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L J Huffman

Publications and source records attributed to L J Huffman.

At least 37 records · Page 2Linked to original sources
PubMed1991

Peripheral vascular resistance and regional blood flows in hypertensive Dahl rats.

The aim of this study was to determine whether different organs undergo similar increases in vascular resistance with hypertension in the Dahl salt-sensitive rat. Cardiac output and organ blood flows were measured with microspheres in anesthetized salt-sensitive and salt-resistant rats fed a high- (7%) or normal- (0.45%) salt diet for 4 wk. High salt intake produced hypertension only in salt-sensitive rats. Cardiac index for the hypertensive group was not different from that for any other group, whereas peripheral resistance index was elevated in proportion to arterial pressure. There were no differences among groups in the fraction of cardiac output supplying the myocardium, intestine, diaphragm, spinotrapezius muscle, or gracilis muscle. The fraction of cardiac output supplying the kidneys was lower in salt-sensitive rats (13%) than in salt-resistant rats (17%) and, among salt-sensitive rats, lowest in the high-salt group. Therefore all the organs studied contribute to increased total peripheral resistance in the hypertensive Dahl rat, with the renal vasculature undergoing the largest resistance increase. Different muscles undergo similar increases in vascular resistance, despite differences in the microvascular abnormalities accompanying salt-induced hypertension.

Animals↗
PubMed1991

Muscarinic modulation of the vasodilatory effects of vasoactive intestinal peptide at the rat thyroid gland.

In the thyroid gland, vasoactive intestinal peptide (VIP) and acetylcholine (ACh) are found in nerve fibers associated with secretory cells and blood vessels. We have, therefore, initiated studies to explore the actions of and interactions between cholinergic agents and VIP in the regulation of thyroid vascular conductance (VC). Thyroid and other organ blood flows were measured using radiolabelled (141Ce) microspheres injected directly into the left cardiac ventricle of anesthetized male rats. The mean systemic arterial pressure was monitored and used in the calculation of organ VC (blood flow/arterial pressure). Plasma TSH, T3, and T4 levels before and after infusions were measured by RIA. The acute administration of ACh (3 x 10(-8) mol/100 g BW) over 4 min increased thyroid VC, whereas nicotine (10(-7) mol/100 g BW) had no such effect. Circulating TSH and thyroid-hormone levels following ACh or nicotine were not different from those in vehicle-treated animals at 20 min or 2 h after infusion. This observation suggested that ACh acts through muscarinic receptors at the thyroid gland to increase VC. In order to extend these observations and to evaluate whether VIP might exert any of its thyroidal effects on VC via muscarinic receptors, we assessed the effects of ACh, methacholine chloride (MCC), and VIP in the presence and absence of the muscarinic receptor blocker atropine. Rats were treated intravenously with saline or atropine (3 mg/kg) 20 min before intravenous infusions of vehicle, ACh (3 x 10(-8) mol/100 g BW), MCC (5 x 10(-9) mol/100 g BW), or VIP (10(-11) mol/100 g BW).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Thyroid vascular conductance: differential effects of elevated plasma thyrotropin (TSH) induced by treatment with thioamides or TSH-releasing hormone.

