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Biomedical subjects

J S Han

Publications and source records attributed to J S Han.

At least 289 records · Page 16Linked to original sources
PubMed1986

Antiopioid activity of the cardioexcitatory peptide in central modulation of cardiovascular functions.

Intracerebroventricular (i.c.v.) injection of [D-Ala2,Leu5]enkephalin produced depressor and bradycardiac responses which were prevented by naloxone or FMRF-NH2 pretreatment. Intrathecal injection of FMRF-NH2 to rats in hemorrhagic shock resulted in a slight but significant increase in blood pressure, and prevented the further decrease in heart rate which was observed in the control group. It is concluded that FMRF-NH2 may act as an antiopioid substance in central modulation of cardiovascular functions.

Animals↗
PubMed1986

Electroacupuncture and morphine analgesia potentiated by bestatin and thiorphan administered to the nucleus accumbens of the rabbit.

The endogenous opioid peptide enkephalin (EK) is known to be degraded mainly by two enzymes, the dipeptidyl carboxypeptidase 'enkephalinase' and aminopeptidase. Microinjection of the enkephalinase inhibitor thiorphan or the aminopeptidase inhibitor bestatin into the nucleus accumbens of the rabbit produced a dose-dependent analgesic effect. This analgesic effect was totally reversed by the narcotic antagonist naloxone or by antibodies against [Met5]enkephalin (MEK) administered to the same site. Antibodies against [Leu5]enkephalin were not effective. Moreover, microinjection of thiorphan or bestatin into the nucleus accumbens resulted in a marked potentiation of the aftereffect of electroacupuncture (EA) produced analgesia, as well as the analgesia induced by a small dose of morphine. It is concluded that the analgesic effect elicited by EA and morphine is mediated, at least in part, by MEK-like immunoreactive substance(s) in the nucleus accumbens.

Amino Acids, Sulfur↗
PubMed1986

Clonidine stimulated the release of dynorphin in the spinal cord of the rat: a possible mechanism for its depressor effects.

The decrease in blood pressure, heart rate and sympathetic nervous discharges (SND) induced by intrathecal injection of clonidine (1 microgram) in the rat was prevented by pretreatment with intrathecal injection of an antiserum against dynorphin. Clonidine (10(-4) M) added to the artificial cerebrospinal fluid perfusing the spinal subarachnoid space of the rat increased the amount of immunoreactive dynorphin in the perfusate. Intrathecal injection of dynorphin (30 micrograms) caused hypotension, bradycardia and a reduction in SND. These results suggest that the release of dynorphin in the spinal cord may constitute one of the mechanisms for the depressor effects of clonidine.

Animals↗
PubMed1986

Reversal of tolerance to morphine but no potentiation of morphine-induced analgesia by antiserum against cholecystokinin octapeptide.

Tolerance to morphine analgesia was induced in rats by chronic treatment with morphine (5-30 mg/kg, t.i.d. for 6 days). Intracerebroventricular (i.c.v.) injection of antiserum against cholecystokinin octapeptide (CCK-8) reversed tolerance to morphine by 50% (P less than 0.001). Intrathecal (ith) injection of the CCK-8 antiserum produced a similar, although less marked, reversal of tolerance to morphine. Rats made tolerant to analgesia induced by morphine developed a cross tolerance to electroacupuncture-induced analgesia. This cross tolerance was also reversed by the CCK-8 antiserum by more than 50% (P less than 0.001). Intracerebroventricular or intrathecal injection of the CCK-8 antiserum per se produced no significant changes in the basal level of the latency of the tail flick response, nor did it affect the analgesia induced by morphine in naive rats. The results suggest that prolonged activation of opioid receptors may trigger the CCK-8 system in the central nervous system to exert a negative feedback control, which may constitute one of the mechanisms for the development of tolerance to opioids.

Analgesia↗
PubMed1986

Cholecystokinin octapeptide (CCK-8): antagonism to electroacupuncture analgesia and a possible role in electroacupuncture tolerance.

The analgesic effect produced by electroacupuncture (EA) stimulation in the rat was dose-dependently antagonized by cholecystokinin octapeptide (CCK-8) administered intracerebroventricularly (i.c.v.) or intrathecally (i.th) at a dose range of 0.25-4 ng. This effect had an immediate onset and lasted for at least 4 h. CCK-8 per se, however, did not affect baseline tail flick latency. Rats subjected to prolonged EA stimulation developed EA tolerance as well as cross-tolerance to morphine. These tolerances could be postponed or reversed by i.c.v. or i.th injection of antiserum against CCK-8. While CCK-8 antagonized opioid analgesia, it did not affect analgesia induced by 5-hydroxytryptamine (5-HT) or norepinephrine (NE). Moreover, CCK-8 antiserum did not alter the basic level of nociception, nor did it potentiate EA analgesia in naive rats. It is concluded that prolonged EA stimulation results in a profound release of opioids which may trigger the release of CCK-8 in the central nervous system to counteract the opioid component of EA analgesia. This mechanism may account, at least in part, for the development of EA tolerance.

