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Biomedical subjects

C E Jones

Publications and source records attributed to C E Jones.

At least 109 records · Page 6Linked to original sources
PubMed1987

Experimental varicocele does not affect the blood-testis barrier, epididymal electrolyte concentrations, or testicular blood gas concentrations.

It has been previously shown that 30-day experimental left varicocele (ELV) in adult rats produces a bilateral increase in testicular blood flow and temperature, as well as a concomitant decrease in epididymal sperm count and motility. In the present study, adult male rats with induced ELV were subjected to a variety of studies to determine the mechanism by which unilateral ELV causes a bilateral testicular response. The results demonstrate that ELV does not alter the blood-testis barrier (BTB) to 3H-inulin (MW 5000), it being largely excluded from entry into the tubule lumen in both control and ELV animals. Neither left nor right cauda epididymidal temperature was altered by ELV. Intraepididymal Na+ and K+ concentrations in the left caput epididymidis were 81.3 +/- 3.8 mEq/l and 26.3 +/- 1.5 mEq/l, respectively. From the cauda epididymidis, these values were 25.0 +/- 2.2 mEq/l and 46.8 +/- 1.0 mEq/l, respectively. These values were similar on the right side and in the left and right epididymis of ELV animals. Left testis arterial pH was 7.3 +/- 0.1, and PO2 and PCO2 were 116.0 +/- 6.4 mm of mercury and 44.3 +/- 3.2 mm of mercury, respectively. Left testicular venous values were 7.3 +/- 0.1 (pH), and 52.6 +/- 2.2 mm of mercury and 49.9 +/- 2.0 mm of mercury. These values were similar for right control testicles and left and right testicles of ELV animals. These results indicate that the mechanism by which unilateral ELV produces a bilateral change in testicular or epididymal function is not by altering the BTB, epididymal temperature or electrolyte concentrations, or testicular blood gas concentrations.

Animals↗
PubMed1987

Response to brief coronary stenosis in conscious dogs after ventricular sympathectomy.

Left ventricular responses to 2-min circumflex occlusion were studied in conscious dogs. In nonsympathectomized controls at 2, 4, and 8 wk after surgery for cardiac instrumentation, segmental shortening in the posterior ventricle significantly decreased by 111, 87, and 81% of the preocclusion values, respectively (P less than 0.05). The decrease in shortening was associated with increases in end-diastolic pressure of 9, 9, and 8 mmHg (P less than 0.05), decreases in the maximal rate of pressure generation of 305, 272, and 340 mmHg/s (P less than 0.05), and increases in heart rate of 28, 21, and 20 beats/min, respectively (P less than 0.05). After 2 and 4 wk of ventricular sympathectomy, posterior segmental shortening declined by 38 and 31%, respectively (P less than 0.05), but these decreases were less than in controls (P less than 0.05). Shortening did not change during occlusion after 8 wk of sympathectomy. Diastolic pressure increased by 6 mmHg (P less than 0.05), and the rate of pressure generation decreased by 232 mmHg/s (P less than 0.05) in the 2-wk sympathectomized ventricle. These variables did not change significantly after 4 and 8 wk of sympathectomy. After 2, 4, and 8 wk of sympathectomy, the increases in heart rate during circumflex occlusion were not different from controls (P greater than 0.05). Thus chronic sympathectomy preserved ventricular function during occlusion. This effect was attributable to a reduced preocclusion mechanical performance with a reduction in blood flow requirement and to an increased collateral perfusion, as indicated by a higher peripheral coronary pressure during occlusion in sympathectomized ventricles.

Animals↗
PubMed1987

Effects of alpha-adrenergic blockade on coronary autoregulation in dogs.

