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The study provides descriptions of two new species of Enterogyrus coexisting in the stomach of the Mozambique tilapia, Oreochromis mossambicus (Peters). Enterogyrus multispiralis n. sp. and Enterogyrus mashegoi n. sp. were collected from hosts sampled at Nwanedi-Luphephe Dam, Limpopo River System, South Africa. The two new species can be differentiated from other members of the genus based on the spirality characteristics of the cirrus. Enterogyrus multispiralis n. sp. has an unique 8/9-2-4 cirrus spiral formula. The length of the cirrus and its spriral formula 5-2-3 make E. mashegoi n. sp. morphometrically unique from other Enterogyrus spp. Sequences of the nuclear ribosomal DNA partial 18S and internal transcribed spacer (ITS1) and 28S were obtained and compared with available sequences of Enterogyrus in GenBank. This is the first record of data on 18S rDNA region of Enterogyrus spp. A phylogenetic comparison was conducted, which included all data available for Enterogyrus spp., but this was limited to 28S data. The closest species to both new species of the present study was an undescribed Enterogyrus sp. 2 from Sarotherodon galilaeus (Linnaeus) described from Senegal (i.e. 2.1 and 2.9% uncorrected pairwise genetic distance to E. multispiralis n. sp. and E. mashegoi n. sp., respectively). These species represent new records for Africa resulting in a total number of 12 described valid species.

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A new species, Emoleptalea nwanedi n. sp. is described from the intestine of Schilbe intermedius, the silver catfish or butter barbel, from the Nwanedi-Luphephe Dam in the Limpopo Province of South Africa. Fish were collected using gill nets where after they were euthanised and dissected. The parasites were sampled, fixed in 70 % EtOH and stained with Van Cleave's haematoxylin. This species represents an addition to the African cluster of Emoleptalea species previously described and differs from the known species due to its unique size, equal size of oral and ventral suckers, position of ovary and seminal receptacle, number of vitelline follicles and their size, as well as the unique ciliated receptors on the wall of the acetabulum. This is the first record of this parasite from the silver catfish and from southern Africa.

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The Oreochromis mossambicus (Peters) population inhabiting Lake Loskop, South Africa, is characterized by a high incidence of obesity and pansteatitis. We investigated potential links between the impaired health of Lake Loskop O. mossambicus and the endocrine system by assessing the expression of selected genes associated with the thyroid and adrenal endocrine axes as well as peroxisome proliferator-activated receptor gamma (pparg). Moreover, contaminant-induced thyroid and/or metabolic modulation in Lake Loskop water was evaluated using juvenile O. mossambicus in laboratory exposures. The expression of thyroid hormone receptor alpha (thra) and type 2 deiodinase (dio2) was higher in Lake Loskop O. mossambicus than fish from another population, suggesting a degree of thyroid disruption. The altered gene expression may be a consequence, rather than cause of obesity. Expression of dio2 and pparg was higher in juvenile O. mossambicus exposed to unfiltered compared to filtered lake water, and our data suggest fasting as causative factor. Micro-organism abundance can therefore be a confounding factor in studies applying molecular markers to test for thyroid modulation by environmental waters. Pansteatitis was not a significant source of variance in the expression of any of the genes investigated, suggesting that the disease is not associated with disrupted endocrine signalling.

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An investigation was conducted into the parasitic infection of an indigenous cichlid, Oreochromis mossambicus, collected seasonally from the Nwanedi-Luphephe dams of the Limpopo River System from July 2007 to April 2009. Of 157 host specimens examined, 115 (73.25%) were infected by at least one gill parasite. In all, 1565 monogenean specimens were collected, belonging to five different species and two genera: Cichlidogyrus (C. halli, C. sclerosus, C. tilapiae and C. dossoui) and Scutogyrus (S. longicornis). Infracommunities were poor, with only 27 (17.20%) hosts harbouring four of the five species observed. Cichlidogyrus halli was the dominant species, with a prevalence of 73.25%. Prevalence values for each of the other four species were less than 50%. The mean intensities for each of the five species were low ( < 8 parasites/host). The parasite abundance and intensity levels were not influenced by either the sex or the size of the host. The abundance of all parasite species except for S. longicornis exhibited seasonal fluctuations, reaching peaks in winter and summer. The spatial distribution of each parasite was studied on different regions of the gill, and positive associations among some species were revealed.

