Biomedical subjects

C L Huang

Publications and source records attributed to C L Huang.

At least 163 records · Page 9Linked to original sources

PubMed1992

A reconstruction of charge movement during the action potential in frog skeletal muscle.

The transfer of intramembrane charge during an action potential at 4 degrees C was reconstructed for a model representing the electrical properties of frog skeletal muscle by a cylindrical surface membrane and 16 concentric annuli ("shells") of transverse tubular membrane of equal radial thickness. The lumina of the transverse tubules were separated from extracellular fluid by a fixed series resistance. The quantity, geometrical distribution and steady-state and kinetic properties of charge movement components were described by equations incorporating earlier experimental results. Introducing such nonlinear charge into the distributed model for muscle membrane diminished the maximum amplitude of the action potential within the transverse tubules by 2 mV but increased the maximum size of the after-depolarization by 3-5 mV and also its duration. However, these changes were small in comparison to the 135-mV deflection represented by the action potential. They therefore did not justify altering the values of the electrical parameters adopted by Adrian R.H., and L.D. Peachey (1973. J. Physiol. [Lond.]. 235:103-131.) and used in the present calculations. Cable properties significantly affected the time course and extent of charge movement in each shell during action potential propagation into the tubular system. Q beta charge moved relatively rapidly in all annuli, and did so without significant latency (approximately 0.3 ms) after the surface action potential upstroke. Its peak displacement varied between 53 and 58% (the range representing the difference fiber edge/fiber axis) of the total Q beta charge. This was attained at 5.4-7.3 ms after the stimulus, depending on depth within the tubules. In contrast, q gamma moved after a 1.7-2.9 ms latency and achieved a peak displacement of up to 22-34% of available charge. Both charge movement species could be driven by repetitive (47.7 Hz) action potentials without buildup of charge transfer. Such stimulus frequencies would normally cause tetanus. Latencies in q gamma charge movement in response to an action potential were resolved into (a) propagation of tubular depolarization required to gain the "threshold" of q gamma charge (0.8-1.5 ms) and (b) dielectric loss processes. The latter took consistently around 1.5 ms throughout the tubular system. Taken with (c) the earlier reports of a minimal latency in delta [Ca2+] signals attributed to tubulo-cisternal coupling following voltage sensing (approximately 2 ms: Zhu, P.H., I. Parker, and R. Miledi., 1986. Proc. R. Soc. Lond. B. Biol. Sci. 229:39-46.). these times can be reconciled to the latency (~ 4-5 ms) reported between the onset of the surface action potential and that of delta [Ca2+] signals (Vergara, J., and M. Delay. 1986. Proc. R. Soc. Lond. B. Biol. Sci. 229:97-110.). This is consistent with a relationship between the q gamma system and excitation-contraction coupling whether as an independent event (e.g.,Adrian, R.H., and C.L.-H. Huang. 1984. J. Physiol. (Lond.). 353:419-434.) or as an end reaction following earlier (q beta) transfers of charge (e.g., Horowicz, P., and M.F. Schneider. 1981. J. Physiol. (Lond.). 314:565-593.; Melzer, W., M.F. Schneider, B.J. Simon,and G. Szucs. 1986. J. Physiol. (Lond.). 373:481-512.)

Action Potentials↗

PubMed1992

Intramembrane charge movements in frog skeletal muscle in strongly hypertonic solutions.

