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Biomedical subjects

J E Faber

Publications and source records attributed to J E Faber.

At least 55 records · Page 3Linked to original sources
PubMed1988

In situ analysis of alpha-adrenoceptors on arteriolar and venular smooth muscle in rat skeletal muscle microcirculation.

The purpose of this study was to determine whether both alpha 1- and alpha 2-adrenergic receptors exist on vascular smooth muscle of microvessels and whether adrenergic constriction of anatomically distinct microvascular segments is differentially subserved by either receptor subtype. The cremaster skeletal muscle of anesthetized rats was acutely denervated and suspended in a Krebs bath containing cocaine, normetanephrine, and propranolol to block uptake1, uptake2, and beta-receptors, respectively. Intravital microscopy was used to study large distributing arterioles (mean diameter, 100 microns), small precapillary arterioles (25 microns), and capacitance venules (140 microns). Concentration-response (diameter change) curves were obtained for bath-added agonists norepinephrine (mixed alpha 1/alpha 2), phenylephrine (alpha 1), and B-HT 933 (alpha 2) in the absence or presence of antagonists prazosin (alpha 1) and yohimbine (alpha 2). Apparent pD2(-log ED50) values for large arterioles and venules were, respectively, as follows: norepinephrine (7.41 and 7.15), phenylephrine (5.95 and 5.41), and B-HT 933 (5.05 and 5.06). Low concentrations of prazosin (10(-8) M) and yohimbine (10(-7) M) produced receptor subtype-selective antagonism and parallel, dextral displacement of norepinephrine curves for large arterioles and venules. The large arteriole pKB (-log KB) was 7.83 +/- 0.65 for prazosin and 7.36 +/- 0.46 for yohimbine. Higher concentrations of prazosin (10(-7) and 3 X 10(-7) M) and yohimbine (10(-6) M) produced further dextral but nonparallel displacement of norepinephrine curves. In contrast, receptor subtype-selective concentrations of only yohimbine inhibited adrenergic constriction of small, precapillary arterioles; but prazosin had no effect at receptor subtype-selective concentrations. These data suggest that adrenergic regulation of large arterioles and venules in skeletal muscle uses both alpha 1- and alpha 2-adrenoceptors. Precapillary arterioles, however, may be subserved predominantly by alpha 2-receptors.

Adrenergic alpha-Antagonists↗
PubMed1988

Microvascular effects of atrial natriuretic factor: interaction with alpha 1- and alpha 2-adrenoceptors.

The cremaster skeletal muscle of anesthetized rats was denervated and extended with intact circulation into a tissue bath. Intravital microscopy was used to measure microvessel diameter at three different anatomical levels within the microcirculation: large distributing arterioles (x control diameter = 100 +/- 7 micron), large capacitance venules (147 +/- 8 micron), and small terminal arterioles (17 +/- 1 micron). Norepinephrine (NE) was added to the cremaster bath to produce intermediate reductions in diameter of large arterioles and venules (55% and 38% of maximum constriction, respectively). In the presence of NE tone, bath-added atrial natriuretic factor (ANF) produced concentration-dependent dilation of both arterioles and venules. Arteriolar IC25 = 18 pmol and IC50 = 1.2 X 10(-10) M; venules exhibited similar sensitivity. However, the highest ANF concentration examined (10(-7) M) only reversed NE-induced tone by 70%. In a second large vessel group ANF completely reversed constriction induced by the alpha 1-adrenoceptor agonist, phenylephrine, in the presence of 5 X 10(-7) M yohimbine. However, vessels constricted with the alpha 2-receptor agonist UK-14,304 (in the presence of 10(-8) M prazosin) were insensitive to ANF. A third group of terminal arterioles, which possess considerable spontaneous "intrinsic" tone, were studied in the absence of alpha-receptor agonists. Significant dilation occurred at greater than 10(-7) M, and the maximal response was only 25% of complete dilation with adenosine. These data indicate that ANF exhibits a high potency and selectivity for reversal of alpha 1-adrenoceptor-mediated constriction of large arterioles and venules. Constriction produced by alpha 2-adrenoceptor occupation or by nonadrenergic "intrinsic" mechanisms appears to be insensitive to ANF. We propose that the ability of ANF to reduce microvascular resistance depends on the relative contribution of alpha 1-, alpha 2-, and intrinsic vasoconstrictor components to the prevailing level of smooth muscle tone. Differences in these components among regional circulations and between arterial and venous smooth muscle may contribute to the systemic hemodynamic pattern produced by ANF.