We have reported previously that thyroid gland blood flow, expressed as vascular conductance (C) per mass, is decreased at very low and increased at very high chronic plasma TSH concentrations, but is apparently unchanged over a broad range of plasma TSH concentrations encompassing normal levels. The aim of the present study was to examine the apparently very steep dose-response relationship between elevated plasma TSH and thyroid vascular C/mass. In the first series of experiments, endogenous plasma TSH concentrations were manipulated by treating male Sprague-Dawley rats (250-280 g) for 6 days as follows: 1) controls (0.5 ml saline/day, ip), 2) propylthiouracil injections (2.0 mg PTU/day, ip), 3) PTU plus partial thyroid hormone replacement (2.0 mg PTU/day and 0.3-0.9 microgram T4 plus 0.075-0.225 microgram T3/100 g.day via continuous sc infusion), or 4) TRH (9-1200 micrograms TRH/100 g.day via continuous iv infusion). The vascular C values of the thyroid gland, salivary gland, kidney, and pancreas were determined using the reference sample version of the radioactive microsphere technique. PTU treatment led to the expected hypothyroidism, increased plasma TSH concentrations (959 +/- 66 vs. 154 +/- 22 ng/dl), increased thyroid weight (9.19 +/- 0.36 vs. 4.60 +/- 0.15 mg/100 g), and increased thyroid vascular C/mass (495 +/- 51 vs. 127 +/- 20 microliters/mm Hg.g/min). PTU-treated rats receiving partial thyroid hormone replacement demonstrated a dose-related suppression of plasma TSH, thyroid weight, and thyroid vascular C. Although, TRH treatments resulted in increased plasma TSH concentrations (e.g. 1200 micrograms TRH, 706 +/- 46 ng/dl) and thyroid weight (e.g. 1200 micrograms TRH, 7.45 +/- 0.41 mg/100 g), thyroid vascular C per tissue mass was not significantly increased after any TRH treatment (e.g. 1200 micrograms TRH, 166 +/- 19 microliters/mm Hg.g/min). Thus, at similarly elevated plasma TSH concentrations, the thyroid vascular C/mass of PTU- and TRH-treated rats constituted separate populations. Both PTU- and TRH-induced thyroid growth were accompanied by similar alterations in thyroid gland morphology (i.e. increased cellular mass with little change in the total amount of colloid). To investigate the mechanisms involved, groups of rats were treated for 6 days as follows: 1) control, 2) PTU or methimazole (25 mg MMI/day, ip), 3) PTU or MMI plus thyroid hormone replacement (1.2 micrograms T4 plus 0.3 microgram T3/d.100 g), 4) TRH (12 micrograms/100 g.day), and 5) PTU or MMI, thyroid hormones, and TRH.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Increases in thyroid gland blood flow after hemithyroidectomy in the rat.

After subtotal thyroidectomy, the thyroid gland remnant undergoes compensatory alterations in function and morphology. Under the trophic stimulation of elevated plasma TSH concentrations, the thyroid remnant responds with an increase in hormone synthesis and secretion and, in addition, increases in mass. We have examined the alterations in thyroid blood flow which accompany increased secretion and growth after hemithyroidectomy (HTX) in male Sprague-Dawley rats (200-220 g). At various times after surgical HTX (1, 2, and 3 weeks), blood samples for the determination of plasma hormone concentrations were obtained and tissue blood flows were determined using 15 +/- 5 microns diameter 141Ce-labeled microspheres in a modification of the reference sample microsphere technique. The microspheres were injected directly into the left cardiac ventricle via a 23-gauge needle passed through the chest wall while a reference blood sample was collected. After the animals were killed, tissues were cleaned and weighed, then tissue and reference blood sample radioactivities were determined. In addition, thyroidal immunoreactive vasoactive intestinal peptide was measured after acetic acid (0.67 N) extraction. After HTX, plasma TSH concentrations were significantly elevated. The plasma concentrations of T4 and T3 fell, but by less than the expected 50%. The mass of the remaining thyroid lobe increased progressively over the 3 weeks post thyroidectomy, reaching approximately 70% of the total thyroid gland weight of sham-operated controls. Thyroid blood flow per gram of tissue was significantly elevated at all times post HTX. HTX did not induce any alterations in thyroidal immunoreactive vasoactive intestinal peptide concentration. Thus, after HTX, the well documented compensatory alterations in thyroid remnant growth and secretion were accompanied by a prompt and striking increase in thyroid blood flow.

Animals↗
PubMed1989

Alterations in thyroid blood flow induced by varying levels of iodine intake in the rat.