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Lamproglena hoi n.sp. species was collected from the gill filaments of largescale yellowfish, Barbus marequensis A. Smith, 1841 and smallscale yellowfish, Barbus polylepis Boulenger, 1907 from the Spekboom River, Mpumalanga, South Africa. The genus Lamproglena is characterized. Morphological features of L. hoi are described and illustrated by means of drawings and scanning electron micrographs. This species is also compared with congener species described from other Barbus spp.

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Substituted carboranes and polyhedral hydroborate salts were observed to be potent anti-neoplastic/cytotoxic agents inhibiting the growth of mouse and human leukemias, human uterine, colon adenocarcinoma, lung bronchogenic and gliomas. Amino-o-carborane-hydrochloride 7, one of the more potent compounds, preferentially inhibited Tmolt3 DNA synthesis. The target of the agent appears to be de novo purine synthesis with significant inhibition of the activities of both regulatory enzymes, PRPP-amido transferase and inosine monophosphate dehydrogenase as well as dihydrofolate reductase. The agent also inhibited nucleoside kinase activities leading to reductions in deoxyribonucleotide pools. The DNA molecule itself was not a target of the agent.

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The boronated nucleosides with varying bases and sugar moieties were shown to be potent hypolipidemic agents in rodents. The 3'- aminocynaoborane dideoxythymidine derivative caused reductions in serum cholesterol and triglyceride levels, tissue lipids, VLDL and LDL cholesterol levels while elevating HDL cholesterol levels in rodents. The agents suppressed rat hepatic acetyl CoA synthetase, HMG-CoA reductase, acyl-CoA cholesterol acyl transferase, phosphatidylate phosphohydrolase and lipoprotein lipase activities while elevating cholesterol-7alpha-hydroxylase activity from 25 to 100 muM.

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Ribose and arabinoside boron nucleoside derivatives were shown to be potent cytotoxic agents in murine and human suspended and solid tumor cell lines. The arabinoside derivative inhibited DNA and RNA synthesis with the protein synthesis requiring a higher concentration of drug for inhibition within 60 min. The purine pathway appeared to be the major target of the arabinoside 1 with inhibition of PRPP amido transferase and IMP dehydrogenase activities. Blockage of this pathway afforded reductions of deoxyadenosine and deoxyguanosine nucleotide pools. The DNA template did not appear to be target of the arabinoside 1, in that there was no change in DNA viscosity, thermal denaturation or absorption of nucleosides of DNA. However, compound 1 when incubated with L-1210 cells for 24 hr. showed a slight shift of the DNA in the gradient and moderate inhibition of ct-DNA topoisomerase II was demonstrated by 1 in vitro.

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The pathogenesis of the hemodynamic abnormalities of diabetic ketoacidosis (DKA) is not well understood. Previous studies suggest that prostacyclin (PGI2) production by adipose tissue is increased in DKA. We investigated the role of PGI2 in the pathogenesis of the reduced vascular resistance in DKA. Rats with streptozocin-induced DKA were anesthetized with pentobarbital sodium, and flow was measured with an electromagnetic probe on the infradiaphragmatic aorta. The plasma level of 6-keto-PGF1 alpha (stable derivative of PGI2) was higher (mean +/- SE 0.91 +/- 0.05 ng/ml) and vascular resistance lower (4.9 +/- 0.2 mmHg.ml-1.min-1.100 g-1 [resistance units, RU]) in 67 rats with DKA than in 21 normal rats (0.34 +/- 0.03 ng/ml, P less than .01, and 9.0 +/- 0.7 RU, P less than .01, respectively). Inhibition of cyclooxygenase activity with either indomethacin or meclofenamic acid reduced the plasma 6-keto-PGF1 alpha level but failed to raise vascular resistance. Infusions of PGI2 in rats with DKA demonstrated that the vasculature was responsive to PGI2. Inhibition of cyclooxygenase activity not only reduced PGI2 production but also suppressed renin release. When the effects of the renin-angiotensin system were excluded by bilateral nephrectomy, indomethacin caused a significant increase (P less than .05) in vascular resistance. Thus, the failure of cyclooxygenase inhibitors to raise vascular resistance in DKA was a result of concurrent suppression of vasodilator (PGI2) and vasoconstrictor (renin-angiotensin system) mechanisms that are activated in DKA. Insulin administration increased vascular resistance (P less than .01) and decreased the level of plasma 6-keto-PGF1 alpha (P less than .01). Combined administration of PGI2 and insulin did not alter vascular resistance, suggesting that the increase in vascular resistance with insulin was predominantly due to the reduction of circulating PGI2. Thus, vascular resistance is decreased in DKA primarily as a result of the vasodilator effects of PGI2 produced by adipose tissue. The activation of the renin-angiotensin system represents a partial compensation. The increase in PGI2 production may contribute to the hypotension and mortality of DKA.