Animals↗
PubMed1987

Renal pressor reflex: involvement of sympathetic vasoconstrictor mechanisms.

We examined whether vasopressin and/or sympathetic vasoconstrictor mechanisms constitute the efferent limb of an afferent renal nerve (ARN)-dependent renal pressor "reflex" produced by acute unilateral renal artery stenosis (RST). Rats that had received sinoaortic denervation (SAD) were implanted with right renal artery occluders and flow probes. After recovery, conscious rats received captopril. Acute RST increased arterial pressure (AP) by 25% and mesenteric and hindquarters resistances by 35 and 51%, respectively. Vasopressin receptor antagonism was without effect on the reflex. Ganglionic blockade (chlorisondamine or trimethaphan) abolished the reflex, as did alfaxalone/alfadolone or urethan-chloralose anesthesia. In an additional study, SAD animals were prepared with chronic T6 spinal cord transection. Increases in AP during RST were unaffected by spinal transection (27 +/- 4 mmHg). However, the increase in hindquarter resistance in the sham-transected animals (57 +/- 12%) was markedly attenuated (19 +/- 4%) in the spinal-transected group. The data suggest that in animals with depressed baroreflexes and renin-angiotensin system responsiveness, acute RST initiates an ARN-dependent pressor reflex with vasoconstrictor nerves comprising the efferent limb of the reflex. The reflex can be integrated at the spinal level and is highly sensitive to anesthesia.

Animals↗
PubMed1987

Role of prostaglandins and kinins in the renal pressor reflex.

In previous studies we identified an afferent renal nerve-dependent pressor reflex elicited by acute unilateral renal artery stenosis (50% decrease in renal blood flow) in conscious, instrumented rats with reduced responsiveness of arterial baroreceptor reflexes and the renin-angiotensin system. The pressor reflex involves a neurogenic increase in peripheral resistance. The present study examined the nature of the intrarenal stimulus underlying this renal pressor reflex. Rats were subjected to sinoaortic denervation and, 7 to 10 days later, were chronically instrumented with Doppler flow probes on the right renal artery, superior mesenteric artery, and abdominal aorta and with an occluder on the right renal artery. Following surgical recovery and inhibition of the renin-angiotensin system (captopril), animals received intravenous isotonic saline, 6% of body weight over 60 minutes. Saline infusion did not alter baseline hemodynamics, vascular neurogenic tone, or responsiveness to tyramine, but it attenuated the reflex by 70%. A second series of experiments examined a possible role for intrarenal prostaglandins, kinins, or adenosine in the activation of renal sensory receptors during renal stenosis. Prostaglandin inhibition with intravenous administration of indomethacin and meclofenamate virtually abolished the reflex in the face of enhanced tyramine responsiveness, whereas kallikrein inhibition (aprotinin) attenuated the reflex pressor response by 33%. Adenosine inhibition with aminophylline or adenosine deaminase had no effect on the reflex; these agents and aprotinin did not affect vascular neuroeffector responsiveness (tyramine). The data suggest that the renal pressor reflex may be mediated by renal sensory nerves, possibly chemoreceptors, whose activation could depend on renal excretory function and synthesis of prostaglandins and kinins.

Adenosine↗
PubMed1987

Inhibitory effect of the contralateral kidney on the renal pressor reflex evoked by ipsilateral renal artery stenosis.