Thyroid hormone biosynthesis depends upon the presence of adequate amounts of thyroidal iodine, and during fluctuations in dietary iodine intake, relatively constant thyroid hormone levels are maintained by various homeostatic mechanisms. These mechanisms include an enhancement of iodide pump efficiency and organification when iodine intake is limited, and significant decreases in iodide uptake and hormone synthesis when excess iodine intake occurs. The present study was designed to determine whether acclimation to different dietary iodine regimens is associated with changes in thyroid blood flow and to assess the time course of any such alterations in relation to pituitary-thyroid axis hormone levels. Male Sprague-Dawley rats were fed a diet containing low (LID), high (HID), or normal (CTR) iodine concentrations. Three, 7, 14, or 133 days after starting these dietary regimens, the animals were anesthetized with ketamine/pentobarbital, and thyroid blood flows were assessed using the reference sample version of the microsphere technique. At the same times and at weekly intervals throughout the 133 days of treatment, blood samples for the determination of TSH, T4, and T3 levels were obtained. Additionally, thyroidal immunoreactive vasoactive intestinal peptide (VIP) was measured at the end of the experiments. LID treatment increased thyroid blood flows to 240%, 350%, and 240% of levels in control rats at 7, 14, and 133 days of treatment, respectively. Thyroid weight was also elevated above levels in control animals at each of these times. A slight decrease in plasma T4 levels occurred over the 133 days of LID treatment; however, this dietary regimen did not alter circulating levels of T3 or TSH or thyroidal VIP concentration. HID treatment had opposite effects, in general, to those of LID. Thyroid blood flows were decreased by 34%, 56%, 46%, and 35% after 3, 7, 14, and 133 days of treatment with HID, respectively. Circulating levels of T4 were increased over the 133 days of HID treatment, whereas plasma levels of T3 and TSH and thyroid weights remained unchanged from those in control rats over this period of study. A small decrease in thyroidal VIP concentrations coincident with the decrease in thyroid blood flow was observed at the beginning of the HID treatment. Neither LID nor HID had any effect on blood pressure, cardiac output, or blood flow in other organs. These data demonstrate that acclimation to changes in dietary iodine intake in the rat include alterations in thyroid blood flow which are reciprocal to the iodine intake level and appear to be independent of circulating TSH levels.

Animals↗
PubMed1988

VIP and its homologues increase vascular conductance in certain endocrine and exocrine glands.

The effects of vasoactive intestinal peptide (VIP) and related structural homologues on tissue vascular conductances were investigated in anesthetized male rats. VIP, peptide histidine isoleucine (PHI), secretin, growth hormone-releasing factor (GHRF), gastric inhibitory peptide (GIP), or saline was infused intravenously over 4 min. Tissue blood flows were measured during this time by use of 141Ce-labeled microspheres. Regional blood flows were normalized for any change in mean arterial blood pressure during infusions, and results were expressed in terms of tissue vascular conductance (C). Circulating thyrotropin (TSH), triiodothyronine (T3), and thyroxine (T4) levels were determined before and at 20 min and 2 h after treatment. Marked increases in thyroid, pancreatic, and salivary gland vascular Cs occurred during peptide infusions with the order of potency (VIP greater than PHI greater than secretin greater than GHRF greater than GIP) correlating with the degree of structural homology to VIP. PHI and secretin produced maximal increases in vascular Cs, which were the same as those obtained with VIP. Circulating TSH, T3, and T4 levels were not different from values in saline-infused rats after peptide treatments that caused striking increases in thyroid vascular C. In the adrenal, kidney, and testis, VIP and its homologues had little to no effect on vascular Cs. We subsequently measured regional vascular Cs during VIP infusions in the presence or absence of secretin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1988

Effects of vasoactive intestinal peptide on vascular conductance are unaffected by anesthesia.

In rats anesthetized with ketamine and pentobarbital (KET/PB), vasoactive intestinal peptide (VIP) increases vascular conductance (VC) in the salivary gland, pancreas, and thyroid gland, whereas no changes in VC are observed in a number of other organs. Because anesthesia may alter the responsiveness of physiological systems, we compared the effects of VIP on organ VC in conscious or anesthetized rats. Chronically catheterized rats were studied in the conscious state or 30 min after induction of anesthesia with KET/PB, isoflurane, or Inactin. Blood flows were measured by the reference sample version of the radioactive microsphere (MS) technique using two MS injections (141Ce-MS/85Sr-MS). Mean arterial blood pressure was monitored and used in the calculation of VC. Organ VCs were similar under basal conditions in conscious and anesthetized rats. VIP infusion caused systemic hypotension and increased VCs in the salivary gland, pancreas, and thyroid gland, and these responses were largely unaffected by anesthesia. These results indicate that the anesthetics used do not alter basal VC or the responsiveness of the vasculature to exogenous VIP.

