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Biomedical subjects

W W Lin

Publications and source records attributed to W W Lin.

106 records · Page 6Linked to original sources
PubMed1990

Infusion of progestins into the hypothalamus of female New Zealand white rabbits: effect on in vivo luteinizing hormone-releasing hormone release as determined with push-pull perfusion.

Previously, we have reported that intermittent infusion of progesterone (P4; 10 ng/ml) into the hypothalamus of conscious unrestrained female New Zealand White rabbits stimulates LHRH release in vivo. To further investigate this phenomenon, in the present studies, the effect of pulsatile (six pulses; 10 min on, 30 min off) and continuous infusion of P4 (Exp I) and 4-pregnen-20 alpha-ol-3-one or 20 alpha-hydroxyprogesterone (20 alpha-OH-P; Exp II) on LHRH release were studied in vivo using push-pull cannulae. Furthermore, the effect of pulsatile infusion (six pulses; 10 min on, 30 min off) of low doses of the following three progestins [5 beta-pregnan-3 beta-ol-20-one (pregnanolone), 5 alpha-pregnan-3 alpha-ol-20-one (3 alpha-5 alpha-P), and 20 alpha-OH-P] into the hypothalamus of does using push-pull cannulae were examined in Exp III. In Exp I, continuous infusion of P4 at 10 ng/ml was unable to stimulate mean LHRH release. However, pulses of P4 at 0.01 ng/ml (n = 4) were found to significantly increase the amplitude of the largest LHRH pulse (control period, 1.18 +/- 0.41; versus treatment period, 3.15 +/- 0.75 pg; P less than 0.035) as well as the frequency of LHRH pulses (control period, 0.72 +/- 0.26; treatment period, 1.37 +/- 0.12 pulses/h; P less than 0.035). On the other hand, there was no effect of pulses of P4 at 0.001 ng/ml (n = 4) on the activity of the LHRH neural apparatus. In Exp II, pulses of 20 alpha-OH-P at 10 ng/ml (n = 4) were found to significantly increase the mean LHRH release (control period, 1.24 +/- 0.10; treatment period, 2.07 +/- 0.52 pg/10 min) as well as the amplitude of the largest LHRH pulse (control period, 0.99 +/- 0.36; treatment period, 8.15 +/- 3.75 pg). Interestingly, continuous infusion of 20 alpha-OH-P (10 ng/ml) also significantly increased the mean amplitude (control period, 0.58 +/- 0.34; treatment period, 1.90 +/- 0.29 pg) as well as the amplitude of the largest LHRH pulse (control period, 0.64 +/- 0.37; treatment period, 4.30 +/- 1.97 pg).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Aortic and pulmonary input impedance in patients with cor pulmonale.

The hydraulic load of the right and left ventricles and the clinical effects of nifedipine were evaluated in 8 normal subjects (mean age: 55 years) and 8 patients with cor pulmonale secondary to chronic obstructive lung disease (mean age: 57 years). It was found that there were differences in the right ventricular resistance (174.62 +/- 25.96 vs 468.57 +/- 178.81 dyne/sec/cm-5), first zero crossing frequency (3.62 +/- 0.34 vs 6.07 +/- 3.56 Hz), steady power (218.95 +/- 32.25 vs 359.44 +/- 37.46 mW) and total power of right ventricle (275.81 +/- 36.18 vs 440.46 +/- 85.16 mW) between the normal and cor pulmonale patients, respectively. However, no significant changes in characteristic impedance, pulsatile power or aortic impedance were observed in the right pulmonary artery. After administration of nifedipine to patients with cor pulmonale, there were significant changes in resistance (468.57 +/- 178.81 vs 256.36 +/- 178.56 dyne/sec/cm-5), steady power (359.44 +/- 37.46 vs 225.51 +/- 114.64) and total power (440.46 +/- 85.16 vs. 289.27 +/- 50.85) of the pulmonary artery, respectively. Otherwise there were no significant changes in aortic input impedance or characteristic impedance of right pulmonary artery and pulsatile power. In conclusion, we found that: 1) the hydraulic vascular load in the right ventricle was higher in patients with cor pulmonale, 2) characteristic impedance that was not increased in cor pulmonale patients may be due to a dilated pulmonary artery, 3) there was no impedance mismatch between left ventricle and systemic arterial system in patients with cor pulmonale, and 4) by reducing the pulmonary vascular resistance through nifedipine administration, the total external right ventricular power might be reduced, without affecting the proximal pulmonary arterial compliance.