We previously identified a sympathoexcitatory pressor reflex that is evoked by acute (90 min) unilateral renal artery stenosis (RST). The reflex is strongly expressed in conscious rats when the renin-angiotensin system and baroreflexes are diminished by captopril and sinoaortic denervation, and is eliminated by denervation of the stenosed kidney. In the present study, dorsal rhizotomy inhibited the reflex, establishing the role of afferent renal nerves (ARN). During sustained (10 h) RST, the reflex reversed within 4 hours after onset of RST, but persisted after removal of the contralateral kidney. Hematocrit measurements did not support pressure diuresis as a mechanism for inhibition by the contralateral kidney. Other studies suggest that ARN signals and/or release of antihypertensive renomedullary lipid from the contralateral kidney are not involved in inhibition of the reflex. These data suggest that the contralateral kidney can oppose, at least acutely by an as yet undefined mechanism, an ARN-dependent pressor reflex evoked by ipsilateral renal artery stenosis.

Animals↗
PubMed1987

Use of blood in transurethral prostatectomy--routine or selective cross-matching?

In our series of 700 transurethral resections of the prostate 464 patients (66%) received no blood transfusions, while 121 patients (17%) received two or more units of blood. A significant relationship was demonstrated between the size of the prostate and the estimated blood loss, as well as between the presence of a preoperative urethral catheter and the blood loss.

Aged↗
PubMed1986

Renal innervation is not required for compensatory renal growth in the rat.

The purpose of this study was to determine whether renal innervation is required for compensatory growth of the remaining kidney following unilateral nephrectomy. In the first study, young (6-week-old) rats were divided into 4 groups and the following surgical procedures were performed. Group 1 animals had their left and right kidneys removed and weighed to provide a measure of control weight prior to compensatory growth. Group 2 and 3 animals underwent right nephrectomy, followed by left kidney denervation (Group 2) or sham denervation (Group 3). Animals from Group 4 were subjected to right sham nephrectomy and sham denervation of the left kidneys. Three weeks later, animals from Groups 2, 3 and 4 were sacrificed and left kidneys were weighed. Relative to control kidney weight (Group 1), left kidney weight increased over 3 weeks by 92% when both kidneys were present (Group 4), representing normal renal growth. Animals with prior nephrectomy but intact renal innervation (Group 3) demonstrated an additional increase in kidney weight of 74% over the same interval, representing compensatory growth. Prior denervation of the left kidney (Group 2) had no effect on the degree of compensatory growth whether expressed in absolute kidney weight or relative to body weight. A second study was performed to determine whether renal innervation influences the initial state of compensatory growth when measured at an earlier time after unilateral nephrectomy. One week after right nephrectomy, left kidney weight was similar in animals with sham left renal denervation (1.08 +/- 0.04 g) when compared to animals with left renal denervation (1.06 +/- 0.02 g). Thus, for a least young rats, renal innervation is not required for full compensatory renal growth following unilateral nephrectomy.

Animals↗
PubMed1985

Afferent renal nerve-dependent hypertension following acute renal artery stenosis in the conscious rat.

Anatomical and electrophysiological evidence indicates that the kidneys contain both mechano- and chemoreceptor nerve endings. We conducted the present study to determine whether conditions of reduced renal blood flow elicit cardiovascular alterations that are dependent on afferent renal nerves. Removal of the renin-angiotensin system with the angiotensin I-converting enzyme inhibitor, captopril, and/or reduction in baroreflex gain by sinoaortic denervation, were combined in conscious rats with acute renal artery stenosis to prevent these systems from potentially obscuring any afferent renal nerve-dependent effects. One week after sinoaortic denervation or sham sinoaortic denervation, each rat was chronically instrumented with Doppler flow probes on the lower abdominal aorta and superior mesenteric and right renal arteries, as well as with intravascular catheters, and a perivascular balloon occluder on the right renal artery. After surgical recovery, sham sinoaortic-denervated animals responded to a 60-minute period of stenosis (50% reduction in renal blood flow) with increases in arterial pressure, regional resistance, and plasma renin activity. Captopril abolished the increases in arterial pressure, hindquarters, and left renal resistance, but both bradycardia and increased mesenteric resistance persisted, indicating that baroreflex activation might be buffering a non-renin-angiotensin system pro-hypertensive mechanism. In support of this, sinoaortic-denervated animals during captopril administration responded to stenosis with substantial increases in arterial pressure (25-30 mm Hg) and regional resistance (30-50%) that were unrelated to the renin-angiotensin system, but which were abolished after denervation of the stenotic kidney. The data suggest that acute reductions in renal blood flow activate an afferent renal nerve-dependent cardiovascular response that is strongly expressed under conditions of reduced gain of the renin-angiotensin and baroreflex systems. We speculate that this reflex may assume particular importance in chronic renal hypertension when baroreflexes become impaired and activation of the renin-angiotensin system is reduced.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Central nervous system action of angiotensin during onset of renal hypertension in awake rats.

