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Biomedical subjects

J E Faber

Publications and source records attributed to J E Faber.

68 records · Page 4Linked to original sources
PubMed1968

Modified biochemical tests for characterization of L-phase variants of bacteria.

Biochemical capabilities of bacterial and L-phase organisms of 15 bacterial strains were examined by using a variety of modified routine diagnostic biochemical tests. The results demonstrated that 13 of the tests examined were suitable for use with L-phase variants, that L-phase variants and revertant bacterial phase organisms retained diagnostically significant capabilities of the respective bacterial or L-phase organisms from which they were derived, and that the 13 biochemical tests could be usefully employed to relate a given L-phase variant to a given bacterial phase organism, to distinguish L-phase variants of different species, and to aid in the identification of nonreverting L-phase variants.

Arginine↗
PubMed1967

Experimental infection of the cotton rat Sigmodon hispidus with Rickettsia rickettsii.

Studies of experimental infection of the cotton rat, Sigmodon hispidus, with the virulent Sheila Smith (R type) and the avirulent Si 7 (U type) strains of Rickettsia rickettsii were undertaken to evaluate the role of this native wild mammal in the ecology of Rocky Mountain spotted fever. The Sheila Smith strain, which was highly lethal for guinea pigs, was nonpathogenic for cotton rats. Serial passage of the R-type strain in the cotton rat did not alter the virulence of the agent for cotton rats or guinea pigs. The U-type strain, which was originally recovered from a wild cotton rat, could not be maintained beyond the first passage in this animal host. Rickettsemia in the cotton rat occurred over a 24-hr period after inoculation of the virulent strain but was detected only 1 hr after inoculation of the avirulent strain. The short period of rickettsemia suggests that the cotton rat probably is not an important reservoir of R. rickettsii. Specific complement-fixing antibodies developed rapidly after infection with either strain, but the antibodies evoked by the R strain attained higher titers and persisted longer. Cotton rats previously infected with the Sheila Smith strain developed rickettsemia after reinfection with the same strain, even though relatively high levels of antibody were still present.

Animals↗
PubMedDate not supplied

Real-time measurement of microvascular dimensions using digital cross-correlation image processing.

A real-time automatic digital image-processing algorithm was developed for measuring microvascular dimensions. Using video microscopic images of the vasculature, the video images are digitized and analyzed using contrast enhancement, frame averaging, and pattern recognition, rather than edge detection. Performance of the algorithm was evaluated for second- and third-order vessels surrounded by the complex interfering features of in vivo skeletal muscle. Graded diameter changes and vasomotion were induced with pharmacological agents. Data obtained by auto-tracking agreed with data obtained by traditional manual methods of measurement. These findings indicate that a pattern recognition algorithm based on cross-correlation analysis provides a highly accurate method for real-time automatic tracking of microvessel diameters.

Animals↗
PubMedDate not supplied

In vitro analysis of alpha-adrenoceptor interactions with the myogenic response in resistance vessels.

The interaction of alpha 1- and alpha 2-adrenoceptor constriction of isolated rat cremaster small arteries (mean diameter +/- SEM, 114 +/- 5 microns) with the myogenic mechanism was examined with in vitro videomicroscopy. Microdissected vessels were double-cannulated with glass micropipets in a tissue bath, and intraluminal pressure was set at 65 mm Hg baseline pressure. Norepinephrine (NE) concentration-response curves were obtained alone and in the presence of prazosin or rauwolscine to establish the concentration of NE required to selectively stimulate alpha 1- or alpha 2-adrenoceptors. A bimodal response was produced by NE alone, indicating interaction with more than one receptor population. Rauwolscine and prazosin each produced dextral displacement at low (< 0.1 microM) NE concentrations. However, while prazosin exhibited competitive antagonism, rauwolscine did not antagonize NE at concentrations > or = EC50 value. Thus, both alpha 1- and alpha 2-adrenoceptors mediate constriction at low NE concentrations, but only alpha 1-receptors contributed to constriction at intermediate and high concentrations. These data are in contrast to previous findings for the same vessels studied in vivo. Diameter responses to increases and decreases in transmural pressure from baseline were examined in the relaxed (passive) state with nitroprusside present, during spontaneous intrinsic tone, and during induced alpha 1- or alpha 2-tone (EC20 concentration of NE plus rauwolscine or prazosin). Myogenic constriction during increases in lumen pressure and myogenic inhibition of tone during decreases in pressure were greatest during alpha 2-tone, less during intrinsic tone and least during alpha 1-tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Neural contribution to renal hypertension following acute renal artery stenosis in conscious rats.