In alpha-chloralose-anesthetized, open-chest dogs, left coronary blood flow and oxygen extraction were measured at perfusion pressures from 25 to 175 mmHg. Pressure-flow relationships were obtained before and after alpha-blockade with prazosin or alpha 2-blockade with yohimbine in the presence of beta-blockade with propranolol. The efficiency of flow autoregulation with increments in pressure was calculated as the closed-loop gain and as the slope of flow to pressure. In all animals the highest gain and the lowest slope were seen when pressure increased from 75 to 125 mmHg. In the prazosin group before alpha-blockade the gain with this pressure increase was 0.76 +/- 0.05, whereas in the yohimbine group before alpha-blockade this gain was 0.75 +/- 0.03. Prazosin reduced the gain within the pressure range of 75-125 mmHg by 41%, and this reduction was statistically significant (P less than 0.05). Prazosin also significantly increased the flow to pressure slope within this range. In addition, at all pressures greater than or equal to 50 mmHg, the level of coronary flow was significantly increased by prazosin. The increase in flow and the reduction in autoregulatory efficiency with prazosin were not attributable to an increase in myocardial oxygen consumption. Yohimbine had no effects on the level of coronary flow or on the autoregulatory efficiency. These data indicate that an alpha 1-adrenoceptor mediated coronary constriction modulates coronary autoregulation.

Adrenergic alpha-Antagonists↗
PubMed1987

Binding of quinine- and quinidine-dependent drug antibodies to platelets is mediated by the Fab domain of the immunoglobulin G and is not Fc dependent.

The antibody domain controlling reactions between platelet membranes and drug-dependent (dd) antibodies from patients with thrombocytopenia induced by cinchona alkaloids was studied using F(ab')2, Fab, and Fc fragments made from purified dd-IgG. By direct binding radioimmunoassay (RIA) measurements, 20,000 to 50,000 antibody molecules bound per platelet equivalent of purified platelet membranes at apparent saturation with three different antibodies. F(ab')2 and Fab fragments bound to platelet membranes drug dependently but Fc fragments did not. The ability of dd-IgG fragments to compete with intact IgG was quantitatively measured by RIA and by complement fixation. F(ab')2 and Fab competed with intact IgG at an 8:1 and greater than 50:1 molar ratio, respectively, in RIA, and at a 1.6-3:1 and 44-75:1 ratio, respectively, by complement fixation assays. Fc did not compete with IgG in either assay. We conclude that the Fab domain supports attachment of dd antibody to the platelet surface.

Autoantibodies↗
PubMed1987

Morphologic correlates of renal growth arrest in neonatal partial ureteral obstruction.

To investigate the morphologic correlates of decreased renal blood flow and growth arrest resulting from chronic partial ureteral obstruction in the neonate, guinea pigs were subjected to unilateral ureteral constriction within the first 2 days of life and were studied at 3 and 8 wk of age. Severity of histologic changes in the obstructed and intact contralateral kidney was assessed by light microscopy. Morphometric glomerular measurements were made using a computerized tracing device. Since contralateral nephrectomy or administration of angiotensin converting enzyme inhibitor (enalapril) result in increased blood flow to the obstructed kidney, morphologic changes were also examined in separate groups of animals subjected to these maneuvers, and were compared to appropriate controls. Ipsilateral chronic partial ureteral obstruction resulted in decreased glomerular volume (p less than 0.0001) and increased glomerular crowding associated with tubular dilatation and progressive glomerular sclerosis, tubular atrophy, and interstitial fibrosis. The intact contralateral kidney underwent hypertrophy with increase in glomerular volume (p less than 0.0001) and decreased glomerular density. Contralateral nephrectomy prevented the decrease in glomerular volume in the obstructed kidney and resulted in decreased glomerular density and reduced tubular atrophy at 3 wk of age. Enalapril prevented the decrease in glomerular volume at 3 wk of age, but glomerular and tubular changes progressed and were unaffected by enalapril at 8 wk. Left kidney glomerular volume was directly related to renal blood flow (r = 0.71, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Contribution of endogenous vasoactive compounds to renal vascular resistance in neonatal chronic partial ureteral obstruction.

