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Biomedical subjects

G S Liu

Publications and source records attributed to G S Liu.

At least 55 records · Page 3Linked to original sources
PubMed1991

Functional and structural impairment in human, rat and guinea-pig atrial muscle in response to in vitro calcium overload: a cytochemical study on cellular calcium distribution.

Critical accumulation of cellular calcium in ischaemic myocardium is involved in irreversible cell damage. In human right atrial trabeculae and in rat and guinea-pig left atria, we investigated whether direct calcium overload by increasing the extracellular calcium concentration, [Ca2+]o, leads to similar impairment of function and ultrastructure as observed after ischaemia. The force of contraction was measured during two consecutive cumulative increases in [Ca2+]o (1-25 mmol/l) separated by 30 min of incubation at low [Ca2+]o. Compared to the first Ca2+ challenge, the positive inotropic effect of increasing [Ca2+]o was depressed during the second one and the after-contractions, and the increase in resting tension developing with high [Ca2+]o tended to be larger. The ultrastructure of the tissue fixed immediately after excision was well preserved. When fixed after the second Ca2+ challenge, half of the cells were severely damaged with various signs of cellular Ca2+ overload similar to those observed after ischaemic damage: the sarcolemma lost its Ca(2+)-binding properties, sarcomeres showed contraction band necrosis, the mitochondria had disrupted cristae and contained either large clusters of Ca2+ precipitate or amorphous densities (Jennings granules). In many cells, calcium precipitates were present in the cytoplasm. The morphological and functional changes were similar in the three species studied. Our results suggest that the deterioration of atrial myocardium after challenge with high [Ca2+]o or after severe ischaemia may be traced back to a common mechanism, i.e. the sarcolemma loses its competence as a permeable barrier for Ca2+ and therefore facilitates excessive Ca2+ entry. However, for the direct demonstration of calcium precipitates as a sign of cytosolic Ca2+ overload, high [Ca2+]o are required with are not normally present in the myocardium.

Animals↗
PubMed1991

Preconditioning causes improved wall motion as well as smaller infarcts after transient coronary occlusion in rabbits.

BACKGROUND: A brief coronary occlusion before a more prolonged occlusion results in less myocardial infarction than the longer occlusion alone. However, the effects of this preconditioning on recovery of systolic function after coronary occlusion have not been determined. METHODS AND RESULTS: Ultrasonic crystals implanted in rabbit myocardium measured segment length in the distribution of a branch of the left coronary artery that was fitted with a snare occluder. Rabbits were randomly allocated to either nonpreconditioned or preconditioned groups. Rabbits in the latter group underwent preconditioning with a 5-minute coronary occlusion followed by 10 minutes of reperfusion. Then the coronary artery was occluded for 20 minutes in all rabbits, after which it was allowed to reperfuse for 90 minutes. The hearts were then excised, and infarct size was measured by staining with triphenyltetrazolium chloride. During coronary occlusion, all hearts except one demonstrated either akinesis or paradoxical bulging. Five minutes after release of the 20-minute occlusion, active shortening had returned in the preconditioned rabbits and averaged 27.9 +/- 16.6% of baseline shortening. At the same time, paradoxical lengthening persisted in nonpreconditioned rabbits (-15.5 +/- 19.8% of baseline). By the end of the 90-minute reperfusion period, segment shortening averaged 40.1 +/- 8.4% of baseline in preconditioned rabbits and only 6.2 +/- 12.0% in nonpreconditioned rabbits (p less than 0.05). Infarct size as a percentage of risk area was significantly smaller in preconditioned rabbits as well (3.0 +/- 1.6% versus 28.8 +/- 7.0%, p less than 0.002) and likely accounted for the improved shortening. CONCLUSIONS: We conclude that a brief coronary occlusion before a more prolonged occlusion results in not only reduced infarct size but also significantly better recovery of systolic function.

Animals↗
PubMed1991

Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart.

BACKGROUND: Preconditioning (5 minutes of ischemia followed by 10 minutes of recovery) renders the heart very resistant to infarction from subsequent ischemia. This study tests whether adenosine receptors might mediate preconditioning protection. METHODS AND RESULTS: We examined the effect on infarct size of pretreatment with either of two adenosine receptor antagonists in both control and preconditioned in situ rabbit hearts. Hearts underwent 30 minutes of regional ischemia plus 3 hours of reperfusion, and infarct size was measured with tetrazolium. Infarct size averaged 39% of the zone at risk in controls but only 8% in preconditioned hearts. Preconditioned and nonpreconditioned hearts receiving either blocker had infarcts not different in size from the controls. A 5-minute intracoronary infusion of adenosine was as effective as 5 minutes of ischemia in protecting parabiotically perfused isolated hearts against infarction from a 45-minute ischemic insult. Similarly, intracoronary infusion of N6-1-(phenyl-2R-isopropyl)adenosine, an A1-selective adenosine receptor agonist, at a dose that delayed conduction but did not dilate the coronary vessels, also limited infarct size. The protection disappeared when we reduced the coronary concentration of drug by intravenous infusion of adenosine, indicating that cardiac rather than peripheral receptors were involved in the protection. CONCLUSIONS: We conclude that adenosine released during the preconditioning occlusion stimulates cardiac A1 receptors, which leaves the heart protected against infarction even after the adenosine has been withdrawn.