The increase in arterial pressure and vascular resistance during acute unilateral renal artery stenosis (RSt) in conscious rats is, in part, dependent on elevated neurogenic vascular tone produced by an indirect neural interaction of angiotensin II (ANG II) with the sympathetic nervous system. The present experiments examined whether this interaction occurs within the central nervous system. Conscious rats that had been chronically instrumented with miniaturized Doppler flow probes for measurement of regional vascular resistance were subjected to a 50% reduction in unilateral renal flow with an implanted pneumatic occluder. Arterial pressure increased by 35% after 60 min of RSt. In animals in which the pressor response to intracerebroventricular (icv) ANG II had been eliminated by prior surgical interruption of the "ANG II pressor pathway" in the anterior hypothalamus, the increase in blood pressure following RSt was attenuated by 44% (P less than 0.01). In a second series, a central action of ANG II during acute renal hypertension (RH) was assessed by central ANG II receptor blockade with icv saralasin. Unlike normotensive controls, acutely RH animals responded to saralasin with significant (P less than 0.01) decreases in arterial pressure (-32%) and hindquarters (-26%) and contralateral renal (-9%) resistance. These changes were accentuated (-57% decrease in pressure) in animals made areflexic by prior sinoaortic baroreceptor denervation. Thus activation of the sympathetic nervous system during the early high-renin phase of RH depends significantly on a central action of ANG II. This mechanism may account for some 40-50% of the pressure increase following acute RSt.

Afferent Pathways↗
PubMed1983

Reflex hemodynamic response to superior laryngeal nerve stimulation in the rat.

In addition to projections through the vagus, cervical sympathetic, and aortic depressor nerves, baroreceptor afferents from the arch of the aorta are thought to rise through a superior laryngeal nerve (SLN) pathway in the rat. We evaluated this possibility, first, by determining the hemodynamic response to electrical stimulation of the SLN in anesthetized rats. Miniaturized pulsed-Doppler flow probes were placed on the right common iliac, superior mesenteric and left renal arteries. Stimulation of the SLN produced frequency-dependent (1-12 Hz) reductions in arterial pressure, heart rate and regional vascular resistance, with the greatest vasodilation occurring in the hindlimb. Right lumbar nerve transection selectively abolished the hindlimb response and attenuated the depressor effect of SLN stimulation. Mesenteric and renal vasodilation were markedly reduced by ganglionic blockade as was the reduction in arterial pressure and heart rate. Vagotomy alone and in combination with propranolol abolished bradycardia to SLN stimulation but had no effect on blood pressure or regional resistance responses, indicating that the reflex reduction in vascular resistance, rather than cardiac output, was the primary determinant of the depressor response. In a second group the pressure and heart rate responses to occlusion for 30 s of the bilateral common carotids (C), subdiaphragmatic aorta (A) and both vessels simultaneously (C + A) were evaluated before and after bilateral SLN transection. Transection of the SLN significantly potentiated the pressure increase produced by C and C + A occlusion. Bradycardia responses during C and A occlusions were converted to tachycardia following SLN transection. These data show that a strong baroreflex response may be elicited by both direct electrical and physiological stimulation of baroreceptor afferents in the SLN and suggest that the SLN may constitute a significant projection pathway for baroreceptors from the region of the aortic arch.