To evaluate the relative contribution of endogenous vasoactive compounds to maintenance of increased renal vascular resistance in neonatal obstructive nephropathy, cardiac output and renal blood flow were measured using radioactive microspheres in 25 +/- 3 day-old guinea pigs subjected to unilateral partial ureteral constriction within the first two days of life. Mass and renal blood flow of the obstructed kidney were significantly lower than those of the contralateral kidney. Following a control period, thromboxane synthesis was blocked by infusion of OKY-046, after which prostaglandin synthesis was inhibited by indomethacin. In a separate group of animals, angiotensin converting enzyme inhibitor, MK-422, was infused before or after administration of OKY-046. While neither OKY-046 nor indomethacin had a consistent effect on vascular resistance, infusion of MK-422 resulted in selective reduction of renal vascular resistance of the obstructed kidney compared to resistance in the intact kidney and other vascular beds. Removal of the contralateral kidney at the time of ureteral constriction in an additional group of animals resulted in hypertrophy and vasodilation of the obstructed kidney which was not altered by thromboxane or cyclooxygenase inhibition. We conclude that in the neonatal kidney subjected to ipsilateral chronic partial ureteral obstruction, vasoconstriction is mediated at least in part by angiotensin II, but not by thromboxane. Furthermore, vasodilation of the obstructed kidney resulting from contralateral nephrectomy is not dependent on prostaglandin synthesis. Renal vascular resistance of the kidney with prolonged partial ureteral constriction in early development thus appears to be inversely related to renal growth and is not significantly mediated by endogenous prostanoids.

Angiotensin II↗
PubMed1986

Adenosine deaminase attenuates canine coronary vasodilation during systemic hypoxia.

The hypothesis that adenosine mediates the coronary vasodilatory response to hypoxia was tested by determining if intracoronary infusion of the adenosine degrading enzyme, adenosine deaminase (ADA), would attenuate this response. Efficacy of ADA was also evaluated by examining its effect on the coronary responses to exogenous adenosine and to 20-s myocardial ischemia. Experiments were conducted in 14 anesthetized, open-chest dogs ventilated 3-5 min with 3% O2-5% CO2-92% N2 to induce systemic hypoxia. Under control, pre-ADA conditions, hypoxia (arterial PO2 19 +/- 2 mmHg) caused left anterior descending (LAD) coronary blood flow to increase from 100 +/- 12 to 382 +/- 47 ml X min-1 X 100 g-1 (+282%). After infusion of ADA (5 U X kg-1 X min-1 for 8-10 min) into the LAD, equally severe hypoxia (arterial PO2 18 +/- 3 mmHg) caused a significantly smaller increase in LAD flow, 79 +/- 9 to 234 +/- 41 ml X min-1 X 100 g-1 (+195%). Oxygen consumption in the LAD perfusion field was unchanged by hypoxia before ADA but fell significantly during hypoxia after ADA. ADA also attenuated significantly the coronary vasodilatory response to exogenous adenosine and to 20-s ischemia. The results of this investigation demonstrate a significant role of adenosine in the coronary vasodilatory response to systemic hypoxia.

Adenosine↗
PubMed1986

Alpha 1-adrenergic constriction limits coronary flow and cardiac function in running dogs.

Modulation of coronary blood flow and cardiac function by alpha 1-adrenergic receptors was examined in dogs during strenuous exercise. Fifteen dogs were chronically instrumented to measure left circumflex blood flow, heart rate, regional left ventricular function (systolic shortening, and rate of shortening), and global left ventricular function (left ventricular pressure, and dP/dt). The specific postsynaptic alpha 1-receptor blocker prazosin (0.5 mg) and nonselective alpha-receptor blocker phentolamine (1.0 mg) were injected through an indwelling circumflex artery catheter to produce local adrenergic blockade of the posterior left ventricular region during exercise. Exercise significantly increased heart rate, left ventricular systolic pressure, dP/dt, segment shortening and rate of shortening, and coronary blood flow. Both prazosin and phentolamine caused similar additional increases in dP/dt by 21 +/- 4%, in rate of shortening in the posterior region by 37 +/- 6%, and in myocardial O2 consumption by 26 +/- 11%, which were associated with a 21 +/- 3% increase in coronary flow during exercise but no change in O2 extraction. Similar results were obtained when dogs were beta-blocked with either atenolol (1.0 mg ic) or propranolol (1.0 mg ic) prior to exercise. These data suggest that an alpha 1-vasoconstriction modulates O2 delivery to myocardial tissue and limits both coronary vasodilation and cardiac function during exercise.