Anesthesia↗
PubMed1988

Vasoactive intestinal peptide treatment that increases thyroid blood flow fails to alter plasma T3 or T4 levels in the rat.

Vasoactive-intestinal-peptide (VIP)-containing nerve fibers impinge upon both follicle cells and blood vessels in the thyroid gland. We have previously shown that VIP induces a specific, dose-related increase in thyroid blood flow in the rat. However, our VIP treatments had no effect on circulating thyroid hormone levels. Since a number of reports have indicated that VIP can enhance thyroid hormone secretion, we have expanded our studies to characterize more completely the conditions under which VIP might stimulate thyroid hormone secretion in the rat. In unanesthetized, unstressed rats with chronic catheters, 33 micrograms VIP/100 g body weight failed to alter triiodothyronine (T3) or thyroxine (T4) levels and did not affect the thyroid secretory response to a submaximal dose of bovine TSH. In euthyroid and hyperthyroid rats, the release of 125I was increased after exogenous TSH, but was not altered by VIP. The only condition in which we observed a rise in circulating T3 levels in response to VIP was during a continuous 2 h infusion of a high dose (0.25 microgram/min, i.v.) of this peptide. However, plasma TSH levels tended to be elevated in these rats, suggesting an indirect effect via TSH. This suggestion is strengthened by our observation that VIP failed to alter T3 or T4 release after topical application (0.1 microgram/microliter for 3 h) in vivo or after in vitro treatment (10(-6) M for 4 h), even though these preparations were fully responsive to bovine TSH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of thyrotropin on the vascular conductance of the thyroid gland.

It is well established that TSH from the anterior pituitary is the principal stimulatory agent in the physiological regulation of the thyroid gland. Chronic elevations of plasma TSH induce hyperplasia and hypertrophy of thyroid follicular cells and enlargement of blood capillaries. At low plasma TSH levels the thyroid gland atrophies. We have examined the vascular conductance (C = blood flow/mean arterial pressure) of the thyroid gland and several other tissues over a wide range of endogenous plasma TSH concentrations and after treatment with bovine TSH (bTSH) in rats. Tissue blood flows were determined using 15 +/- 5-microns diameter 141Ce-labeled microspheres in a modification of the reference sample microsphere technique. The microspheres were injected directly into the left cardiac ventricle via a 23-gauge needle passed through the chest wall, while the reference blood sample was collected and systemic arterial blood pressure was monitored through femoral arterial catheters. After the animals were killed, tissues were cleaned and weighed, and the tissue radioactivity was determined. Blood samples for determination of plasma hormone levels were obtained from the jugular vein before the injection of microspheres. In the first series of experiments, the vascular C per mass of thyroid gland was significantly decreased 4 and 8 days after hypophysectomy. Treatment of hypophysectomized rats with bTSH (185 mU/100 g.day as a continuous iv infusion for 2 or 6 days) restored thyroid vascular C per mass of tissue to control levels. In the second series of experiments, we manipulated circulating plasma TSH levels in intact rats by 6 days of treatment with propylthiouracil (2.0 mg/day, ip), thyroid hormones (1.5 micrograms T4, 0.4 micrograms T3 or 3.0 micrograms T4, plus 0.8 micrograms T3/100 g.day, sc by continuous infusion), TRH (240 micrograms/day, iv, by continuous infusion), bTSH (800 mU/day, iv, by continuous infusion), or combinations of these treatments. The vascular C per mass of thyroid gland was significantly decreased at very low chronic plasma TSH levels and increased at very high chronic plasma TSH levels. Thyroid vascular C per mass was unchanged, however, over a broad intermediate range of plasma TSH concentrations encompassing normal values, despite alterations in the size and function of the thyroid gland. At these intermediate levels of TSH stimulation, the thyroid gland may respond by adding or subtracting functional units without changing the blood flow per unit. The amount of blood flow per functional unit may be altered only at very high or very low levels of TSH stimulation.

Adrenal Glands↗
PubMed1987

Changes in episodic luteinizing hormone secretion leading to puberty in the lamb.

