皮下环精索封闭疗法治疗急性附睾-睾丸炎疗效观察

目的评价急性附睾-睾丸炎皮下环精索封闭疗法的疗效.方法对80例急性附睾-睾丸炎病例随机分为两组,对照组给予传统治疗方法,而治疗组除了传统疗法外,加用皮下环精索封闭治疗.结果治疗组所有患者1～3d内发热、疼痛症状缓解,4～6 d内附睾睾丸肿胀明显减退,97.5%的病例2周内治愈;而对照组40%的患者1～3d内发热、疼痛症状缓解,75%的患者4～6d内附睾睾丸肿胀减退,80%患者2周内治愈,治疗组疗效优于对照组.结论皮下环精索封闭疗法可以迅速缓解临床症状,缩短病程,提高治愈率,是治疗急性附睾-睾丸炎的有效方法.     

Intubating conditions and onset of neuromuscular block of rocuronium (Org 9426); a comparison with suxamethonium

The intubating conditions and neuromuscular blocking profile following 600 micrograms.kg-1 rocuronium (Org 9426) have been investigated in patients under various experimental conditions. They were compared with conditions following 1.5 mg.kg-1 suxamethonium, preceded by a precurarising dose (10 mg) of gallamine, and with those in a control group in the absence of a muscle relaxant. Rocuronium produced good to excellent intubating conditions at 60 as well as at 90 s after administration, even though there was only a partial blockade of the adductor pollicis muscle. Intubating conditions following suxamethonium were comparable with those after rocuronium. Half of the control patients could be intubated. The clinical duration and the recovery time of 600 micrograms.kg-1 of rocuronium were 24(4) and 9(3) min (mean(s.d.)), respectively. Rocuronium may have a major advantage over existing non-depolarising muscle relaxants due to the early presence of excellent intubating conditions. The results indicate that rocuronium may replace suxamethonium in procedures in which rapid sequence induction is required.     

Pharmacological evaluation of natural product analogues. I. Preliminary pharmacological evaluation of O-methylgortschakoine and O-methylpetaline

The synthesis of O-methylgortschakoine and O-methylpetaline was achieved through an unambiguous route. Pharmacological testing of O-methylgortschakoine in comparison to papaverine and 7,8-dimethoxy-N-methyltetrahydroisoquinoline, indicated that it possesses hypotensive, neuromuscular blocking and smooth muscle relaxant activities. 7,8-Dimethoxy-N-methyltetrahydroisoquinoline showed only nonspecific smooth muscle relaxation in our testing system. The 1-(p-methoxybenzyl)-substituent of O-methylgortschakoine appears to be required for this hypotensive and neuromuscular blocking effect. The quaternary analogue O-melthylpetaline was found to possess a more potent neuromuscular blocking activity.     

Heart failure: Effects of beta receptor antagonists on left ventricular function in patients with clinical evidence of heart failure after myocardial infarction. A double-blind comparison of metoprolol and xamoterol Echocardiographic results from the Metoprolol and Xamoterol Infarction Study (MEXIS)

Two hundred and ten patients with clinical evidence of heartfailure, developing after an acute myocardial infarction, wererandomized to treatment with the ß₁ antagonist metoprolol50–100mg b.i.d. (n=106) or the ß₁ partial agonistxamoterol 100–200 mg bid. (n=104). Left ventricular systolicand diastolic function were assessed with echocardiography andtransmitral Doppler cardiography before and after 3 and 12 monthsof double-blind treatment. E-point septal separation and percent left ventricular fractional shortening were used as indicesof systolic function. The ratio between peak early and latemitral diastolic flow (E/A ratio) and isovolumic relaxationtime were used as indices of diastolic function. In the xamoterol group, there was a deterioration in E-pointseptal separation (P<0·05). A difference between thetreatment groups was present both at 3 months (E-point septalseparation 11·4 vs 13·0 mm, P<0·0l,fractional short ening 271 vs 252%, P<005) and 12 months(E-point septal separation Ill vs 13·2 mm, P<0·05fractional shortening 26·9 vs 25·0%, P<0·05).E/A ratio increased in the metoprolol group (P<0·05)but not in the xamoterol group. At 3 months there was a significantdifference (0·85 vs 0·67, P<0·005 betweenthe groups but not at 12 months. In comparison with the ß₁-receptor antagonist metoprolol,the ß₁ partial agonist xamoterol impaired left ventricularsystolic function in patients with clinical evidence of heartfailure after an acute myocardial infarction.     