Animals↗
PubMed1986

Cardiac and coronary effects of prazosin and phenoxybenzamine during coronary hypotension.

Left coronary perfusion pressure was reduced to 50 mm Hg in alpha-chloralose-anesthetized open chest dogs, causing significant reductions in coronary blood flow and left ventricular oxygen consumption (P less than .05). Infusion of the specific alpha-1 adrenergic antagonist prazosin (0.1 mg/min i.c.) during coronary hypotension significantly increased coronary flow and oxygen consumption within 6 to 8 min. These effects of prazosin were not attenuated by beta adrenergic blockade with propranolol. In the absence of propranolol, infusion of the nonspecific alpha adrenergic antagonist phenoxybenzamine (0.37 mg/min i.c.) increased coronary flow and oxygen consumption within 10 to 15 min, and these increases were significantly greater than with prazosin. In the presence of propranolol, phenoxybenzamine caused increases in coronary flow and oxygen consumption that were not different from those caused by prazosin. The results indicate that 1) prazosin increases coronary flow and oxygen delivery by abolition of a coronary constrictor tone mediated by postsynaptic alpha adrenoceptors; 2) the increases in coronary flow and oxygen consumption caused by phenoxybenzamine in the absence of beta adrenergic blockade were due to antagonism of pre- and postsynaptic alpha adrenoceptors; and 3) the increases in coronary flow and oxygen consumption caused by phenoxybenzamine after beta adrenergic blockade were due entirely to antagonism of coronary postsynaptic alpha-1 adrenoceptors.

Animals↗
PubMed1985

Androgens in male rat reproductive tract fluids: hypophysectomy and steroid replacement.

The control of androgen concentrations in the intraluminal fluids of the male reproductive tract is not well understood. The present experiments were performed to determine the effects of hypophysectomy, hypophysectomy plus testosterone (T), and hypophysectomy plus pregnenolone treatment on intraluminal androgen concentrations in the adult rat testis and epididymis. T and 5 alpha-dihydrotestosterone (DHT) concentrations were determined in the vascular, interstitial, and intraluminal compartments of the epididymis. Testicular and epididymal morphology also were examined under light microscopy. Hypophysectomy of at least 5 days duration significantly reduced T and DHT concentrations in serum, tissues, and intraluminal fluids of the reproductive tract. T replacement for 14 days, which produced peripheral T concentrations of 5 ng/ml, did not support intraluminal androgen concentrations in the seminiferous tubules equivalent to controls; rete testis androgen concentrations were similar to controls, however. Pregnenolone administration at 2 mg X rat-1 X day-1 for 14 days did not maintain spermatogenesis nor intraluminal T concentrations in the seminiferous tubules equivalent to controls; however, a low level of spermatogenesis continued when intraluminal and tissue androgen concentrations were maintained at 10-20% of controls by either the testosterone and pregnenolone treatments.

Androgens↗
PubMed1985

Adenosine antagonist aminophylline attenuates pacing-induced coronary functional hyperemia.