Aorta↗
PubMed1990

Contributing factors to formation of left atrial spontaneous echo contrast in mitral valvular disease.

The formation of left atrial spontaneous echo contrast may relate to blood stasis. This study analyzed the factors contributing to the formation of that contrast. Transesophageal echocardiography, transthoracic echocardiography, cardiac catheterization, and left ventricular angiography were performed in 139 patients, divided into five groups. Predominant mitral stenosis with atrial fibrillation was found in 36 patients (group I); normal porcine valve in the mitral valvular area with atrial fibrillation in 31 (group II); predominant mitral stenosis with normal sinus rhythm in 26 (group III); moderate to severe mitral regurgitation with atrial fibrillation in 25 (group IV); atrial fibrillation with normal mitral valve in 21 (group V). The results showed left atrial spontaneous contrast echo was found in only 1 of 139 patients by transthoracic echocardiography and 62 of 139 cases were detected by transesophageal echocardiography. There was a high incidence of left atrial spontaneous echo contrast in cases of mitral obstruction with atrial fibrillation and enlarged left atrium (group I, 88%; group II, 74%), but a lower incidence in cases with normal sinus rhythm (group III, 4%), atrial fibrillation alone (group V, 16%), and increased left atrial flow velocity (group IV, 9.5%). The diameter of the left atrium was significantly different between presence and absence of left atrial spontaneous contrast echo (54.3 +/- 9.2 mm vs. 48.3 +/- 8.6 mm, p less than 0.01). The mean pressure gradient was similar in groups I and III (14.6 +/- 0.6 mHg and 14.4 +/- 2.8 mHg, respectively) but different in group II (10.9 +/- 3.2 mHg, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Hemodynamic effects of hydralazine in mitral valve prolapse with regurgitation.

Vasodilators cause the earlier occurrence of click and prolong the duration of regurgitation murmur in mitral valve prolapse (MVP), meanwhile, they also decrease the intensity of murmur. To investigate the net effects of vasodilators on mitral regurgitation (MR) caused by MVP, we studied the hemodynamic responses to intravenous hydralazine in 10 patients with MVP and associated MR. The results showed that hydralazine reduced systemic vascular resistance by 28% (1705 +/- 307 to 1223 +/- 227 dyne-sec-cm5 p less than 0.001) and produced a 30% increase in cardiac output (4.4 +/- 0.7 to 5.7 +/- 0.7 l/min, p less than 0.001). The forward stroke volume increased by 18% (56 +/- 12 to 66 +/- 11 ml, p less than 0.001), while regurgitant stroke volume fell by 14% (46 +/- 22 to 40 +/- 23 ml, p less than 0.05), with a resultant slight fall in pulmonary capillary wedge v wave (13 +/- 5 to 11 +/- 3 mmHg, p = 0.05). We thus suggest that hydralazine has beneficial hemodynamic effects on MVP with regurgitation, and may be effective in the treatment of these patients.

Adult↗
PubMed1989

Two subtypes of acetylcholinesterase isoenzymes distinguishable by Angusticeps-type toxin F7.

1. Toxin F7, a toxin isolated from Dendroaspis angusticeps (green mamba) venom, exhibited a potent inhibition on the acetylcholinesterase of Bungarus snake venoms and homogenized brains and muscles of Bungarus and Trimeresurus snakes as well as that of mammalian tissues. 2. The acetylcholinesterase in the venoms and tissues of Naja (cobra) species as well as that in avian tissues, however, was found to be about 1000 times less susceptible towards inhibition by toxin F7. 3. It is concluded that there exist at least two subtypes of acetylcholinesterase isoenzymes distinguishable by an angusticeps-type toxin F7.

Acetylcholinesterase↗
PubMed1989

Sequence characterization of venom toxins from Thailand cobra.