Intramembrane charge movements were studied in intact, voltage-clamped frog (Rana temporaria) skeletal muscle fibers in external solutions made increasingly hypertonic by addition of sucrose. The marked dependence of membrane capacitance on test potential persisted with increases in extracellular sucrose concentration between 350 and 500 mM. Charge movements continued to show distinguishable early monotonic (q beta) decays and the strongly voltage-dependent delayed (q gamma) charging phases reported on earlier occasions. In contrast, a further increase to 600 mM sucrose abolished the most steeply voltage-sensitive part of the membrane capacitance. It left a more gradual variation with potential that closely resembled the function that resulted when q gamma charge was abolished by tetracaine in the presence of 500 mM sucrose. Charging transients were now simple monotonic (q beta) decays and lacked delayed (q gamma) transients. Furthermore, tetracaine (2 mM) altered neither the kinetic nor the steady-state features of the charge left in 600 mM sucrose. However, Ca2+ current activation in the same fibers persisted through such tonicity increases under identical conditions of temperature, external solution, and holding voltage. Tonicity changes thus accomplish an independent separation of q gamma and q beta charge as defined hitherto through their tetracaine sensitivity. Their effects on q gamma charge correlate with earlier observations of osmotic conditions on delta[Ca2+] signals (1987. J. Physiol. (Lond.) 383:615-627.) and the parallel effects of other agents on excitation-contraction coupling and q gamma charge. In contrast, they suggest that Ca2+ current activation does not require q gamma charge transfer whether by itself or as part of the excitation-contraction coupling process.

Animals↗

PubMed1992

Voltage-sensitive elevation of cytosolic [Ca2+] in guinea-pig cardiac myocytes elicited by calcitonin gene-related peptide.

We have studied the effect of the 37-amino acid cardioactive peptide, calcitonin gene-related peptide (CGRP) on cytosolic [Ca2+] in guinea-pig ventricular myocytes following depolarization. Cytosolic [Ca2+] was measured in single myocytes using fura-2. The application of 20 mM K+ led to a transient rise of cytosolic [Ca2+] followed by an exponential decline. The subsequent application of 2 nM CGRP resulted in a marked increase in cytosolic [Ca2+]. In contrast, no such response was obtained without prior depolarization. The results suggest a basis for the cardiotropic effects of CGRP through an influence on cytosolic [Ca2+].

Animals↗

PubMed1992

Endothelin inhibits osteoclastic bone resorption by a direct effect on cell motility: implications for the vascular control of bone resorption.

The abundance of endothelin (ET)-producing endothelial cells in bone marrow and the proximity of these cells to bone-resorbing osteoclasts prompted us to evaluate the action of ET-1 on osteoclast function. Osteoclasts disaggregated from neonatal rat long bones were settled onto devitalized cortical bone substrate, and resorption was quantified by morphometry. The supernatant tartrate-resistant acid phosphatase activity was determined by a spectrophotometric method using paranitrophenol phosphate as substrate. Cell motility was quantified by time lapse video- and computer-assisted image processing using an empirical procedure for morphometric analysis. Cytosolic free calcium levels ([Ca2+]i) were measured in single cells by an indo 1-based microspectrofluorimetric method. Using the area of bone resorbed per slice as response, we found that ET-1 caused a significant (P = 0.011) concentration-dependent inhibition of osteoclastic bone resorption (EC50 = 2.5 nM) without inhibiting acid phosphatase secretion. Exposure of isolated osteoclasts to ET-1 also led to a marked concentration-dependent inhibition of osteoclast motility (EC50 = 7.9 nM; P = 0.013; t1/2 = 18 min) without significant effects on cell spread area. These effects of ET-1 were reversible after removing the peptide, and the cells remained viable during the experiments. In addition, ET-1 did not elevate [Ca2+]i at the concentrations tested. The results suggest that ET-1 specifically interacts with an osteoclast receptor to inhibit osteoclastic bone resorption and cell motility. As the concentration of ET-1 required for osteoclast inhibition was similar to that reported for smooth muscle contraction, it is possible that ET-1, produced locally from the bone marrow endothelial cell, might play a primary role in osteoclast regulation.

Acid Phosphatase↗

PubMed1992

Regulation of cytosolic free calcium in isolated rat osteoclasts by calcitonin.