In this study, we monitored episodic luteinizing hormone (LH) secretion throughout development in eight April-born ewe lambs to determine if a change in LH pulse patterns preceded first ovulation at puberty. LH pulses were measured in samples collected every 12 min for 6 h once in July, twice a month from 22 August to 2 October, and then weekly until puberty. Progesterone concentrations, measured in samples taken 3/wk, were used as an index of first ovulation, which occurred at 29.3 +/- 0.7 wk of age. LH pulse frequencies throughout most of this period ranged from 0 to 2 pulses/6 h, with no change over time. However, during the week prior to the first progesterone rise, there was a significant increase in pulse frequency to a level seen during the follicular phase in post-pubertal lambs. This increase in pulse frequency was evident in 7 of 8 lambs; pulses were not analyzed in the last lamb because samples were taken during the LH surge. In contrast, LH pulse amplitude did not increase prior to puberty. In fact, pulse amplitude declined linearly during the 3 wk before first ovulation and then increased during the follicular phase in post-pubertal animals. These results support the hypothesis that an increase in the frequency of episodic LH secretion is a key event leading to the onset of ovarian cycles in the lamb. Whether an increase in pulse amplitude is also necessary remains unclear. If so, it must occur just before the LH surge, since it was not detected in any samples taken before puberty in this study.

Animals↗
PubMed1984

Immunocytochemical studies of the peptidergic innervation of the thyroid gland in the Brattleboro rat.

An indirect immunofluorescence technique was used to study the peptidergic innervation of the thyroid gland in homozygous Brattleboro rats (DI) and normal Long-Evans rats (LE). The primary goal of this study was to determine whether the previously demonstrated decrease in thyroid responsiveness to TSH in DI might be due to an abnormality in the innervation of the thyroid. Thyroids from both types of rats were found to contain nerve fibers containing immunoreactivity for vasoactive intestinal peptide (VIP), substance P (SP), neuropeptide Y (NPY), and peptide HI (PHI). All four types of fibers were found in close association with both follicle cells and blood vessels. Well developed networks of fibers surrounding blood vessels were particularly apparent in the case of NPY. The density of fibers associated with follicle cells in DI was at least as great as that in LE in regard to SP, NPY, and PHI. Fibers containing VIP were found in greater abundance in DI than in LE. Additional studies revealed no evidence of thyroid fibers containing either somatostatin or neurophysin, which was used as a marker for vasopressin. We conclude that the reduced responsiveness of the thyroid in DI is not due to an inadequate supply of any of the neuropeptides included in this study. Since VIP is known to enhance thyroid secretion, we suggest that the apparent proliferation of VIP-containing fibers in DI may be a reflection of a neural mechanism attempting to compensate for a thyroid gland deficiency analogous to the humoral mechanism by which TSH secretion increases in response to thyroid deficiency.

Animals↗
PubMed1983

Influence of left ventricular receptor stimulation on plasma vasopressin in conscious dogs.

The current study was undertaken to determine whether receptors in the left ventricle are capable, when stimulated, of inhibiting plasma arginine vasopressin (AVP) in the conscious dog. Dogs were instrumented to measure aortic pressure and heart rate. In addition, a catheter was implanted in the left circumflex coronary artery. Left ventricular receptors were stimulated by the intracoronary infusion of veratrine, which evoked a hypotension and bradycardia. Control experiments consisted of intravenous infusion of veratrine. Plasma AVP, osmolality, and sodium and potassium concentrations were measured at intervals following the infusion. Similar experiments were done during the intravenous infusion of sodium nitroprusside (NP) to lower aortic pressure to the same extent as that seen with intracoronary infusion of veratrine. Experiments were also performed in chronic sinoaortic-denervated dogs. Intracoronary infusion of veratrine resulted in a significant decrease in aortic pressure from 93.9 +/- 2.8 to 70.5 +/- 4.5 mmHg. Control plasma AVP averaged 2.13 +/- 0.25 pg/ml and did not change significantly during this time. NP infusion lowered aortic pressure to a similar degree, and plasma AVP rose to 21.17 +/- 3.79 pg/ml after 5 min. There were no significant changes in any other plasma constituents. The results were similar in sinoaortic-denervated dogs. We conclude from the results of this study that receptors in the left ventricle are not capable of decreasing plasma AVP from low basal levels or from augmented levels.