Adenosine↗
PubMed1991

[Freeze-etch study on the brush border structure of Cysticercus cellulosae].

The images of C. cellulosae detected by freeze-itch technique were exactly similar to those observed in the thin section. The scolex microtriches might be divided into two parts, a thick proximal portion and a thinner spinal distal end, the former measuring about 0.2-0.4 micron in length, the latter measuring about 1-2 microns in length. On the extracellular surface of the proximal portion of microthrix, 1 or 2 particles could occasionally be seen, while numerous particles appeared on the protoplasmic fracture face (PF face) of the proximal portion. The PF face were closely packed and irregularly distributed with membranous particles, which were spherical or subspherical in shape, measured 0.01-0.02 micron in diameter. The extracellular fracture face (EF face), of proximal portion and all four membranous faces of spinal end were smooth. The tegumentary plasmic membrane was 0.02 micron in thickness, with smooth ES face. The PF face of this membrane packed closely with numerous particles, which were similar with those on the PF face of the microthrix. Numerous globular or discoidal vesicles scattered at random in the tegumentary matrix. Most mitochondria were near the basement membrane of the matrix. In the parenchymal layer, the parenchymal cells, calcareous corpuscles and flame-cells could easily be seen. Most of the calcareous corpuscles and flame-cells were located closely beneath the muscle layer. The flame-cell of C. cellulosae mainly consisted of three portions, cell body, a bundle of cilia and a filtered cell lumen. The flame-cell body had a large nucleus and relatively few cytoplasm with several mitochondria.(ABSTRACT TRUNCATED AT 250 WORDS)

Actin Cytoskeleton↗
PubMed1991

Ketanserin in the treatment of hypertension: a multicentre dose-finding study in China.

The effect of ketanserin at 5 mg, 10 mg and 20 mg twice daily for 3 months was studied in Chinese patients with hypertension. Both 10 mg and 20 mg doses twice daily effectively reduced systolic and diastolic pressures, while 5 mg twice daily was not effective. The 20 mg regimen was more effective than 10 mg in reducing diastolic, but not systolic pressures. Blood pressure reduction was progressive up to 1 month of treatment but not thereafter. Neither first-dose hypotension nor postural hypotension were seen. There were no effects on body weight or heart rate. A nominally significant 6 msec increase in QTc was seen with 10 mg, but not with 5 or 20 mg twice daily; this could be a chance finding. The side-effect burden was light, and decreased with time.

Blood Pressure↗
PubMed1990

Beta adrenoceptors and regenerating corneal epithelium.

Beta blockers inhibit corneal re-epithelialization. This may be due to beta-2 receptor controlled mechanisms. To investigate this possibility we performed a randomized, double-masked study involving 60 rabbit iatrogenic induced corneal ulcers produced with iodine vapour. Two beta specific drug compounds were tested, namely, betaxolol hydrochloride 0.25% (Alcon) (beta 1) and L132-468 (Sandoz, Basel) 0.25% (beta 2), and phosphate-buffered solution (PBS) as control. There was no statistical difference in the wound healing rates among all groups at 24 hours but there were significant differences at 48 hours (p less than 0.01). At 72 hours, the L132-468 treated groups showed significantly less healing than the betaxolol hydrochloride treated group. The PBS-treated group was healed at this time. By 20th post burning day, SEM revealed that betaxolol hydrochloride treated corneas were completely healed with normal epithelial microvilli. The L132-468 treated corneas were also healed but desquamation and abnormal cells were observed. In conclusion, beta-2 blockers inhibit corneal re-epithelialization more potently than beta-1 blockers.

Administration, Topical↗
PubMed1990

Inhibition of protein synthesis does not block myocardial protection afforded by preconditioning.