It is now established that calcium is a second messenger mediating the action of calcitonin on the osteoclast. We have demonstrated that an increase in the concentration of intracellular free calcium ([Ca2+]i) is associated with (and possibly mediates) the functional effects of calcitonin, including an acute reduction of cell spread area (the R effect) and, in the longer term, a reduction in enzyme release. The present study addresses questions relating to mechanisms of calcitonin action on osteoclast [Ca2+]i. We have used asusuberic(1-7) eel and human calcitonin as agonists, and an indo-1-based dual-emission microspectrofluorimetric method for the measurement of [Ca2+]i in single osteoclasts. Whilst asusuberic(1-7) eel calcitonin caused a biphasic increase in [Ca2+]i, human calcitonin produced only a monophasic [Ca2+]i response of a much lower magnitude. Each biphasic response consisted of a rapid initial transient increase, occurring within seconds of exposure, followed by a sustained increase in [Ca2+]i. The magnitude of the latter response was more variable, but was consistently below the peak value of [Ca2+]i. The sustained phase of the calcitonin effect was abolished in extracellular Ca(2+)-free medium. This phase is therefore dependent on extracellular [Ca2+] ([Ca2+]e) whilst the rapid transient increase appeared to be dependent on Ca2+i redistribution. The effects of calcitonin on [Ca2+]i were concentration-dependent, with neither latency nor oscillations. Repetitive 30-s exposures to calcitonin failed to produce subsequent responses. There was a marked concentration-dependent correlation between changes in osteoclast [Ca2+]i and the magnitude of the R effect. Thus the likely components of the biphasic [Ca2-]i response are a rapid redistribution followed by the transmembrane flux of Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Two-site monoclonal antibody-based immunoradiometric assay for measuring prostate secretory protein in serum.

We developed a double-determinant immunoradiometric assay for measuring serum prostate secretory protein (PSP), using monoclonal antibodies (MAb) against two different epitopes: MAb PSP-19 was the capture antibody and MAb PSP-6 was the tracer antibody. Assay sensitivity was 0.1 microgram/L. Analytical recovery of PSP was 93.5-104.6%, whereas the intra- and interassay mean CVs were 4.2% and 6.9%, respectively. In 92 normal men, ages greater than 50 years, the mean PSP concentration was 5.7 micrograms/L, with 10 (10.9%) men having concentrations greater than 10 micrograms/L. In contrast, 20 of 49 (40.8%) patients with benign prostate hyperplasia (BPH; mean PSP concentration 9.4 micrograms/L) and 46 of 100 (46%) patients with prostate cancer (mean PSP concentration 22.2 micrograms/L) had PSP concentrations greater than 10 micrograms/L. Mean serum PSP concentrations of the BPH (P less than 0.05) and prostate cancer (P less than 0.01) groups were significantly different from those of age-matched normal men. In a small group of patients, serial PSP concentrations correlated with the clinical course during therapy. Thus, PSP may be a useful marker for evaluating patients with prostate cancer.

Antibodies, Monoclonal↗

PubMed1991

Selective antagonism of calcitonin-induced osteoclastic quiescence (Q effect) by human calcitonin gene-related peptide-(Val8Phe37).

Exposure of isolated rat osteoclasts to calcitonin (CT) leads to an abrupt cessation of cell motility (Q effect) followed by cell retraction (R effect). We have previously shown that these effects are mediated by two G proteins that appear to activate separate post-receptor pathways. The present study demonstrates that the Q but not the R effect of CT (0.006 microM) is abolished in the presence of human calcitonin gene-related peptide (CGRP)-(Val8Phe37) (0.5 microM), a fragment analogue of human CGRP. This selective antagonism suggests that the Q effect could result from an action of CT upon a site that is distinct from that producing the R effect. The former site ('amylin site') also appears to interact with related peptides, amylin and CGRP, whilst the latter site ('CT site') specifically interacts with CT.

Animals↗

PubMed1991

Single pulses of cytoplasmic calcium associated with phagocytosis of individual zymosan particles by macrophages.

We have measured cytosolic free calcium levels ([Ca++]i) in individual macrophages during the phagocytosis of single zymosan particles. We report here that the contact of a macrophage with zymosan results in a rapid transient elevation of [Ca++]i. Each [Ca++]i pulse is symmetrical lasting for up to 30 seconds. In contrast, macrophage spreading is associated with repetitive [Ca++]i spiking occurring in salvos of up to four smaller spikes, each lasting for between 8 and 18 seconds. These qualitative and kinetic differences might suggest that the role of [Ca++]i in phagocytosis is distinct from its role in spreading.