Several toxins with distinct pharmacological properties were isolated from the venom of Thailand cobra (Naja naja siamensis) by cation-exchange chromatography. Two neurotoxins and one basic toxin with cardiotoxic activity were further purified and sequenced. The neurotoxins characterized were closely similar to the previously reported long- and short-chain neutrotoxins. The complete sequences of one minor neurotoxin and one cardiotoxin analogue were determined with the automatic protein sequencer in non-stop single runs of Edman degradation coupled with C-terminal sequence determination with carboxypeptidase digestion. The minor neurotoxin consists of 62 amino-acid residues with 8 cysteine residues and is found to be almost identical to cobrotoxin, a major toxic component of Formosa cobra (Naja naja atra). The sequence comparison of the 60-residue cardiotoxin with other reported cytotoxins of snake venoms indicates that 8 cysteine residues at the positions 3, 14, 21, 38, 42, 53, 54, and 59 are invariant among all sequences, with only two conservative changes at other positions along the sequence. The upshot of this report exemplified the facile sequence analysis of venom toxins by the application of pulsed-liquid phase protein sequencer and also revealed new analogues of a minor neurotoxin and one major cardiotoxin reported previously on the same species of Thailand cobra.

Amino Acid Sequence↗
PubMed1989

Is direct cardiotoxicity the primary cause of death following i.v. injection of the basic phospholipase A2 from Naja nigricollis venom?

The primary cause of death following i.v. injection of the basic phospholipase A2 (PLA2) from Naja nigricollis venom has been attributed to its direct cardiotoxicity. In view of our recent findings that cardiac failure caused by the basic PLA2 from Naja m. mossambica is primarily due to hyperkalemia resulting from cellular damage and possibly also from hemolysis, the cause of death due to the basic PLA2 from Naja nigricollis was re-investigated. In the anesthetized mice and rats, the PLA2 (0.3 micrograms/g, i.v.) produced a transient hypotension followed by recovery and subsequently by cardiac failure with ECG changes suggestive of hyperkalemia, such as P-R prolongation, tall T-wave, biphasic QRS-T complex, low voltage of QRS, A-V block, etc. Analysis of blood chemistry revealed marked increases in the plasma levels of K+, CPK, LDH, GOT, GPT, inorganic phosphate and hemoglobin (probably a mixture of hemoglobin and myoglobin). In the atrial preparation, however, no marked cardiotoxicity was observed except for a slight negative inotropic effect at 30 micrograms/ml. When 200 micrograms of the enzyme was injected into the coronary circulation in the Langendorff preparation, also no marked cardiotoxic effect was observed except for a decrease (about 40%) of coronary flow. From these results, it is concluded that the primary cause of death following i.v. injection of the basic PLA2 from Naja nigricollis is apparently cardiac failure due to hyperkalemia, resulting from cellular damage and possibly also from hemolysis, rather than direct cardiotoxicity.

Animals↗
PubMed1989

The effect of intravenous captopril on the left ventricular function-an acute study by hemodynamics and radionuclide angiography.

Acute hemodynamic effects of intravenous captopril were measured, and left ventricular function was analyzed by radionuclide angiography in 11 patients with moderate to severe hypertension. All subjects received 1 mg captopril bolus injection initially, and followed in 10 minutes intervals by 2 mg or 5 mg injections according to their blood pressure response. Eight patients experienced an acute reduction of blood pressure; three patients remained unresponsive. The onset of action occurred within 5 minutes with peak effect at 5 to 10 minutes and a duration of action of 20 to 30 minutes. The hemodynamic effects were characterized by arteriolar dilation (reduced systemic vascular resistance P less than 0.01), and apparent venous dilatation (reduced right atrial, pulmonary wedge pressure P less than 0.05 & 0.01 respectively). Pulmonary vascular resistance was not altered. Ejection fraction remained unchanged. Isovolumic relaxation period lengthened (109 +/- 20.1 vs 137.39 +/- 21.15 msec, P less than 0.05) and coronary perfusion pressure gradients dropped (113.8 +/- 5.6 vs 101.1 +/- 11.3 mmHg P less than 0.001) following intravenously administered captopril. Intravenous captopril may reduce arterial pressure by inducing arterial dilatation with minimal adverse effect. The prolongation of isovolumic relaxation period should mainly attribute to the decrease of coronary filling load.