It is currently unknown how preconditioning the heart with brief periods of ischemia makes it resistant to infarction from a subsequent ischemic insult. The protein synthesis inhibitors, cycloheximide and actinomycin D, were used to determine whether preconditioning involves synthesis of a protective protein. Ischemia was produced by occlusion of a branch of the left coronary artery in open-chest anesthetized rabbits. All groups were subjected to 30 min of ischemia followed by 3 h of reperfusion. The first two groups served as noninhibited controls. Group 1 was subjected to ischemia with no preconditioning. Group 2 was preconditioned with two 5-min ischemic periods each followed by 10 min of reperfusion, before the 30-min ischemic period. Groups 3 and 4 were the same as groups 1 and 2, respectively, except that cycloheximide was administered before coronary occlusion. Groups 5 and 6 were also the same as groups 1 and 2 except that actinomycin D was administered before coronary occlusion. After 3 h of reperfusion all hearts were removed and the size of the ischemic zone and infarct were determined. The percent of the ischemic zone infarcted was small and similar in all preconditioned groups (3.3 +/- 1.1% for group 2, 7.4 +/- 3.3% for group 4, and 0.5 +/- 0.7% for group 6). All nonpreconditioned groups had large infarcts with no differences between groups (39.0 +/- 8.5% for group 1, 31.6 +/- 6.3% for group 3, 30.8 +/- 5.9% for group 5). Because neither cycloheximide nor actinomycin D could block protection afforded by preconditioning, it seems unlikely that synthesis of a protective protein is the mechanism of protection.

Animals↗
PubMed1990

Neurogenesis of respiratory rhythm and pattern: emerging concepts.

We present three hypotheses related to the nervous system control of breathing in mammals: 1) that neural mechanisms controlling breathing change with state and that the relationship between mechanisms in different states can be described in terms of either modulation or a basic transformation of properties, or both; 2) that the mechanisms generating respiratory rhythm and pattern are separate; and 3) that conditional pacemaker cell activity is the basis for respiratory rhythm in highly reduced states.

Animals↗
PubMed1990

Neural mechanisms generating respiratory pattern in mammalian brain stem-spinal cord in vitro. I. Spatiotemporal patterns of motor and medullary neuron activity.

1. An analysis of the spatial and temporal patterns of activity of neurons of the respiratory motor-pattern generation system in an in vitro neonatal rat brain stem-spinal cord preparation is presented. Impulse discharge patterns of spinal and cranial moto-neurons as well as respiratory neurons in the medulla were analyzed. Patterns of motoneuronal discharge were characterized at the population level from recordings of motor-nerve discharge and at the single-cell level from intracellular recordings. These patterns were compared to patterns generated in the neonatal rat and adult mammal in vivo to establish the correspondence between in vitro and in vivo states. 2. The in vitro system generated a complex spatiotemporal pattern of spinal and cranial motoneuron activity during inspiratory (I) and expiratory (E) phases of the respiratory cycle. The respiratory cycle consisted of three distinct phases of neuronal activity (I, early E, and late E phase) similar to the temporal organization of the cycle in the intact mammal. The spike discharge pattern of motoneurons during the I phase consisted of a rapidly peaking-slowly decrementing discharge envelope with a high degree of synchronization on a time scale of 25-50 ms (approximately 20-40 Hz). A similar pattern was generated in the neonate in vivo under conditions comparable with the in vitro state (i.e., nervous system isolated from mechanosensory afferent inputs). However, the I-phase-motoneuron discharge pattern and cycle-phase durations differed from those characteristic of the intact neonatal or adult systems in vivo. This difference could be accounted for primarily by removal of vagal mechanosensory afferent inputs. 3. The synaptic drive potentials of spinal motoneurons during the I phase in vitro consisted of a rapidly peaking-slowly decrementing potential envelope similar in shape to the spike-frequency histogram of single motoneurons and the envelope of the motoneuron-population discharge. The drive potentials had prominent high-frequency amplitude fluctuations superimposed on the slower drive-potential envelope that were temporally correlated with the generation of motoneuron action potentials. The dominant frequency components of these fast-membrane-potential oscillations (20-35 Hz) were similar to the frequency components of the amplitude fluctuations in the motoneuron-population discharge. One class of medullary neurons with I-phase discharge also exhibited a rapidly peaking-slowly decrementing pattern of impulse discharge and synaptic drive potential with similar high-frequency components.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Budd-Chiari syndrome. Surgical treatment of 45 cases.

Fourty-five patients with Budd-Chiari syndrome were treated surgically from December 1985 to May 1988. The procedures consisted of cavoatrial shunt, mesoatrial shunt, transcardiac membranotomy, splenopneumopexy, portal vein-systemic vein shunt and re-opened umbilical vein-right auricle shunt, etc. Two of the patients died postoperatively. Others showed improvement after follow-up for 3-24 months. Recurrent hemorrhage from varices did not occur after operation in all patients. The diagnosis, surgical indications, and various methods of surgery for Budd-Chiari syndrome were discussed.

