Peripheral embolization during thrombolytic therapy for left atrial thrombus.
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Embolism↗
Biomedical subjects
C McGowan
Publications and source records attributed to C McGowan.
Experimental induction of chronic aflatoxicosis in chickens by purified aflatoxin B1 and its reversal by activated charcoal, phenobarbital, and reduced glutathione.
Aflatoxin B1 (AFB1) caused dose-dependent reductions in weight gain and feed consumption when day-old Hubbard X Hubbard broiler type chicks were maintained on a diet contaminated with either 0, 2.5, 5, or 10 ppm purified AFB1 for 8 weeks. Although changes in these parameters were detected at the 2.5 and 5 ppm, the most profound changes were evident at 10 ppm contamination. The concentration of cytochrome P-450 in hepatic microsomes, measured at the end of 8 weeks, also showed dose-dependent decreases. Cytochrome P-450 content in chickens receiving 2.5, 5, and 10 ppm AFB1 was 16, 28, and 65%, respectively, less than the control. Microsomal benzphetamine N-demethylase activity was not inhibited by 2.5 or 5 ppm, but ingestion of 10 ppm AFB1 reduced its activity by more than 40%. Serum glutamic oxalacetic transaminase (SGOT) levels of chickens receiving 10 ppm AFB1 increased by more than 100%, indicating substantial liver damage. However, birds simultaneously receiving 10 ppm AFB1 and activated charcoal (.1% in the feed) or either reduced glutathione (.05%) or phenobarbital (.05%, given intermittently) in their drinking water showed a trend of improvement in feed consumption (less than 10% reversal) and weight gain (less than 28% reversal) over the birds receiving 10 ppm AFB1 alone. The results also indicate that the simultaneous presence of these agents with AFB1 considerably prevented the inhibitory effect of AFB1 on the microsomal cytochrome P-450 and benzphetamine N-demethylase activity. Furthermore, these agents were able to provide moderate protection against AFB1-induced liver injury manifested by elevation of SGOT activity.
Aflatoxin B1↗
Vascular reactivity during the development of two-kidney, one-clip Goldblatt hypertension in conscious dogs.
This study evaluates the sequential changes in vascular reactivity in conscious dogs during the early and late phases of two-kidney, one-clip Goldblatt hypertension (2-KGH) produced by unilateral renal artery constriction (URAC). The in vivo responses to serotonin (5-HT), norepinephrine (NE), angiotensin II (Ang II), prostacyclin (PGI2), acetylcholine (ACH), and nitroglycerin (GTN) were reproducible and stable throughout the 32-day period of study in dogs subjected to sham URAC. The vascular responses to 5-HT, Ang II, and PGI2 were enhanced day 1 post-URAC, before mean arterial pressure (MAP), cardiac output (CO), or total peripheral resistance (TPR) increased. The magnitude of the enhanced reactivity progressed on days 4 and 32 post-URAC, as hypertension developed. The pressor responses to NE did not change from pre-URAC values until CO and MAP were elevated. The vasodepressor responses to ACH and GTN diminished over a 12-day period post-URAC, in parallel with the change in CO, but prior to any increase in TPR. These data suggest that in dogs with 2-KGH changes in vascular reactivity precede the development of the increased MAP and TPR of hypertension. The lack of uniformity of the onset of the reactivity changes to the different agonists suggests that both intrinsic factors and pressure changes modify the vascular wall in the early and later stages of 2-KGH.
Angiotensin II↗
Effect of an increased cardiac output on vascular responses to vasoactive agents in two-kidney, one-clip Goldblatt hypertension.
The effect of the increased cardiac output of two-kidney, one-clip Goldblatt hypertension (2-KGH) on the altered vascular responses to vasoactive agents was examined in the conscious, chronically instrumented dog. The early stage of 2-KGH is characterized by an increased arterial pressure, an increased aortic flow, a decreased total peripheral resistance, and enhanced responses to angiotensin II and serotonin. As the aortic flow increases the responses to norepinephrine are enhanced, and the dilator responses to acetyl-choline and nitroglycerin are depressed. Aortic flow then returns to control values and the increased arterial pressure is maintained by an increase in peripheral resistance. When the increased aortic flow is prevented by occluding the vena cava to maintain flow at control values, the vascular responses to each of the agonists do not differ from that obtained when the aortic flow is elevated. Moreover, the temporal development and magnitude of the elevation in arterial pressure resulting from the increased vascular resistance is similar in dogs with an increased and normal aortic flows. The results suggest that increased aortic flow is not essential for the increased vascular resistance or the vascular changes in the canine model of 2-KGH.
Acetylcholine↗
Pulmonary vascular smooth muscle function in porcine splanchnic arterial occlusion shock.
