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C Hermans

Publications and source records attributed to C Hermans.

80 records · Page 5Linked to original sources

Thalamonal, droperidol and fentanyl in induced hypovolaemic shock in the conscious dog.

Previous studies had shown that Thalamonal exerts a protective activity against hypovolaemic shock in experimental animals as well as in patients. The purpose of the present study was to make a long-term evaluation of the value of single doses of Thalamonal fentanyl and droperidol as shock-protecting agents in conscious dogs which received no replacement of blood loss. The study was conducted in 20 animals in which devices were implanted for measuring heart rate, arterial and venous blood pressure, left ventricular and left atrial blood pressure. The dogs were divided into 4 groups, receiving 20 ml of an i.v. injection containing either 0.025 mg/kg fentanyl, 0.625 mg/kg droperidol, 0.25 ml/kg Thalamonal (0.625 mg/kg droperidol + 0.0125 mg/kg fentanyl), or saline. Thalamonal allowed a 100 per cent survival of the dogs, one of the 5 animals survived in the droperidol group, whereas fentanyl and saline were completely ineffective. As a possible mechanism of action the interruption of the vicious sequence of blood loss, vasoconstriction and circulatory arrest at a peripheral and/or central level is discussed. The hypothesis of intracorporeal blood volume correction under the influence of Thalamonal as an anti-vasoconstrictor seems to be logical but needs further investigation.

Animals↗

The effect of domperidone on pyloric activity in dog and in man.

In a study in dogs using ultrasonic transducers to measure degree of pyloric dilatation, it was found that i.v. domperidone (0.35 and 0.7 mg/kg) significantly increased the diameter of the pyloric lumen without affecting the frequency of pyloric relaxations. A subsequent study involving 59 patients referred for upper digestive tract endoscopy, confirmed this increase in diameter of the pylorus which indicates a potential use of domperidone (either i.v. or oral) in the treatment of some forms of dyspepsia characterized by delayed gastric emptying.

Animals↗

Ultrastructural damage and Ca2(+)-shifts in the canine myocardium subjected to regional incomplete ischemia.

The role of Ca2+ in the pathogenesis leading to ischemic myocardial cell death is still controversial. To gain insight into this phenomenon a cytochemical procedure, the phosphate pyroantimonate method, was used to localize different subcellular Ca2(+)-pools at the ultrastructural level. After 45 min of left anterior descending coronary artery (LAD) occlusion, the coronary arteries were perfused with triphenyltetrazoliumchloride staining (TTC) to identify viable ischemic and infarcted tissue. In non-ischemic tissue, Ca2(+)-deposits were confined to the sarcolemma, sarcolemma-derived vesicles, transverse tubules, and intercalated disks. In infarcted tissue (TTC-negative), the sarcolemma lost its Ca2(+)-binding capacity and mitochondria were either overloaded with Ca2(+)-precipitate or they contained amorphous densities. In viable ischemic areas (determined with the TTC-technique) the sarcolemma was virtually devoid of Ca2(+)-deposits. Mitochondria in this area frequently showed clumping of the cristae, associated with an accumulation of Ca2(+)-precipitate in between the clustered cristae. The results of this study indicate that Ca2(+)-shifts occur in ischemic myocardial cells before the occurrence of other ultrastructural signs of irreversible injury which, therefore, narrows the possibility that Ca2(+)-overload is only a consequence of ischemic cell death.

Animals↗

Pericarditis induced by high-dose cytosine arabinoside chemotherapy.

Pericarditis is a rare side effect of chemotherapy. We report here the case of a patient treated with high-dose cytosine arabinoside (HD ara-c) who developed severe pericarditis. Interruption of HD ara-c and initiation of corticosteroid treatment were effective in resolving the pericardial effusion. This case illustrates this rare but potentially life-threatening cardiac complication of HD ara-c therapy as well as the beneficial effect of corticosteroid treatment.

Adult↗

Correlation of HSP110 expression with all-trans retinoic acid-induced apoptosis.

In a previous study, we observed the strong expression of a stress protein of the HSP100/Clp family (HSP110) in apoptotic mesectodermal cells during early mouse facial development. In the present study, we describe the strong expression of the same HSP110 in mesectodermal cells undergoing apoptosis after all-trans retinoic acid (RA) administration. We used a teratological model known to increase cell deaths mainly in the first and second branchial arches during mammalian cephalogenesis: the treatment of E9 mouse embryos with all-trans RA, which results in craniofacial malformations comparable to those that characterize mandibulofacial dysostosis in man. Pregnant NMRI mice were treated with 60 mg/kg body weight of all-trans RA, given orally on day 9 of gestation; embryos were taken 4, 12 or 24 hr after RA administration. The apoptotic pattern of RA-induced cell deaths was confirmed using the dUTP biotin nick-end labeling (TUNEL) method and transmission electron microscopy (TEM). HSP110 expression was detected using an immunohistochemical approach. The increase in the number of TUNEL-positive cells and HSP110-positive cells after all-trans RA administration was quantified in the first branchial arch using a computerized method. Twelve hours after RA administration, the increase in the number of HSP110-positive cells is greater than the increase in the number of TUNEL-positive cells. Twenty-four hours after RA administration, only TUNEL-positive cells remain strong in number. We suggest that HSP110 expression could represent a biochemical event of apoptotic cell death induced by RA, associated with early stages of the apoptotic process. In order to find out if HSP110 expression resulted from neosynthesis, we performed in situ hybridization, which demonstrated that the expression of HSP110 occurred at the level of mRNA.

Animals↗