Absence of enhanced detoxication of permethrin in pyrethroid-resistant house flies

The mechanisms of resistance to pyrethroids were studied in a permethrin-selected (147-R) strain of the house fly, Musca domestica L. Approximately 12-fold synergism was obtained with a mixture of (1R)-trans-permethrin:piperonyl butoxide (1:5) so that the resistance decreased from 97-fold to 22-fold. Tests with the esterase inhibitor S,S,S-tributyl phosphorotrithioate produced very little synergism in either the resistant (R) strain (1.6-fold) or the susceptible (S) strain (1.9-fold). An investigation of the microsomal components revealed that compared to the S strain, the R strain demonstrated twice as much cytochrome P-450 and cytochrome b₅ and double the rate of NADPH-cytochrome c reductase activity. In addition, the rate of p-nitroanisole O-demethylation was found to be six times greater in the R strain. An in vivo accumulation study showed that the R strain displayed a decreased rate of penetration of trans-[¹⁴C]permethrin. When treated at equitoxic doses the R strain was found to tolerate 50-fold more internal permethrin than the S strain. An in vitro metabolism study indicated that there was no difference between strains in the overall rate of metabolism of trans-[¹⁴C]permethrin. The evidence obtained supports the conclusion that several resistance factors are involved but that decreased sensitivity of the nervous system to the action of pyrethroids is the principal mechanism of resistance in the 147-R strain.     

CLINICAL EXTRACORPOREAL OXYGENATION FOR RESPIRATORY INSUFFICIENCY

There is today a large group of patients who die for the simple reason that their lungs can no longer transport sufficient oxygen to meet the demands of the body. The projected number of deaths resulting from acute respiratory insufficiency in 1977, in the United States is 86,000. The average age of these patients will be 46 years.¹ This establishes a rather high priority for developing newer methods of prevention and treatment of this syndrome. Prevention is the most important facet of this syndrome and many of its contributing etiological factors will be better clarified and, subsequently, better managed in the next decade.     

Versuche mit einem Prostaglandinanalog zur Zyklussynchronisation beim Rind unter hormonanalytischer und klinischer Kontrolle

1. Durch intramuskulare Injektion von 0,5 mg des Prostaglandinanalogs ICI 80 996 beim Rind während der Gelbkörperphase des Zyklus kann nach 15–24 Stunden ein Abfall der Progesteronwerte unter 1 ng/ml Blutplasma und damit eine nachhaltige Luteolyse erreicht werden. Die sich anschließende Brunst ist ovulatorisch und feral. Das Präparat wird ohne Nebenwirkungen vertragen. 2. Durch zweimalige Injektion (d. h. je 1 mal 0,5 mg i. m.) im Abstand von 11 Tagen kann dieser Luteolyseeffekt zu Brunstsynchronisationen herangezogen werden; dabei ist eine Zykluskontrolle oder Brunstbeobachtung nicht erforderlich. 3. in 8 Feldversuchen konnte bei 213 Tieren ein Synchronisationserfolg von 90,6 % und, nach KB in der 1. induzierten Brunst, ein Konzeptionsergebnis von 54,7 % (bzw. von 60,1 %, wenn man die Auswertung auf die erfolgreich synchronisierten Tiere beschränkt) erzielt werden. Die KB bei 119 nicht behandelten Kontrolltieren, die in 5 dieser 8 Versuche zur Verfugung standen, war zu 60,3 % erfolgreich. 4. In einem Problembestand konnte die Fertilitätslage durch das biotechnische Vorgehen der Prostaglandinanwendung unmittelbar nicht verbessert werden 5. Die palpatorischen Ovarbefunde zum Zeitpunkt der KB ergaben, daß Tiere mit aprungbereiten Follikeln'zu 65 %, mit kleinen, nicht reifen Follikeln zu 50,8 % und mit bereitsgesprungenen Follikeln zu 15,8 % konzipierten. 6. Die bei einem Teil der Versuche eingesetzte zusdtzliche Behandlung mit 1,0 bzw. 1,5 mg des Gonadotropin-Releasinghormons (LRH-Hoechst 471) i. m. zum Zeitpunkt der Besamung zeigte bezüglich des Konzeptionsergebnisses eine positive Tendenz.     

Etiology of patent ductus arteriosus in dogs

Patent ductus arteriosus (PDA) is the most common congenital heart disease in dogs and usually causes heart failure and death unless corrected at a young age. Previous histologic studies in a line of dogs derived from Miniature Poodles with hereditary PDA identified varying degrees of hypoplasia and asymmetry of ductus-specific smooth muscle and the presence of aortalike elastic tissue in the ductus wall sufficient to cause patency. To determine if similar structural abnormalities cause PDA in other dogs, serial-section, 3-dimensional histology of ductal architecture was studied in 8 non-Poodle purebred dogs with PDA with no immediate family history of PDA. Morphologic abnormalities were observed in 7 of 8 dogs with PDA and essentially were the same as those in dogs known to have a hereditary form of PDA. These findings suggest that apparently sporadic PDA in these breeds is caused by a genetic defect in the structure of the ductus arteriosus that is similar or identical to that in the Poodle. The relatives of dogs with PDA, particularly parents, offspring, and siblings, should be screened for evidence of PDA. Dogs with PDA should not be used for breeding, regardless of breed.     

Methemoglobinemia and eccentrocytosis in equine erythrocyte flavin adenine dinucleotide deficiency

This report describes erythrocyte biochemical findings in an adult Spanish mustang mare that exhibited persistent methemoglobinemia, eccentrocytosis, and pyknocytosis that were not related to the consumption or administration of an exogenous oxidant. The methemoglobinemia was attributed to a deficiency in cytochrome-b5 reductase (Cb5R) activity, and the eccentrocytes and pyknocytes were attributed to a marked deficiency in reduced nicotinamide adenine dinucleotide phosphate-dependent glutathione reductase (GR) activity that resulted in decreased reduced glutathione concentration within erythrocytes. The GR activity increased to a near-normal value after addition of flavin adenine dinucleotide (FAD) to the enzyme assay, indicating a deficiency of FAD in erythrocytes. The methemoglobinemia, eccentrocytosis, and pyknocytosis were attributed to deficiency of FAD in erythrocytes because the GR and Cb5R enzymes use FAD as a cofactor. This deficiency in FAD results from a defect in erythrocyte riboflavin metabolism, which has not been documented previously in animals.