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Elevation of extracellular osmolality reduces the extent of myocardial and endothelial cell swelling that accompanies acute ischemia, and the reduction of cell swelling is associated with an increase in collateral blood flow to the ischemic area. However, little is known about the effects of hyperosmolality on the vascular resistance of the collateral coronary vasculature. We compared the effects of hyperosmolar mannitol with those of nitroglycerin and dipyridamole on the vascular resistance of large collateral coronary vessels and of the small arterial vasculature in an isolated heart model of regional ischemia. Elevation of osmolality by mannitol increased collateral blood flow to the ischemic region through at least two mechanisms. First, increasing osmolality resulted in dilation of large arterial conductance vessels, similar to that produced by nitroglycerin. In addition, mannitol produced an effect on the coronary circulation at a microvascular level which, per se or in combination with its effect on larger collateral conductance vessels, increased collateral blood flow to ischemic regions.

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This study examines the neurogenic effect of alpha 2-adrenoceptor stimulation on skeletal muscle vascular resistance and its relation to the level of background sympathetic activity. The isolated, separately perfused, neurally intact canine gracilis muscle preparation was used since it permits deliberate and quantifiable alterations in background sympathetic activity, as measured by skeletal muscle vascular resistance. Systemic intravenous UK-14304, a highly selective alpha 2-adrenoceptor agonist, produced a precipitous, neurogenic vasodilation that lowered vascular resistance below the subsequently denervated resistance, thus indicating that an active vasodilation was involved. The overall magnitude of the vasodilation was much greater in animals that had been hemorrhaged to elevate background sympathetic activity than in animals that had been transfused to lower background activity. The neurogenic vasodilation was unaffected by baroreceptor and cardiopulmonary receptor denervation and by prior cholinergic-receptor blockade of the gracilis muscle. Prior H1- and H2-histaminergic-receptor blockade, on the other hand, eliminated the active vasodilation but not a vasodilation down to the subsequently denervated resistance. Prior alpha 1-adrenoceptor blockade lowered resistance down to the subsequently denervated resistance and greatly attenuated the active vasodilation. The present study demonstrates that withdrawal of sympathetic activity by alpha 2-adrenoceptor stimulation produces an active vasodilation resulting from histamine release in skeletal muscle as well as a passive vasodilation resulting from lysis of peripheral vasoconstrictor tone.

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The role of alpha 2-adrenergic receptor stimulation in the regulation of systemic vascular capacity and venous return, a major determinant of cardiac output, is not well understood. With the influence of the central nervous system isolated from the systemic circulation, the direct peripheral vascular effects of two specific, chemically distinct alpha 2-adrenergic receptor agonists, UK 14,304 and B-HT 920, were investigated in 19 dogs on total cardiopulmonary bypass with constant arterial perfusion and central venous pressure. Five-minute intra-arterial infusions of UK 14,304 (200 micrograms/min) resulted in increased arterial resistance (mean arterial pressure increased 18 +/- 4 [SEM] mm Hg; p less than 0.01) and a decrease in systemic vascular capacity (81 +/- 20 ml; p less than 0.01). This decrease in systemic vascular capacity appears to result from vasoconstriction, since there was no decrease in transhepatic resistance to portal flow and no significant change in hepatic vein flow to suggest redistribution of arterial blood flow. Yohimbine abolished both the arterial and systemic capacity effects, whereas prazosin did not. Intra-arterial administration of B-HT 920 (200 theta grams/min) in five dogs produced similar changes in arterial resistance and systemic capacity. These findings provide direct evidence for beta 2-adrenergic control, not only of arterial resistance but also of systemic vascular capacity, which in the intact animal would increase venous return to the heart.