Animals↗

PubMed1991

Platelet-derived growth factor-mediated Ca2+ entry is blocked by antibodies to phosphatidylinositol 4,5-bisphosphate but does not involve heparin-sensitive inositol 1,4,5-trisphosphate receptors.

Elevation of intracellular Ca2+ by platelet-derived growth factor (PDGF) and other growth factors involves both release of Ca2+ from intracellular Ca2+ stores and Ca2+ entry from the extracellular medium. Release from intracellular stores is believed to be mediated by inositol 1,4,5-trisphosphate (IP3) and the heparin-sensitive IP3 receptor. We studied the mechanism by which entry of extracellular Ca2+ is induced by PDGF. Intracellular free Ca2+ (Ca2+i) was measured in single cultured rat vascular smooth muscle cells using fura 2 microspectrofluorometry. In nominally Ca2(+)-free medium, PDGF (recombinant BB, 10 ng/ml) raised intracellular Ca2+ transiently (less than 5 min); addition of 2 mM Ca2+ to the bathing medium after 5 min caused a second, prolonged increase in intracellular Ca2+. Repeated changes in extracellular Ca2+ from 0 to 2 mM over 90 min caused rapid, parallel changes in Ca2+i of approximately 200 nM. This change in Ca2+i in response to changes in extracellular Ca2+ was virtually undetectable in control or thrombin-treated cells. The intracellular response to changes in medium Ca2+ after PDGF was completely blocked by 10 mM CoCl2, but not by 10(-7) M nicardipine. Microinjection of monoclonal antibodies to phosphatidylinositol 4,5-bisphosphate (PIP2) (kt 10, 2 mg/ml) totally abolished both mobilization of intracellular Ca2+ stores and entry of extracellular Ca2+. Consistent with this finding, maintenance of Ca2+ entry required ongoing receptor occupancy, since displacement of PDGF from its receptor with suramin (1 mM) eradicated extracellular Ca2+ entry in less than 5 min. To determine whether extracellular Ca2+ entry involves the heparin-sensitive IP3 receptor, cells were microinjected with heparin (4 mg/ml) prior to addition of PDGF. Heparin, but not chondroitin sulfate, prevented mobilization of intracellular Ca2+ stores but did not affect extracellular Ca2+ entry. We PDGF requires ongoing receptor occupancy and involves PIP2 or PIP2 metabolism. However, the signal which mediates PDGF-induced Ca2+ entry does not require the heparin-sensitive IP3 receptor.

Animals↗

PubMed1991

Sphingosine reverses growth inhibition caused by activation of protein kinase C in vascular smooth muscle cells.

In certain cell systems, including neonatal vascular smooth muscle (VSM) cells, phorbol esters are growth inhibitory. Here we show that 1,2-dioctanoyl-sn-glycerol (DiC8), when added 2 h after alpha-thrombin, reverses by greater than 95% the induction of DNA synthesis in VSM cells by alpha-thrombin. Sphingosine, a naturally occurring lysosphingolipid inhibitor of protein kinase C, and its synthetic analogues N-acetylsphingosine and C11-sphingosine were used to investigate this phenomenon further. Neither phorbol 12-myristate 13-acetate (PMA;200 ng/ml) nor sphingosine (up to 10 microM) alone had any effect upon basal DNA synthesis in VSM cells. Like DiC8, PMA totally blocked the induction of DNA synthesis by alpha-thrombin. This inhibitory effect of PMA was reversed by sphingosine in a dose-dependent manner with complete reversal at 10 microM. Neither N-acetylsphingosine nor C11-sphingosine exhibited any effect on DNA synthesis in VSM cells. The effect of sphingosine and its analogues on the activity of protein kinase C extracted from VSM cells was measured by histone III-S phosphorylation. Protein kinase C activity was inhibited 50% by 300 microM sphingosine, but less than 15% by similar concentrations of N-acetylsphingosine and C11-sphingosine. To assess the effects of sphingosine and analogues on protein kinase C in intact cells, we examined the effect of the lipids on [3H]phorbol dibutyrate binding. Sphingosine (at greater than 5 microM), but not N-acetylsphingosine or C11-sphingosine, blocked [3H]phorbol dibutyrate binding in a dose- and time-dependent fashion. Thus the mechanism of growth inhibition by DiC8 and PMA in neonatal VSM cells appears to be through activation of protein kinase C by these compounds. Sphingosine reverses this growth inhibition through interference with the binding to protein kinase C of phorbol esters or other activators of this enzyme.