The role of adenosine in pacing-induced hyperemia was examined in 10 dogs. Left coronary blood flow (LCBF), left ventricular O2 extraction [(a-v)O2], and myocardial O2 consumption (MVO2) were monitored. Heart rate (HR) was initially paced at 120 beats/min and then increased to 180 beats/min to elicit a hyperemic response (delta LCBF). During the hyperemia, the vasodilatory response to exogenous adenosine (FAd) was tested. HR was then returned to the initial level, and 20 min after injection of aminophylline (100 mg iv) HR was again increased to 180 beats/min. The response to adenosine was again tested. The pacing-induced increase in MVO2 (delta MVO2) was not affected by aminophylline (P greater than 0.05). However, after aminophylline, the flow response slope delta LCBF/delta MVO2 was decreased by about 20% (P less than 0.05), and the extraction-response slope delta (a-v)O2/delta MVO2 was increased by 100% (P less than 0.05). FAd was also decreased by aminophylline, and the magnitude of the reduction was correlated with the decrease in the flow-response slope (r = 0.82). These results suggest that endogenous adenosine may play an important role in coronary functional hyperemia induced by increases in heart rate.

Adenosine↗
PubMed1985

Local endogenous opiate activity in dog myocardium: receptor blockade with naloxone.

The participation of endogenous opiates in myocardial performance and coronary blood flow was investigated. Heart rate, left ventricular contractile force (LVCF), left coronary blood flow (LCBF), and left ventricular oxygen extraction were monitored in anesthetized dogs before and after intracoronary opiate receptor blockade with naloxone. LVCF consistently increased in a dose-dependent fashion following intracoronary naloxone. The increasing LVCF was accompanied by significant increases in LCBF and myocardial oxygen consumption, without changes in heart rate. Rapid onset of responses suggested the presence of endogenous opiates operating locally within the myocardium. Similar effects did not follow right atrial injection of naloxone, ruling out a systemic mechanism. Furthermore, naloxone injected into the isolated left anterior descending artery selectively increased contractile force in that perfusion territory while the adjacent untreated circumflex territory showed no change. The administration of dynorphin into the coronaries produced a depression of LVCF qualitatively consistent with these effects. The effect of dynorphin was subsequently reversed with naloxone. These results support the concept that endogenous opiates participate in the regulation of myocardial function through local mechanisms at the myocardial level.

Animals↗
PubMed1985

Alpha 1-adrenergic blockade increases coronary blood flow during coronary hypoperfusion.

Coronary hypoperfusion was elicited in alpha-chloralose-anesthetized open-chest dogs by reducing left coronary perfusion pressure to 50 mmHg. Left coronary blood flow, as well as left ventricular oxygen extraction, oxygen consumption, and contractile force were measured. The reduction in perfusion pressure caused significant reductions in coronary flow, oxygen consumption, and peak reactive hyperemic flow. During hypoperfusion in 11 dogs, intracoronary infusion of the specific alpha 1-adrenergic antagonist prazosin (0.1 mg/min) increased coronary flow and oxygen consumption by 22 and 16%, respectively. Peak increases were observed after 6-8 min of prazosin infusion (0.6-0.8 mg prazosin), and both increases were statistically significant (P less than 0.05). In seven additional dogs, beta-adrenergic blockade with propranolol (1.0 mg ic) did not significantly affect the actions of prazosin. In five additional dogs, the specific alpha 2-adrenergic antagonist yohimbine (1.3 mg ic) in the presence of propranolol (1.0 mg ic) did not affect coronary flow or oxygen consumption during coronary hypoperfusion. Those results suggest that an alpha 1- but not an alpha 2-adrenergic constrictor tone was operative in the left coronary circulation under the conditions of these experiments.

Adrenergic alpha-Antagonists↗
PubMed1984

Absence of generalized immunosuppression in C57BL/6J mice implanted with Lewis T241 fibrosarcoma or Lewis lung carcinoma.