Animals↗
PubMed1982

Microvascular response to blockade of prostaglandin synthesis in rat skeletal muscle.

The contribution of endogenous prostaglandins (PGs) to the control of arteriolar diameter in the microcirculation is incompletely defied and has only been studied in drug-anesthetized animals. To test the possibility that endogenous PGs are tonically released to exert a net dilator influence at certain levels in the microcirculation, television microscopy was used to quantitate the arteriolar responses in the rat cremaster muscle to local blockade of PG synthesis with indomethacin. Rats were decerebrated by a midcollicular transection and were allowed to recover from surgical anesthesia. The cremaster muscle with intact circulation and innervation was suspended by sutures in a temperature-controlled Krebs bath. Diameters, vasomotion frequency, and vasomotion amplitude of arterioles at several anatomic levels were measured before and after local inhibition of PG synthesis in the presence and absence of alpha-adrenergic receptor blockade. Inhibition of PG synthesis produced marked constriction (42-66% of control) at all arteriolar levels, with greater responses occurring in the smaller arterioles. PG synthesis blockade increased vasomotion frequency in arterioles that exhibited spontaneous vasomotion during control periods, and blockade induced vasomotion in vessels lacking spontaneous vasomotion. Pretreatment with phentolamine significantly attenuated the constriction and augmentation of vasomotion. These data indicate that dilator PGs participate in the moment-to-moment regulation of arteriolar tone and local blood flow in skeletal muscle. Further, their mechanism of action may involve alterations in neuronal norepinephrine release or alpha-receptor sensitivity.

Animals↗
PubMed1982

Anesthetic depression of microcirculation, central hemodynamics, and respiration in decerebrate rats.

The objectives of this study were the development of a skeletal muscle microcirculatory preparation, in which the complications of drug anesthesia were minimized, and the quantitation of the effects of urethan and chloralose anesthesia on the microcirculation. Rats were initially anesthetized with urethan and chloralose and decerebrated by a midcollicular transection. The cremaster skeletal muscle, with intact circulation and innervation, was prepared for intravital microscopy by placement in a tissue bath. Arterioles (9-70 micrometers diam) at several anatomic levels were observed during the initial period of urethan-chloralose anesthesia (period 1), after recovery from the anesthesia (period 2), and again following reanesthetization (period 3). During period 2, respiratory rate, heart rate, and mean arterial pressure were significantly greater than during periods 1 and 3. Smaller arterioles (8-50 micrometers diam) exhibited vasomotion (mean amplitude 35% of mean diameter; mean frequency 31 cycles/min) during period 2. Urethan-chloralose anesthesia during periods 1 and 3 inhibited vasomotion and increased arteriolar diameters by 16-36%. This study quantitates the depressant effects of urethan-chloralose anesthesia on the cardiovascular system and demonstrates the feasibility of using decerebration to circumvent the necessity of continuous drug anesthesia for in vivo microvascular studies.

Animals↗
PubMed1969

Effect of cultural environment on the blood group activity of microorganisms.

Blood group activity was proven to be a property of the bacterium per se which possesses it, although such activity was influenced by the cultural environment of the organism. High concentrations of peptones having blood group activity were able to transfer this activity to inactive organisms; however, the conferred activity was proportional to the concentration. As a result of the low concentrations, the blood group activity of peptones was eliminated upon incorporation in culture media, and the activity of the peptones had no effect on the blood group activity levels of microorganisms when grown in these media. Conversely, the vitamin content of culture media did affect blood group active organisms. Multiple vitamins in media decreased the activity levels by blocking the reactive sites of the active organisms on which activity detection depended. Blood group activity levels were highest in media of minimal or no vitamin content. Therefore, it can be concluded that a choice of cultural medium becomes an important factor in the quantitation of bacterial blood group activity.

Blood Group Antigens↗