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Recent work has documented both centrally mediated vasoconstriction and, paradoxically, a withdrawal of sympathetic activity in response to cardiac glycosides. In the present study the possibility that these different neurogenic responses might be dose related was investigated by infusing ouabain (5, 10, and 20 micrograms) for 5 min into the right common carotid artery of 51 anesthetized mongrel dogs. Effects on vascular resistance in the isolated, separately perfused but innervated gracilis muscle were measured. A 5-microgram infusion of ouabain (n = 6) produced a prolonged decrease in gracilis vascular resistance (GVR) of 19.4 +/- 5.4% (SE) from 43.4 +/- 6.7 (SE) to 33.7 +/- 4.2 mmHg.ml-1.100 g muscle.min (resistance units, RU). This vasodilatory response was not present in nine additional dogs following denervation of the carotid bifurcation. A 10-microgram infusion had no significant effect on GVR (n = 5), but the 20-microgram infusion of ouabain (n = 8) caused a rapid increase in GVR from 42.1 +/- 5.0 to 47.6 +/- 5.7 RU, an increase of 14.4 +/- 5.6%, which was not influenced by denervation of the carotid bifurcation (n = 8). This vasoconstriction was transient returning toward the control levels by 20 min following the infusion. These data indicate important dose-related differences in vascular responses to ouabain that are directionally opposite and mediated by separate neurogenic mechanisms. At high doses a centrally mediated vasoconstriction dominates, whereas at low doses carotid bifurcation mediated vascular dilatation occurs.

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Since the gradient between aortic pressure and left ventricular diastolic pressure is a major determinant of coronary blood flow, a change in left ventricular relaxation by its effect on early diastole could diminish early diastolic coronary flow. Two interventions that resulted in impaired left ventricular relaxation, hypothermia, and reperfusion following a left anterior descending coronary artery occlusion were studied to evaluate whether there were associated changes in coronary blood flow. With both interventions, there was a significant prolongation of left ventricular relaxation (p less than 0.01) accompanied by a significant decrease in early diastolic coronary blood flow (p less than 0.01). Verapamil did not have a significant effect on these hemodynamic changes during hypothermia. However, verapamil significantly blunted the effects of reperfusion following ischemia on ventricular relaxation (p less than 0.002) and early diastolic coronary blood flow (p less than 0.01). Thus, impaired left ventricular relaxation has an adverse impact on early diastolic coronary blood flow, which, under the condition of reperfusion following regional myocardial ischemia, can be alleviated with calcium channel blockade.

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The present study examines both the local and neurally mediated effects of sufentanil, a new synthetic opioid, on the vascular resistance of the isolated, separately perfused canine gracilis muscle. Infusions (50 micrograms/min) of sufentanil into the gracilis arteries of nine denervated gracilis muscles did not produce a direct vascular effect. Because morphine has been previously shown to produce a central sympatholytic effect, the neural effect of sufentanil was examined in 12 innervated muscles under conditions of either low or high background sympathetic activity produced by either hemorrhage or transfusion of the dog. After i.v. sufentanil (20 micrograms/kg), all dogs experienced a rapid parallel fall in gracilis vascular resistance (GVR) and mean arterial pressure. The GVR decreased under conditions of high and low sympathetic activity. With low sympathetic tone, the GVR decreased from a control value of 24.1 +/- 4.4 S.E.M. to 6.6 +/- 0.8 resistance units (RU), a value below the subsequently denervated level (13.2 +/- 2.5 RU) (P less than .05). In hemorrhaged animals with elevated control sympathetic tone, resistance declined from 38.4 +/- 9.1 to 26.1 +/- 4.4 RU (P less than .05) but did not reach the denervated level (12.4 +/- 2.7 RU). Local intra-arterial pharmacologic blockade of the gracilis muscle was performed in animals with low sympathetic tone. Intra-arterial atropine did not effect the neurogenic vasodilatory response to sufentanil, whereas prazosin abolished it. Intra-arterial H1 and H2 receptor blockade prevented the decline of GVR secondary to sufentanil below the denervated level. Thus, vasodilation associated with sufentanil administration is mediated solely through neurogenic mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