To assess the hemodynamic changes during acute renal artery stenosis (RSt) and their dependence on alterations in the renin-angiotensin and sympathetic nervous systems, we studied conscious rats chronically instrumented with miniaturized pulsed-Doppler flow probes. Probes were implanted on the superior mesenteric and both renal arteries, and on the lower abdominal aorta for measurement of mesenteric (MR), renal (RR), and hindquarters (HQR) vascular resistance. Unilateral RSt, with a pneumatic cuff occluder that reduced flow by approximately 50%, increased mean arterial pressure (MAP) by 32%, reduced heart rate, and increased MR, nonstenotic (contralateral) RR and HQR. The hypertension was renin-dependent since plasma renin activity increased 6-fold and the angiotensin II (AII) antagonist, saralasin, significantly reduced MAP and regional resistances. The acute hypertension was also associated with increased neurogenic vasoconstrictor tone since hexamethonium markedly reduced MAP, MR, HQR and non-stenotic RR. Hexamethonium similarly decreased MAP during hypertension induced by AII infusion, whereas hypertension produced by the "pure" peripheral vasoconstrictor, phenylephrine, was unaffected by ganglionic blockade. In animals with peripheral sympathectomy produced by 6-hydroxydopamine, acute RSt produced hemodynamic changes similar in magnitude to intact animals; however, PRA increased 3-fold more than in intact rats. We conclude that hypertension induced by acute RSt in conscious rats is not only renin-dependent, but is also associated with inappropriately high neurogenic vasoconstrictor tone, presumably activated by indirect neural actions of AII.

Angiotensin II↗
PubMedDate not supplied

Regional hemodynamic effects of antihypertensive renomedullary lipids in conscious rats.

Renomedullary tissue has been proposed to exert an antihypertensive endocrine-like action. The antihypertensive polar renomedullary lipids (APRL) and neutral renomedullary lipids (ANRL) are potential mediators of this action. We evaluated the blood pressure and regional hemodynamic responses to APRL administered peripherally (i.v.) and to the central nervous system (CNS) in normal rats and rats with sinoaortic deafferentation (SAD) to remove baroreflex buffering. Rats were chronically instrumented with Doppler flow probes for measurement of mesenteric, renal, and hind-quarter vascular resistance, with arterial pressure and intravenous catheters, and with lateral cerebroventricular cannuli for intracerebroventricular (i.c.v.) administration. Intravenous APRL (0.01 to 1.0 micrograms) produced a dose-dependent decrease in blood pressure, tachycardia, and dilation of all vascular beds studied. The dose-response relationships were shifted to the left in SAD animals. APRL administered i.c.v. had no effect on intact or SAD rats. Pressor and regional vasoconstrictor responses to norepinephrine, angiotensin, and vasopressin were markedly reduced in SAD animals during constant infusion of APRL. In a second group of conscious SAD animals instrumented for blood pressure and heart rate measurements, intravenous ANRL (500 micrograms) decreased both arterial pressure (-45 +/- 16 mm Hg) and heart rate (-50 +/- 16 bpm). When given i.c.v., however, ANRL (10-100 micrograms) had no significant effect on resting blood pressure or heart rate. These studies suggest that APRL and ANRL produce no significant cardiovascular effects that are mediated through the CNS. However, both lipids are potent depressor agents, and APRL exhibits a strong peripheral vasodilator action and nonspecifically reduces reactivity to vasoconstrictor agents.

Animals↗
PubMedDate not supplied

Selective antagonism of humoral versus neural vasoconstrictor responses by nisoldipine.

The effects of nisoldipine administration on vascular reactivity to humoral and neural vasoconstrictor stimuli were examined in the intact rat. For these experiments, rats were instrumented with miniaturized pulsed Doppler flow probes to allow continuous measurement of renal, mesenteric, and hindquarters blood flow. In conscious and anesthetized rats, intravenous doses of angiotensin II (75 and 150 ng/kg), norepinephrine (0.6 and 1.2 microgram/kg), and epinephrine (0.6 and 1.2 microgram/kg) caused dose-dependent increases in arterial pressure and renal and mesenteric vascular resistance. Nisoldipine (0.7 microgram/min) administration significantly attenuated (p less than 0.05) the pressor and regional vasoconstrictor actions of all three circulating pressor agents; however, nisoldipine infusion had little effect on neurally mediated regional vasoconstrictor responses elicited by electrical stimulation of the posterior hypothalamus or greater splanchnic nerve. These data indicate that nisoldipine depressed vascular responsiveness to humoral vasoconstrictor agents, while neural vasoconstrictor responses were unaffected. Thus nisoldipine appears to exert preferential antagonistic effects on humoral rather than on neural vasoconstrictor stimuli.

Angiotensin II↗