The immune status of C57BL/6J mice implanted with Lewis T241 fibrosarcoma or Lewis lung (LL) carcinoma was investigated on days 14 and 28 after implantation. Splenic lymphocyte responses were assessed in mitogen (Con A, LPS) mixed lymphocyte culture (MLC), natural killer (NK), graft-vs-host (GVH), and interleukin production assays. Except for NK-cell cytotoxicity, all other immunologic parameters were either comparable to those in medium-implanted controls or augmented. NK cytotoxicity was reduced in both tumor-bearing groups on day 28. The provision of NK potentiation therapy (beta-interferon, polyinosinic: polycytidylic acid) to T241 mice under various treatment conditions did not have any significant effect on lung metastasis or survival. The results of this study do not support the thesis that T241- or LL-bearing C57BL/6J mice are generally immunosuppressed. Indeed, when immune functions were assessed on the basis of total splenic activity, each of the measured immunologic parameters was substantially greater in animals with tumors than without. Further it seems improbable, considering the magnitude of the NK-cell defect in T241 mice on days 14 and 28 after implantation and the absence of a therapeutic response to NK-cell stimulants, that NK-cell cytotoxicity is intrinsically associated with resistance to tumor progression in this model.

Animals↗
PubMed1984

On the androgen microenvironment of maturing spermatozoa.

Adult anesthetized male rats were submitted to in vivo micropuncture of the seminiferous and epididymal tubules and reproductive tract vasculature to obtain fluids for analysis of testosterone, 5 alpha-dihydrotestosterone, and androgen-binding protein (ABP). Androgen and ABP concentrations were determined by RIA. The highest concentrations of testosterone (73.14 +/- 5.12 ng/ml) were in testicular interstitial fluid. A significant downhill concentration gradient exists between testosterone concentrations in testicular interstitial fluid and seminiferous tubule fluid (50.24 +/- 2.26 ng/ml); another significant decrease occurs between seminiferous tubule fluid and rete testis fluid (17.85 +/- 2.11 ng/ml). 5 alpha-Dihydrotestosterone concentrations were highest in intraluminal caput epididymidal fluids (58.73 +/- 6.48 ng/ml) as were ABP concentrations (33.30 +/- 2.40 mu leq/microliter). Intraluminal sperm concentrations were also determined, and from these data, fluid reabsorption by the efferent ducts and epididymal tubules were calculated. Eighty-nine percent of the fluid leaving the testis is reabsorbed between the rete testis and caput epididymidis, and 96% is reabsorbed between rete and cauda. It was calculated that large losses of androgen and ABP also occur from the lumen of the excurrent duct system. These losses may be due to metabolism, diffusion from the lumen, or uptake by cells.

Androgen-Binding Protein↗
PubMed1983

Radioimmunoassay of the immunomodulator erythro-9-(2-hydroxy-3-nonyl)-hypoxanthine in human serum and urine.

A radioimmunoassay was developed for the measurement in human serum and urine of erythro-9-(2-hydroxy-3-nonyl)-hypoxanthine. Antisera were produced in rabbits by immunization with an erythro-9-(2-hydroxy-3-nonyl)-hypoxanthine hemisuccinate-bovine serum albumin conjugate. The competitive antigen was erythro-9-(2-hydroxy-3-nonyl)-hypoxanthine labeled with carbon-14 on the purine ring. Cross-reactivities were measured against three metabolites and the naturally occurring purine bases inosine and hypoxanthine. Sensitivity of the method was 1 ng/ml in serum and 10 ng/ml in urine. Precision at clinical levels was +/- 15% in serum at 2 ng/ml and +/- 3% in urine at 200 ng/ml.

Adjuvants, Immunologic↗
PubMed1983

Radioimmunoassay for immunoglobulin G autoantibody on the surface of mouse erythrocytes.

A radioimmunoassay (RIA) for the determination of autoantibody on the surface of erythrocytes from New Zealand Black (NZB) mice is described. This method was adapted to hemagglutination plates in order to facilitate the separation of bound and unbound 125I-labeled rabbit anti-mouse immunoglobulin G with an automated cell harvester. Intra- and interday precision, over the useful quantitative range of the standard curve, was 3.9 and 12.9%, respectively. The RIA was five to ten times more sensitive than the direct antiglobulin test which, unlike the RIA, provided little quantitative information on a group of 20 experimental NZB mice. This is publication number 562 from the Department of Basic and Clinical Immunology and Microbiology, Medical University of South Carolina.

Animals↗