Acupuncture Therapy↗
PubMed1986

Studies on the mesolimbic loop of antinociception--II. A serotonin-enkephalin interaction in the nucleus accumbens.

In a previous report we have shown that the antinociceptive effect elicited by microinjection of morphine into the periaqueductal gray is due, at least in part, to the activation of an ascending serotonergic pathway which releases 5-hydroxytryptamine in the nucleus accumbens. We now report that antinociception induced by intra-periaqueductal gray injection of morphine can be attenuated also by the narcotic antagonist naloxone or the enkephalin antibodies administered into the nucleus accumbens, and potentiated by D-phenylalanine, a putative inhibitor of the degradation of enkephalins. Moreover, the antinociceptive effect induced by 5-hydroxytryptamine administered into nucleus accumbens could be blocked by naloxone injected into the same site, whereas the antinociception elicited by intra-accumbens injection of [D-Ala2,D-Leu5]enkephalin was not affected by cinanserin, a 5-hydroxytryptamine blocking agent. It is concluded that morphine administered to the periaqueductal gray is capable of activating an ascending serotonergic pathway to release 5-hydroxytryptamine in the nucleus accumbens, which in turn activates an enkephalinergic mechanism within the same nucleus, resulting in an antinociceptive effect.

Animals↗
PubMed1986

Comparison of nuclear magnetic resonance imaging and computed tomography in the diagnosis of upper cervical spinal cord compression.

Because of its ability to visualize soft-tissue structures in greater detail than any previous radiographic modality, nuclear magnetic resonance (NMR) has been heralded as one of the greatest advances in recent years. It is particularly well suited in diagnosis of spinal disorders since it can visualize the spinal cord and cerebrospinal fluid without intrathecal contrast agents. This is a preliminary report of our experience of NMR examination in 106 patients studied since November 1982 at Case Western Reserve University Hospital. One of the best applications of NMR is for compressive lesions of the upper cervical spine because "functional" images can be obtained. The information from NMR was compared with computed tomography (CT) in 14 patients with various etiologies of neural compression--atlanto-occipital subluxation in Down's syndrome, fixed post-traumatic atlantoaxial subluxation, rheumatoid atlantoaxial subluxation and basilar impression of the odontoid, ossification of the posterior longitudinal ligament, Klippel-Feil syndrome, congenital spinal stenosis, cervical spondylosis, Arnold-Chiari malformation, etc. Unlike CT, NMR can directly image in the sagittal plane without computer reformatting of axial cuts. This readily provides direct images of the spinal cord in neutral, flexion, and extension to show the mechanism of neural compression. Disadvantages of NMR compared with CT include poorer image resolution, slightly increased imaging time, and no patients with intracranial aneurysm clips or cardiac pacemakers can be studied. Advantages include no radiation exposure, no intrathecal contrast agent is required to differentiate CSF from neural tissue, and direct sagittal, coronal, and oblique images can be obtained. As a result of this preliminary experience, computed tomography and nuclear magnetic resonance imaging appear to be complimentary studies--CT provides better osseous detail, whereas NMR offers superior soft tissue resolution.

Adult↗
PubMed1986

Cervical radiculopathy: prospective evaluation with surface coil MR imaging, CT with metrizamide, and metrizamide myelography.

A prospective study was undertaken to compare the accuracy of surface coil magnetic resonance (SCMR) imaging, metrizamide myelography (MM), and computed tomography with metrizamide (CTM) in the determination of cervical radiculopathy. Surgical findings were the objective measure of accuracy. Fifty-two patients underwent all imaging studies. Studies were evaluated for disease location and type (bone vs. soft tissue). Twenty-eight patients underwent subsequent cervical surgery at 39 levels form an anterior interbody approach. Predictions made with SCMR imaging were surgically confirmed in 74% of patients, with CTM in 85%, and with MM in 67%. There was 90% agreement with surgical findings when SCMR imaging and CTM were used jointly, and 92% agreement when CTM and MM were used jointly, In general, SCMR imaging was as sensitive as CTM for identification of disease level, but not as specific for type of disease. MM was the modality least specific for disease type. The major advantage of CTM was its ability to distinguish bone from soft tissue, for which contrast material is unnecessary. SCMR imaging is a viable alternative to MM and, together with computed tomography, if needed, provides a thorough examination of the cervical region.

Adult↗