Animals↗
PubMed1980

Communicating hydrocephalus caused by Aspergillus flavus.

A patient with a past history of sporadic parenteral drug abuse had communicating hydrocephalus associated with arachnoiditis over the lumbar spinal cord. The diagnosis of aspergillosis was made by a newly described immunofluorescent staining procedure and was later confirmed by culture. The spectrum of central nervous system aspergillosis associated with drug abuse is reviewed.

Adult↗
PubMed1979

Intravenous metronidazole therapy for Bacteroides fragilis meningitis.

A 69-year-old man developed meningitis due to Bacteroides fragilis and Streptococcus MG-intermedius, which progressed during chloramphenicol and nafcillin therapy to the extent that he seemed near death, with frank pus covering the spinal cord at surgery. Treatment with intravenous metronidazole and penicillin G was curative. After multiple trauma, a 20-year-old man developed meningitis due to Escherichia coli and B fragilis. He failed to respond to chloramphenicol alone, but responded to combined treatment with chloramphenicol and metronidazole. The right frontal sinus and epidural space abscesses were drained and a right frontal lobe abscess was excised. Metronidazole may be a uniquely effective agent for treatment of meningitis due to susceptible strains of Bacteroides fragilis.

Adult↗
PubMedDate not supplied

Renal function and pituitary hormone release during cerebral osmostimulation and TRH in dogs.

The effects of increases in serum osmolality on renal function and plasma levels of radioimmunoassayable prolactin (PRL) and luteinizing hormone (LH) were examined during intracarotid (IC) infusions of hypertonic NaCl in conscious dogs with a sustained water diuresis (SWD). A 10 minute bilateral IC infusion of 45 mumole/kg X min X artery of NaCl during SWD which raised jugular osmolality by 10.1 mOsm/kg, without significantly altering peripheral venous osmolality, produced a significant decrease in free water clearance (CH2O) at 20 to 40 minutes postinfusion. IC infusions of 0.9% NaCl did not produce an antidiuretic response. No change in heart rate or blood pressure from preinfusion control values occurred during NaCl infusions. Elevations in cerebral osmolality did not result in changes in circulating levels of LH or PRL which qualitatively differed from levels of these hormones recorded during IC infusions of 0.9% NaCl. Although fluctuations in levels of LH occurred during experiments, renal function was not concomitantly affected. The results suggest that a specificity exists in the hormonal response to selective elevations of cerebral osmolality. The administration of TRH 3.8-4.2 micrograms/kg produced a transient increase in blood pressure and inhibited a water diuresis, the latter possibly as a result of releasing antidiuretic hormone.

Animals↗
PubMedDate not supplied

Lack of effect of vasoactive intestinal peptide antagonists on blood flow in the rat thyroid.

We used three putative vasoactive intestinal peptide (VIP) antagonists: 1) [4C1-D-Phe6,Leu17]VIP, 2) [N-Ac-Tyr1,D-Phe2] GRF(1-29)-NH2, and 3) VIP(10-28) to assess the involvement of endogenous VIP in the regulation of thyroid hormone secretion and thyroid blood flow (BF). We measured thyroid BF in ketamine-pentobarbital-anesthetized rats using the microsphere technique. Increases in thyroid BF induced by VIP administration (30 pmol-1.5 nmol/100 g b.wt.) were not affected by any of the three compounds tested at doses 10-100 times higher than that of VIP. These compounds (3-15 nmol/100 g b.wt.) also failed to affect basal thyroid BF or hormone secretion. Increases in pancreatic and salivary gland BFs induced by VIP (30 pmol/100 g b.wt.) were also not affected by [4C1-D-Phe6,Leu17]VIP or [N-Ac-Tyr1,D-Phe2]GRF(1-29)-NH2 (3 nmol/100 g b.wt.). These results indicate that the three compounds tested are not effective inhibitors of VIP receptors in the thyroid vasculature and, therefore, they cannot be used in the investigation of the functional significance of endogenous VIP in the regulation of thyroid BF.

Animals↗