Animals↗

PubMed1991

Divalent cations mimic the inhibitory effect of extracellular ionised calcium on bone resorption by isolated rat osteoclasts: further evidence for a "calcium receptor".

Osteoclast activity is thought to be regulated by calcitonin, as well as by the level of ionised calcium generated locally as a result of bone resorption. The exposure of isolated osteoclasts to elevated ambient calcium levels has been shown to lower resorptive activity and to reduce rates of enzyme release. We have attempted to determine whether these effects are mediated by a divalent cation-sensitive "calcium receptor," as has been reported for the parathyroid chief cells. Thus, we compared the effect of alkaline earth metal cations on osteoclast function using a morphometric measure of bone resorption and a spectrophotometric method for measuring the activity of the released enzyme, acid phosphatase. The exposure of resorbing osteoclasts to between 5 and 20 mM extracellular ionised calcium ([Ca2+]e) inhibited bone resorption and enzyme release to an extent similar to that seen with 0.1 to 10 microM ionomycin. The effect of combining submaximal concentrations of [Ca2+]e (15 mM) and ionomycin (0.1 microM) resulted in additivity, suggesting that the influence of [Ca2+]e on bone resorption was mediated by elevated intracellular calcium levels ([Ca2+]i). The other cations studied (Mg2+, Ba2+) were effective and elicited similar effects, although some required higher concentrations. Thus, whilst Ca2+ and Mg2+ were effective at 10 to 15 mM levels, Ba2+ was effective only at high (20 mM) concentrations. These findings are consistent with an influence of [Ca2+]e on osteoclast activity through an action on a surface membrane "calcium receptor" that can also bind other divalent cations, rather than by passive changes of [Ca2+]i with [Ca2+]e elevation.

Acid Phosphatase↗

PubMed1991

Separation of intramembrane charging components in low-calcium solutions in frog skeletal muscle.

The inactivation of charge movement components by small (-100 to -70 mV) shifts in holding potential was examined in voltage-clamped intact amphibian muscle fibers in low [Ca2+], Mg(2+)-containing solutions. The pulse protocols used both large voltage excursions and smaller potential steps that elicited prolonged (q gamma) transients. Charge species were distinguished through the pharmacological effects of tetracaine. These procedures confirmed earlier observations in cut fibers and identified the following new properties of the q gamma charge. First, q gamma, previously defined as the tetracaine-sensitive charge, is also the component primarily responsible for the voltage-dependent inactivation induced by conditions of low extracellular [Ca2+]. Second, this inactivation separates a transient that includes a "hump" component and which has kinetics and a voltage dependence distinct from the monotonic decay that remains. Third, q gamma, previously associated with delayed charge movements, can also contribute significant charge transfer at early times. These findings suggest that the parallel inhibition of calcium signals and charge movements reported in low [Ca2+] solutions arises from influences on q gamma charge (Brum et al., 1988a, b). They also reconcile reports that implicate tetracaine-sensitive (q gamma) charge in excitation-contraction coupling with evidence that early intramembrane events are also involved in this process (Pizarro et al., 1989). Finally, they are relevant to hypotheses of possible feedback or feed-forward roles of q gamma in excitation-contraction coupling.

Animals↗

PubMed1991

An investigation into the influence of vasopressin on perfusion of the cortex and papilla of the rat kidney.