Captopril↗
PubMed1988

Effect of sea nettle (Chrysaora quinquecirrha) venom on isolated rat aorta.

The venom from sea nettle (Chrysaora quinquecirrha) (1-10 micrograms/ml) produced an irreversible contraction of the isolated rat aortic ring that was slow in onset, increased with time, and reached maximum in about 10-20 min. The contraction was not inhibited by pretreatment with phenoxybenzamine, atropine, indomethacin, tetrodotoxin, ouabain, low Na+ or Na+-free medium, however, it was markedly decreased by the Ca2+ channel blockers, nifedipine and verapamil. In Ca2+-free medium, no increase in tension was produced by the venom. It is concluded that sea nettle venom causes a contraction of the rat aortic ring by increasing Ca2+ influx through the voltage-dependent Ca2+ channels.

Animals↗
PubMed1988

Effect of pulsatile infusion of progesterone on the in vivo activity of the luteinizing hormone-releasing hormone neural apparatus of awake unrestrained female and male rabbits.

Eight female and eight male New Zealand White rabbits were outfitted with push-pull cannulae aimed at the tuberal region of the hypothalamus and were used in 19 perfusion experiments. Animals were treated under 2 conditions: a control condition in which female (n = 4) and male (n = 4) rabbits were perfused only with artificial medium for 5-9 h, and an experimental condition in which female (n = 4) and male (n = 5) rabbits were subjected to perfusion with artificial medium, followed by 6 pulses of progesterone (P4) (10 min on, 30 min off; 10 ng/ml) during a 240-min period. Two female rabbits were also subjected to perfusion with artificial medium, followed by 6 pulses of cholesterol (10 min on, 30 min off; 10 ng/ml) during a 240-min period. The LHRH concentration in perfusates collected every 10 min was measured by RIA. In the 4 females undergoing 6- to 7-h control push-pull perfusions, spontaneous pulses were observed, with about 1 pulse every 60 min, and a variable amplitude of the LHRH signal, with a mean release of about 0.91 pg/10 min. In the 4 does treated with pulsatile P4 at 10 ng/ml, the mean LHRH release rate increased significantly from 0.91 +/- 0.13 to 1.66 +/- 0.20 pg/10 min (P less than 0.035), primarily due to an increase in the amplitude of the LHRH pulses, which were significantly greater than controls. This response occurred with an apparent mean latency of about 50 min. Cholesterol pulses did not affect the spontaneous activity of the LHRH neural apparatus. In the 4 males undergoing 5- to 9-h control push-pull perfusions, spontaneous LHRH pulses were observed with about 1 pulse every 60 min, and the mean release increased from 1.25 +/- 0.56 to 1.54 +/- 0.55 (P less than 0.035, by Wilcoxon's matched pairs signed rank test) in the late afternoon primarily due to an increase in the amplitude of the pulses. P4 pulses did not affect the spontaneous activity of the LHRH neural apparatus compared to that in the control animals. Overall, these results clearly demonstrate that although spontaneous pulsatile LHRH release from the hypothalamus of awake unrestrained female and male rabbits is similar, pulses of P4 can activate only the female LHRH neural apparatus, with an apparent latency to peak LHRH release of approximately 50 min. In addition, there appears to be an increase in LHRH mean release levels in the late afternoon to early evening in male rabbits.

Anestrus↗
PubMed1987

Pharmacological study on phospholipases A2 isolated from Naja mossambica mossambica venom.