Adolescent↗
PubMed1989

Percutaneous superfine-needle aspiration biopsy of intrathoracic lesions guided by simulator.

The result of percutaneous superfine-needle aspiration biopsy in 100 patients with intrathoracic lesions guided by simulator is reported. The success rate of aspiration biopsy was 94%, and no major complication was observed. The method of localization by simulator had advantages such as accuracy in localization, no limitation of mass size and site, and a high rate of puncture success. Cell smears obtained by superfine needle were similar to those obtained by fine- or large-bore needles, but fewer complications were encountered. This is a useful technique that can provide early cytological diagnosis, especially for the peripheral type of pulmonary mass.

Adult↗
PubMed1989

Ultrastructural effects of topical betoptic, betagan, and timoptic on the rabbit corneal endothelium.

Scanning and transmission electron microscopy was used to evaluate the cytotoxic effect of three commercially available beta adrenergic blockers (Betoptic 0.5%, Betagan 0.5% and Timoptic 0.5%), and preservative (benzalkonium chloride 0.01%) on rabbit corneal endothelium. Evaluation was performed on groups including intact corneas, de-epithelialized corneas, full-thickness corneal grafts with intact epithelium, and de-epithelialized corneal grafts. Both Betoptic and Betagan produced minor damage to endothelial microvilli in the intact epithelial group. The de-epithelialized and the grafted-cornea groups had less damage induced by Betoptic than Betagan. Timoptic produced more endothelial damage than Betoptic and Betagan in all groups. Benzalkonium chloride produced minimal endothelial damage. Results indicate that Betoptic produces less endothelial toxicity than the two non-specific beta blockers when corneal epithelium is damaged and after penetrating keratoplasty.

Administration, Topical↗
PubMed1989

The toxic effects of pilocarpine gel and drops on rabbit cornea.

Pilocarpine drops and gel were applied daily for 3 months to rabbit cornea to determine their cytotoxic effects. The corneas were examined clinically with slit lamp biomicroscopy and histologically with scanning and transmission electron microscopy. The gel-treated corneas developed edema and desquamation of the superficial epithelial layers. Vacuoles, swollen mitochondria and amorphous deposits were detected in the basal epithelial layers. The drop-treated corneas developed endothelial cell damage characterised by cytoplasmic vacuoles, swelling and degeneration of the intracellular organelles. The study confirms the clinical impression that pilocarpine gel can produce anterior corneal damage. The toxic effect of pilocarpine gel on the corneal endothelium was much less than the effect produced with pilocarpine drops.

Administration, Topical↗
PubMed1988

Toxic effects of topically administered Betagan, Betoptic, and Timoptic on regenerating corneal epithelium.

Re-epithelialization of 40 iatrogenic cornea ulcers produced in rabbits with iodine vapour burn were studied after topical administration of Betagan, Betoptic or Timoptic. At 24 hours there was no statistical difference in the wound healing rates among all the treated animal groups. At 48 hours, all the drug-treated groups were significantly different from the control group (p less than 0.05). There was no difference between the Betagan and Betoptic treated groups but the Timoptic-treated group was slower (p less than 0.05) than the Betoptic treated group, while the difference between the Timoptic and Betagan treated groups is not significant. At 72 hours the re-epithelialization rate of the Timoptic treated group was significantly slower than both the Betagan and Betoptic treated groups (p less than 0.05). By the 16th day following ulceration SEM examination revealed the Timoptic treated group had extensive epithelial cell desquamation, as well as hole formation and plasma membrane disruption. The Betagan treated corneas had mild superficial epithelial changes with loss of microvilli or slight desquamation. The Betoptic treated corneas were completely healed. In conclusion, Betagan is less toxic than Timoptic. Betoptic is the least toxic of the three drugs to regenerating rabbit corneal epithelium.

Administration, Topical↗
PubMed1987

Ultrastructural changes of the rabbit corneal epithelium and endothelium after Timoptic treatment.

The purpose of this study was to determine whether timolol maleate (Timoptic) is cytotoxic to the cornea. The drug was applied as topical drops for 1 month to control rabbit eyes and rabbit eyes from which the epithelium had been removed or to de-epithelialized full-thickness autografts. Clinically all corneas and grafts remained clear. Scanning and transmission electronmicroscopy however revealed is drug induced epithelial damage, defective epithelial wound healing, and endothelial changes. The endothelial changes were most prominent in the group of rabbits that underwent de-epithelialization before corneal grafting.

Animals↗