An investigation was undertaken to examine the effects of vasopressin on blood pressure and perfusion of the cortical and papillary regions of the kidney, and to determine the receptor subtype involved. Pentobarbitone-anaesthetized rats were used and laser-Doppler flowmetry applied to measure regional renal haemodynamics. Infusion of vasopressin at 10, 20 and 40 mU kg-1 min-1 caused dose-related increases in blood pressure and reductions in cortical and papillary perfusion of approximately 21, 35 and 41%, respectively at the highest dose. Administration of the V1-receptor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(o-methyl)tyrosine]-Arg8-vasopressin, at 1 microgram kg-1 plus 5 micrograms kg-1 h-1 or four times this dose had no effect on the basal levels of any variable. Vasopressin administration during the low dose of antagonist increased blood pressure and reduced papillary perfusion, the magnitudes of which were only slightly less than those obtained in the absence of the drug, whereas there was a significant attenuation of the response in cortical perfusion. During infusion of the V1 antagonist at 4 micrograms kg-1 plus 20 micrograms kg-1 h-1, vasopressin had no effect on either blood pressure or renal haemodynamics. Infusion of the V2 antagonist, [d(CH2)5, D-Phe2, Ile4, Arg8, Ala9-NH2]-vasopressin at 1 microgram kg-1 plus 5 micrograms kg-1 h-1, and twice this dose had no effect on the basal value of any variable and had no effect on the ability of vasopressin to induce an increase in blood pressure or cause reductions in renal cortical and papillary perfusions. However, the administration of the V2 antagonist at 4 micrograms kg-1 plus 20 micrograms kg-1 h-1 significantly attenuated blood pressure, cortical and papillary perfusion responses to the vasopressin. These studies have shown that vasopressin, given at doses which increased blood pressure, caused dose-related decreases in perfusion of renal cortex as well as the papilla. The data further show that these systemic and renal actions were mediated primarily by V1-receptors and that the contribution of V2-receptors at these vascular beds was very small.

Angiotensin Receptor Antagonists↗

PubMed1991

A study of the action of angiotensin II on perfusion through the cortex and papilla of the rat kidney.

The effect of angiotensin II on blood pressure and perfusion of blood through the cortex and papilla regions of the kidney was determined in pentobarbitone-anaesthetized rats which were subjected to laser-Doppler flowmetry to estimate regional renal haemodynamics. Angiotensin II was infused at 10, 45 and 150 ng (kg body weight-1 min-1) which caused dose-related increases in blood pressure of 3, 12 and 24%, respectively, and decreases in cortical perfusion of 9, 15 and 24%, respectively. Papillary perfusion did not change at any dose of angiotensin II. This pattern and magnitude of responses to angiotensin II in blood pressure, cortical and papillary perfusions was essentially unaffected (a) following blockade of cyclo-oxygenase activity with indomethacin (1.3 mg kg-1 plus 2 mg kg-1 h-1), (b) during infusion of a bradykinin antagonist, at 1.3 micrograms min-1, (c) when renal perfusion pressure was regulated at control levels and (d) following Methylene Blue administration to inhibit potential endothelial-derived relaxing factor production. By contrast, infusion of phenylephrine at 5, 10 and 20 micrograms kg-1 min-1 caused dose-related increases in blood pressure and decreases in both cortical and papillary perfusions reaching some 28, 7 and 17% respectively at the highest dose of phenylephrine used. These results showed that both cortex and papilla were sensitive to vasoconstrictor agents. They are compatible with the suggestion that angiotensin II regulates cortical but not papillary perfusion in the kidney, and that these responses do not depend on prostaglandin, bradykinin, renal perfusion pressure or endothelium-derived relaxing factor.

Angiotensin II↗

PubMed1991

Correlates of osteoclast function in the presence of perchlorate ions in the rat.