The pharmacological properties of three phospholipases A2 (CM-I, CM-II and CM-III) purified from Naja mossambica mossambica venom were studied. The order of their catalytic and indirect hemolytic potencies was CM-I = CM-II greater than CM-III. Among them, only CM-III had a direct hemolytic action on the guinea-pig RBC, which was greatly inhibited by heparin. In the chick biventer cervicis nerve- muscle preparation, both CM-II and CM-III caused neuromuscular blockade with a gradual contracture and a decreased sensitivity to ACh and KCl, whereas no complete neuromuscular block was observed with CM-I up to 30 micrograms/ml. In the mouse phrenic nerve-diaphragm preparation, these three PLA2s abolished twitches evoked by indirect stimulation earlier than those by direct stimulation. Contracture was also produced by CM-II and CM-III. However only the latter was inhibited by pretreatment with heparin. These PLA2s caused myonecrosis in the hind-leg muscle of the mouse when injected intramuscularly. From these results, it is concluded that all of these PLA2s are both neurotoxic and myotoxic.

Animals↗
PubMed1985

Pharmacological study on angusticeps-type toxins from mamba snake venoms.

Five angusticeps-type toxins, F7, F8 and C10S2C2 from Dendroaspis angusticeps and C and FS2 from D. polylepis polylepis, were tested for action on the chick biventer cervicis nerve-muscle, the frog rectus abdominis muscle and the mouse phrenic nerve-diaphragm preparations. In the chick muscle, none of these toxins exhibited any stimulatory effect up to 100 micrograms/ml. In the frog muscle, the response to acetylcholine, but not to carbachol, was enhanced dose dependently by F7 and C. No appreciable effect was observed with the other three toxins. In the mouse diaphragm, also only F7 and C augmented responses to indirect stimulation and produced spontaneous fasciculations. On tetanic stimulation, a marked Wedensky inhibition was observed. Their stimulatory effect was abolished by d-tubocurarine. In the presence of d-tubocurarine as well as in the denervated mouse diaphragm, neither toxin increased responses to direct stimulation. In low-calcium (0.6 mM) or high magnesium (4.2 mM) medium, the stimulatory effect of both toxins was markedly attenuated. The resting membrane potential of the mouse diaphragm was not changed. The amplitude and frequency of MEPPs and the quantal content and the half-decay time of EPPs was increased. Both toxins also produced a stimulatory effect on the isolated guinea-pig ileum, which was abolished by atropine. In the rat atrial preparation, both toxins caused negative inotropic and chronotropic effects, which were reversed by atropine. If pretreated with atropine, these effects were completely prevented. Both F7 and C markedly inhibited the cholinesterase activity of the homogenized mouse diaphragm and frog rectus abdominis muscle but not that of the chick biventer cervicis muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal Muscles↗
PubMedDate not supplied

Potentiation of lipopolysaccharide-induced IL-6 release by uridine triphosphate in macrophages: cross-interaction with cyclooxygenase-2-dependent prostaglandin E(2) production.

Our previous study has demonstrated the potentiation by uridine triphosphate (UTP) of nitric oxide (NO) and prostaglandin E(2) (PGE(2)) production in lipopolysaccharide (LPS)-stimulated murine J774 macrophages. In this study, we found that the amount of interleukin-6 (IL-6) release in response to LPS stimulation was greatly enhanced in the presence of UTP. This enhancement exhibited concentration dependence and occurred after 8 h of treatment with LPS. RT-PCR analysis indicated that the steady-state level of IL-6 mRNA induced by LPS was apparently increased upon co-addition of UTP. The potentiation by UTP was inhibited by the treatment with U73122 (a phosphatidylinositol-phospholipase C inhibitor), BAPTA/AM (an intracellular Ca(2+) chelator), KN-93 (a selective inhibitor of calmodulin-dependent protein kinase) or PDTC (a nuclear factor kappaB inhibitor). To understand the cross-regulation among NO, PGE(2) and IL-6, all of which are dramatically induced after LPS stimulation, the effects of L-NAME (a nitric oxide synthase inhibitor), indomethacin (a cyclooxygenase inhibitor), NS-398 (a cycloxygenase-2 inhibitor) and IL-6 antibody were tested. The results revealed the positive regulation between PGE(2) and IL-6 synthesis because NS-398 and indomethacin inhibited LPS plus UTP-induced IL-6 release, and IL-6 antibody attenuated LPS plus UTP-induced PGE(2) release. Taken together these results reinforce the role of UTP as a regulatory element in inflamed sites by demonstrating the capacity of this nucleotide to potentiate LPS-induced release of inflammatory mediators.

Animals↗