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Low flow myocardial ischemia in the distribution of the left anterior descending coronary artery was established in 32 anesthetized dogs. The early development of irreversible myocardial injury was identified using 125I-antimyosin (Fab')2--a specific immunological marker of myocardial necrosis. The simultaneous injection of 131I-nonspecific (Fab')2 controlled for variables unrelated to specific antimyosin activity. It was also possible to calculate the relative uptake of 125I-antimyosin (Fab')2 in the ischemic area. In order to prevent recirculation of the (Fab')2, and to limit the time of exposure to the myocardium, the fragments were injected directly into the coronary circulation during diversion of the coronary sinus effluent. The antibody fragments were given either two, three or five hours after the onset of low flow in different groups of dogs and the animals were sacrificed 60 minutes later. Selective accumulation of 125I-antimyosin (Fab')2 in the ischemic area occurred between two and three hours after the onset of low flow ischemia indicating that necrosis was already established at this time. Macroautoradiographs of cross sections of the left ventricle and autoradiographs of microscopic sections of the ischemic myocardium independently confirmed selective accumulation of 125I-antimyosin (Fab')2 and hence necrosis, at three hours after the onset of low flow. In this study the use of 125I-antimyosin (Fab')2, in contrast to the use of histology, as a marker of necrosis avoided error due to sampling and also permitted the detection of cell death early during the ischemic process. The demonstration, within a narrow time frame, of early necrosis in this low flow preparation provides a potential model with which to evaluate agents for myocardial preservation in obstructive coronary disease.

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To study the effects of alveolar hypoxia on canine bronchopulmonary shunt flow, a biventricular bypass preparation was employed. The preparation allowed a constant and sensitive measure of changes in pulmonary venous blood flow. In 16 of 18 dogs with intact bronchial arteries, alveolar hypoxia caused an increase in pulmonary venous return both under conditions of constant pulmonary arterial inflow and under conditions of no pulmonary arterial inflow, suggesting bronchopulmonary shunting. This effect was accompanied by systemic vasodilation despite vagotomy and ganglionic blockade, and was abolished by division of all bronchial vessels. Ibuprofen, 3 mg/kg, and indomethacin, 15 mg/kg, in dogs with intact bronchial vessels, abolished both the increase in pulmonary venous return and the systemic vasodilatation caused by hypoxia. Thus, alveolar hypoxia directly augments bronchopulmonary flow, most likely through release of one or more vasodilating prostaglandins.

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Hypoxia has been demonstrated to cause impairment of myocardial relaxation. This impairment of relaxation is particularly pronounced during early reoxygenation. This study was undertaken in 24 isometric cat papillary muscles at 38 degrees C to determine if nifedipine can influence the impairment of relaxation produced during reoxygenation following hypoxia. A dose of nifedipine was chosen that produced only a minimal depression of peak systolic tension and no change in the half time to relaxation (RT 1/2) under well-oxygenated conditions. Thirty minutes of hypoxia were produced in 12 muscles, and systolic tension decreased by the same amount in muscles treated or not treated with nifedipine. During early hypoxia in the absence of nifedipine, RT1/2 was significantly prolonged (P less than 0.01) from 104 +/- 7 to 126 +/- 9 ms. After pretreatment with nifedipine, the change in RT1/2 with hypoxia was not significant. More striking was the near abolition of the marked impairment of relaxation seen during early reoxygenation (238 +/- 33 ms without nifedipine and 128 +/- 8 ms with nifedipine, P less than 0.01). These data establish that, although nifedipine only minimally attenuates the relaxation impairment early during hypoxia, this agent can substantially reduce the impairment of relaxation produced by early reoxygenation.

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