The effects of perchlorate anion (ClO4-) on osteoclast properties were investigated through a number of independent in vivo and in vitro procedures. Intravenous infusion of ClO4- significantly reduced plasma [Ca] in young (50 g) Wistar rats, in the absence of changes in plasma [Mg] or [albumin]. This effect was maximal at 20 min after administration, and at a dose of 600 mumol/rat. Scanning electron-microscope images suggested that the presence of 10 mM-perchlorate reduced both the total area of cortical bone resorbed by freshly disaggregated rat osteoclasts, and the number of osteoclastic excavations in vitro. Similar effects were observed in the presence of 5 mM [Ca2+]. The effects of Ca2+ were potentiated by otherwise ineffective (1 mM) doses of perchlorate. Indo-1 dual-emission microspectrofluorimetry indicated a transient sixfold elevation of cytosolic free [Ca2+], in isolated cultured osteoclasts, with addition of 10 mM-perchlorate. Records of time-lapse video images indicated that this was followed by a marked and sustained cell retraction, by up to 70% of control cell area. Such effects were not observed at thiocyanate concentrations (10 mM) that would have produced comparable lyotropic effects as perchlorate. However, perchlorate did not alter morphometric measures for pseudopodial motility and cell migration. Nor did it influence supernatant concentrations of tartrate-resistant (osteoclastic) acid phosphatase in cultures of resorbing osteoclasts. These findings suggest that perchlorate is a potent inhibitor of osteoclast function, and acts through an influence on intracellular [Ca2+], and in turn upon the degree of cell retraction.

Acid Phosphatase↗

PubMed1991

Serum biochemical and histological changes in caerulein-induced acute pancreatitis in rats: a correlative study.

We investigated correlations between serum biochemical changes and pathological alterations in caerulein-induced acute pancreatitis in rats. Seven consecutive doses of caerulein consisting of 50 mu g/kg, were given intraperitoneally, in 40 male Sprague-Dawley rats at hourly intervals. Serum biochemical and histological changes of the rats were studied at hours 7, 9, 12, 18, 24 and 36 after the first injection, as well as day 3 and 5 respectively. Serum amylase in the controlled rats (n = 6) was 2549 +/- 221 U/L (mean +/- SE). It was elevated to twenty times that of the baseline value (52630 +/- 11397 U/L) at the seventh hour, declined to about two times the control (5520 +/- 800 U/L) at the 18th hour, and returned to the baseline level at the 24th hour after the first caerulein injection. Serum lipase, elevated since the 7th hour, reached its peak value (631 +/- 34 U/L) at the 12th hour, then declined abruptly to the baseline value (0 U/L) at the 24th hour, after the first injection. However, severe histological changes of the pancreas were apparent at the 7th hour, reaching maximal destruction at the 18th hour, with severe inflammatory changes at the 24th hour; all after the first injection. The frank inflammation did not subside until 5 days after the first injection. These results suggest that, in the case of acute pancreatitis, normalization of serum biochemistries does not indicate recovery of the pancreas from acute inflammation.

Acute Disease↗

PubMed1991

[Poly-lactic-acid (PLA) sternal pins for the closure of median sternotomy--report of a case].

Poly-lactic-acid (PLA) sternal pins were used for the closure of median sternotomy in a case of bilateral pneumothorax. After placement 7 sutures of polyester and 2 wires, PLA sternal pins were inserted into the bone marrow of the sternum. The wires were then twisted and tightened, and all sutures were tightened, and the wires were removed. No significant postoperative complications, i.e., osteomyelitis and mediastinitis, sternal dehiscence, or bone marrow dysfunction, were observed. In addition, the PLA sternal pins were absorbed. In the closure of median sternotomy, PLA sternal pins provide stable sternal adhesion, which is essential to the prevention of sternal dehiscence and other complications. Moreover, with the use of PLA sternal pins, the retention of steel wires in the body is unnecessary.

Adolescent↗

PubMed1991

[Old pulmonary embolism causing intrabronchial bleeding].

A 51-year-old man was admitted because of hemoptysis. Physical examinations and chest XP revealed no abnormal findings. Fiberoptic bronchoscopy showed pulsatile bleeding at the orifice of right B6. Right bronchial arteriography showed a markedly dilated and tortous bronchial artery and shunting to the pulmonary arterial system in the middle and lower lobes. Pulmonary arteriography showed complete obstruction of the right middle lobar and lower lobe segmental arteries (A6, 9, 10). The hemoptysis was thought to be due to increased blood flow of the right bronchial artery, which compensated for reduced right pulmonary arterial flow. Right middle and lower lobe resection was done to prevent further hemoptysis. The resected specimen revealed old thromboemboli in the right middle and lower lobe pulmonary arteries. In this case old pulmonary embolism should be considered as a cause of intrabronchial bleeding.

Bronchial Arteries↗