Pulmonary complications are a major cause of death in patients in various forms of shock. The exact causes of the pulmonary complications are unknown. This study evaluates the functional characteristics of intralobar pulmonary arteries (IPA) and veins (IPV) obtained from swine subjected to splanchnic arterial occlusion (SAO) shock ans subsequent cardiovascular collapse and sham-shocked swine subjected to surgery but no occlusion. The contractile response of pulmonary arteries to norepinephrine (NE) and serotonin (5-HT) were depressed when obtained from pigs subjected to SAO shock. The depression in the sensitivity to 5-HT and maximal tension development to 5-HT and NE was selective, since the responses to potassium ion were not depressed. IPA obtained from swine with SAO shock were more sensitive to the relaxant actions of arachidonic acid, a precursor for bisenoic prostaglandins, than were IPA from sham-shocked swine. This was not observed when prostaglandins were used as agonists. This suggests that synthesis of prostaglandin differs in the pulmonary vasculature of sham-shocked and SAO-shocked animals. IPV obtained from swine in SAO shock were less sensitive to 5-HT and NE but more sensitive to arachidonic acid and 9 alpha, 11 alpha-epoxymethano-PGH2, a thromboxane like compound. IPV obtained from swine in SAO shock converted more arachidonic acid into a substance with the chromatographic mobility of thromboxane B2. The data suggest that alterations in the prostaglandin system within the pulmonary artery and vein may contribute to the pulmonary complications of SAO shock. The alterations appear to include an enhanced synthesis of prostacyclin as well as thromboxane-like substance. Because the veins were more sensitive than the arteries to 9 alpha, 11 alpha-epoxymethano-PGH2, thromboxanes or endoperoxides may elevate venous tone and contribute to the pulmonary edema associated with shock states.
Animals↗
In vivo and in vitro effect of chelating agents on drug metabolizing enzymes of the rat.
Rats given calcium disodium ethylenediaminetetraacetic acid (CaNa2EDTA), diethylenetriaminepentaacetic acid (DTPA), dimercaprol, p-aminosalicylic acid (PAS), or d-penicillamine (penicillamine) i.p. for 7 successive days showed a significant decrease in the activity of hepatic microsomal benzphetamine N-demethylase. There was no appreciable change in the microsomal cytochrome P-450 concentration. In vitro incubation of the chelating drugs with liver microsomes isolated from rats pre-treated with phenobarbital caused no significant loss of the hemoprotein. The decreased rate of benzphetamine metabolism in microsomal preparations from rats, pretreated with the chelating drugs, may be attributed partly to hepatic depletion of essential trace elements by the chelating drugs.
Aminosalicylic Acid↗
The hind limb musculature of the brown kiwi, Apteryx australis mantelli.
The most complete account of the hind leg muscles of the kiwi was published a century ago by Sir Richard Owen, in his seventy-fifth year. This extensively-cited work has several omissions and errors, and while certain of these were corrected by subsequent authors, sufficient uncertainty remains to warrant a reinvestigation. In the present study a detailed description of the hind leg musculature is given, based upon dissections of two frozen specimens. An indication of the possible function of each muscle is given by assessing its size, action, and fiber-arrangement, together with tentative data on the relative abundance of twitch and tonus fibers. The correlation between surface features of bones and muscle attachments is investigated with a view to interpreting palaeontological material. Although the limb and pelvic bones are marked by numerous features which suggest muscle attachments, relatively few can be positively identified with specific muscles. Only 23% of the muscle origins and insertions can be identified, and, with three possible exceptions, no indication of relative size is given by the scars. The possibility of being able to reconstruct the musculature of the kiwi from its skeletal anatomy, much less that of its extinct relatives, is remote.
Animals↗
The effects of agents that bind to cytochrome P-450 on hypoxic pulmonary vasoconstriction.
The relationship between pulmonary arterial pressure (Ppa) and blood (Q) was determined during normoxia and hypoxia in ventilated pig lungs perfused in situ with the animal's own blood. Hypoxia shifted the Ppa-Q relationship to the right and decreased its slope, indicating pulmonary vasoconstriction. Carbon monoxide (11.5% in the inspired gas) and metyrapone ditartrate (10 mg/min into the perfusate) caused vasodilation when oxygenation was normal and reduced the vasoconstriction caused by hypoxia. Since the only pharmacological property CO and metyrapone are thought to have in common at the concentrations employed is the ability to bind to the heme iron of cytochrome P-450, these results are consistent with the hypothesis that desaturation of this cytochrome leads to pulmonary vasoconstriction. Prostaglandin F2alpha, infused into the pulmonary artery at 0.01 mg/min, when oxygenation was normal, had effects on the Ppa-Q relationship similar to those of hypoxia. The F2alpha response was also reduced by CO and metyrapone, suggesting either that P-450 was involved in the F2alpha response or that CO and metyrapone were toxic to pulmonary vascular smooth muscle. Proadifen hydrochloride (1 mg/min), which is thought to bind to the protein moiety of P-450 also reduced the hypoxic response, but was a vasoconstrictor during normoxia and did not affect the F2alpha response.
Animals↗
Lead toxicity in chickens. Interaction with toxic dietary levels of selenium.
Two experiments were conducted in which varying levels of lead (up to 2000 ppm as lead acetate trihydrate) and selenium (up to 40 ppm as Na2SeO3) were fed, either alone or in combination, to chicks from day-old through 18 or 20 d. Lead additions depressed growth in a dose-dependent manner without affecting mortality. Selenium addition at 20 ppm was severely growth inhibitory, but mortality was not affected. The growth inhibition of 20 ppm Se was partially alleviated by feeding it in combination with 2000 ppm Pb; however, mortality was increased significantly by the combination. In contrast 40 ppm Se resulted in almost complete cessation of growth and 85% mortality, whereas the combination with 2000 ppm Pb partially overcame the growth inhibition and eliminated the excess mortality. When Pb or Se were fed alone, hepatic levels of the fed element were elevated. There were further significant elevations of hepatic levels of both elements when fed in combination at identical dietary concentrations as the single element additions. The results suggest that Pb and Se are antagonistic. The nature of the interaction of these elements is such that although 2000 ppm Pb partially overcomes the growth inhibition by 20 or 40 pm Se, the reverse (relief of Pb inhibition by Se) is not observed.
Animals↗
Helenin inhibition of liver microsomal enzymes.
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Animals↗