes, focal hydropic degeneration of basal epidermal cells, focal thickening of the basement membrane zone and dermal lichenoid infiltrations with mononuclear and plasma cells. A diagnosis of cutaneous or discoid lupus erythematosus was made on the basis of these clinical, physical and specific histopathological changes. The dogs were treated systemically with immunomodulating drugs and good results were obtained.
Mesenteric volvulus was diagnosed in 12 dogs over a nine-year period. Each case was presented with abdominal distension and shock. Haematochezia, which is frequently reported in association with mesenteric volvulus, was present in only two of the dogs. The diagnosis, which in all cases was based on radiography, was followed by immediate treatment for shock and surgical intervention whenever possible. In five of the 12 cases, the volvulus was treated successfully and these patients survived. This indicates that the prognosis for mesenteric volvulus might be better than is currently believed, and immediate laparotomy is recommended if mesenteric volvulus is suspected.
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To induce diarrhoea and hypovolaemia, newly-weaned conventionally bred piglets (3- to 4-weeks-old), were either given secretagogues or were inoculated with enterotoxigenic Escherichia coli (ETEC). Choleratoxin (n = 2), E. coli heat-labile enterotoxin (n = 2) or castor oil (n = 2) were given intragastrically or piglets were intraperitoneally injected with DL 5-hydroxytryptophan (n = 3). These substances induced a transient diarrhoea without clinical symptoms of dehydration. Therefore, a combination of castor oil and DL 5-hydroxytryptophan was given two times a day during 3 consecutive days to 3 piglets. Although diarrhoea lasted for 5 days, still no hypovolaemia occurred. Probably the secretagogues have to be given continuously to mimic the continuous release of enterotoxins during secretory colibacillary diarrhoea. It was, therefore, tried to reproduce colibacillosis in the just-weaned piglets. Animals were inoculated with K88ac fimbriae producing ETEC strains (O149:K91:K88ac; LT, STa and STb positive) (n = 7), or pretreated with chloramphenicol followed by the ETEC inoculation (n = 8), or pretreated with the antibiotic, inoculated with an enteropathogenic coronavirus, transmissible gastroenteritis virus (TGEV), and subsequently inoculated with ETEC (n = 18). Only the last procedure induced a reproducible diarrhoea (93%) and dehydration resulting in a mortality of 80%. It was concluded that the latter experimental procedure could be used to study diarrhoea and hypovolaemia in newly-weaned piglets and to evaluate the effect of potentially antisecretory drugs on postweaning diarrhoea in piglets.
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In conscious pigs the influence of intravenous infusion of live E. coli (7 x 10(8)/kg), of the equivalent amount of endotoxin (20 micrograms/kg) or of a high dose of endotoxin (2.5 mg/kg) on the hemodynamic, clinical and pathological parameters and on survival rate was studied. E. coli and endotoxin infusion resulted in pulmonary hypertension, systemic arterial hypotension, a decrease in cardiac output and an increase in heart rate. Clinical signs were characterized by respiratory and nervous disturbances, whereas necropsy revealed hemorrhages and edema in several organs. Although these findings were similar in the three groups, a marked difference in lethality was observed. Infusion of E. coli or of the high dose of endotoxin resulted in a significant mortality, whereas all pigs survived the infusion of the low dose of endotoxin. This suggests that the lethal pathophysiological mechanisms may only become activated when a sufficient amount of endotoxin is released into the circulation.
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In anesthetized piglets the influence of an LD100 of Escherichia coli endotoxin (0.5 mg/kg IV, bolus injection) on several hemodynamic parameters and on survival time was studied. Endotoxin provoked a pronounced decrease in arterial pressure and cardiac output and an increase in portal venous and pulmonary arterial pressure and heart rate. Total peripheral and mesenteric vascular resistances displayed an initial increase followed by a sustained decrease, whereas pulmonary vascular resistance revealed a pronounced biphasic increase. All pigs died within 210 min following endotoxin administration. Pretreatment with the 5-HT2-antagonists R 41468 and R 50970 and with the prostanoid-synthesis inhibitor flurbiprofen induced a significant attenuation of the increase in pulmonary vascular resistance and beneficial effects on survival. Best survival results were obtained with prednisolone sodium succinate, although these results can only partly be ascribed to beneficial hemodynamic effects. The experiments with the opiate antagonists, however, point to detrimental effects.
In the present review, an attempt has been made to describe the modern concept of circulatory shock (Part I). The shock inducing insults (low circulatory volume/vascular capacity equation, heart failure, or disturbance of cellular metabolism induce physiological defense mechanisms, which result in peripheral vasoconstriction in order to maintain adequate blood pressure and perfusion of vital organs (compensatory phase). However, when the insult is too aggressive or too prolonged, deterioration of the cardiovascular system and cellular function ensues as a result of anaerobic metabolism, loss of vascular tone, reperfusion injury, depression of the reticuloendothelial system, disseminated intravascular coagulation, and myocardial failure (decompensatory phase). This leads to widespread cellular destruction, autodigestion, and finally death of the patient. Recent features of shock therapy will be discussed in part II of this review.
In Part II of this review, recent aspects in shock therapy are discussed. Treatment of an animal in a state of shock is not an easy task, it is time-consuming and expensive. The basic aims of shock therapy are to remove the inciting cause (wherever possible), to increase the circulating blood volume in order to stimulate the cardiac output and tissue perfusion (by infusion of fluids and eventually vasoactive substances), and to reduce or correct the injurious effects of shock (oxygenation, corticosteroids, antibiotics, energy or substrates, vasoactive substances, diuretics, regulation of the acid-base balance, stimulation of RES, and treatment of DIC).
In anesthetized piglets the intravenous injection of a lethal dose of endotoxin, 0.5 mg/kg, resulted in a progressively evolving deterioration of the cardiovascular system (hypotension, decrease in cardiac output), in an increase in pulmonary vascular resistance and in the death of all animals within 210 min following endotoxin administration. Endotoxin induced a significant increase in immunoreactive (i) i-6-oxo-PGF1 alpha, i-TXB2, and i-15-oxo-13,14-dihydro-PGF2 alpha levels in peripheral plasma. Pretreatment with the PG-synthesis inhibitor, flurbiprofen, abolished the profound rise in PG-levels, whereas cardiovascular performance was more sustained. The results suggest the involvement of several prostanoids during the evolution of endotoxic shock in the piglet.
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The influence of intraarterial infusions of lysine-vasopressin and oxytocin on mesenteric vascular resistance has been studied in anaesthetized young pigs. Vasopressin provokes a pronounced vasoconstrictor effect, whereas oxytocin induces a biphasic response: a transient vasodilation, followed by a more pronounced and sustained vasoconstriction. The comparison of the plasma concentrations of these hormones during parturition and hemorrhage in the pig with the minimal effective doses infused, suggests a possible mesenteric vasoconstrictor effect of oxytocin during parturition and of lysine-vasopressin during hemorrhage.
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