Selective modification at the N-terminal region of human growth hormone that shows antagonistic activity

A new analogue of recombinant human growth hormone (hGH), hGH des(1–6,14) was expressed in Escherichia coli, refolded and purified to homogeneity. The mutation decreased the hormone's ability to bind lactogenic and somatogenic receptors through its site 1, and almost completely abolished its ability to bind these receptors through site 2, as evidenced by both binding and gel-filtration experiments. More specifically, the binding to prolactin receptors (PRLRs) from various species or their soluble recombinant extracellular domains (ECDs) was decreased 1.5–4-fold, whereas the binding to hGH receptor (hGHR) was decreased 10–85-fold. These changes caused an almost total loss of hormone agonistic activity in several in vitro bioassays and subsequently, the hGH des(1–6,14) analogue acquired antagonistic properties. This antagonistic activity was dependent upon modification of site 1. In those cases in which the binding was reduced only slightly, e.g. binding to rabbit PRLRs, hGH des(1–6,14) acted as a strong antagonist, whereas in others in which the binding of site 1 was reduced to a higher degree, such as other PRLRs and, in particular, hGHR, the antagonistic activity was correspondingly weaker. Circular dichroism spectra of the analogue suggested that these changes do not result from a decrease in overall -helix content, but rather from minor local structural modifications at the N-terminus.     

Differential effect of pancuronium at the adductor pollicis, the first dorsal interosseous and the hypothenar muscles. An electromyographic and mechanomyographic dose-response study

Cumulative dose-response curves were constructed from evoked compound electromyographic (EMG) recordings in man to compare the sensitivity to pancuronium of the adductor pollicis, the hypothenar and the first dorsal interosseous muscles. Also, the EMG and mechanomyography-based sensitivity of the adductor pollicis muscle were compared. The EMG and the mechanomyogram were evaluated in random sequence in each of 21 adult thiopental, fentanyl and diazepam anesthetized patients. The EMG-based ED50 were 36-38 micrograms.kg-1 with no differences between muscles. The EMG-based ED90 of the adductor pollicis and the hypothenar muscles were 62-65 micrograms.kg-1 compared to the 60 micrograms.kg-1 of the first dorsal interosseous muscle (P < 0.05). ED50 (34 micrograms.kg-1), and ED90 (56 micrograms.kg-1) obtained from the adductor pollicis mechanomyogram were significantly lower than those based on the EMG (P < 0.05). It is concluded that differences in sensitivity to pancuronium exist between the three muscles when evaluated from the EMG, and that the apparent sensitivity of a given muscle to a muscle relaxant may depend upon whether the response is evaluated using EMG or mechanomyography.     

肝钳与肝门阻断的肝损害及其防治的实验研究

本实验观察不同阻断时刻肝钳与肝门阻断的肝损害以及预防性应用抗氧化剂的缓解作用。结果表明：（１）ＳＧＰＴ、ＴＢ在肝钳组的变化比肝门阻断组表现得更为一过性。而肝门阻断给药组的改变要比非给药组的轻微且恢复得快。（２）肝门阻断时，ＭＤＡ含量显著升高，机体的Ｔ－ＡＯＣ和ＳＯＤ下降。而给药组可明显减轻上述改变。（３）随着肝门阻断时间的延长，肝组织损害也相应加重，抗氧化剂的给予缓解了肝缺血和再灌注造成的组织损害。肝钳组由于健肝血供未受干扰，因此，不同阻断时刻肝组织学形态与对照组相似无甚改变。结论：（１）肝钳较肝门阻断的肝损害轻，且实用安全。（２）肝门阻断预防性使用抗氧化剂，可明显减轻肝缺血再灌注损害。（３）肝门阻断时经门静脉较外周静脉输注抗氧化剂，其保护作用更直接、明显     

Differential potentiation by calcium antagonists of neuromuscular blockade induced by pancuronium and succinylcholine in cats in vivo

Summary The effects of several calcium antagonists (verapamil, nicardipine and two diltiazem isomers, d-cis and l-cis diltiazem) alone and associated to non-depolarizing (pancuronium) and depolarizing (succinylcholine) neuromuscular blockers, were evaluated on sciatic nerve-tibialis anterior muscle preparations from cats in vivo. The calcium antagonists used (at 0.1 and 0.5mg/kg iv) did not modify the height of muscular twitches elicited indirectly. However, these agents potentiated in a dose-dependent way the neuromuscular blockade induced by iv pancuronium (2–40g/kg) and succinylcholine (6–200g/kg). The order of potency in increasing the effects of pancuronium was nicardipine d-cis diltiazem verapamil, whereas the order of potency in enhancing succinylcholine effects was d-cis diltiazem verapamil nicardipine. The effects of diltiazem were stereoselective, thus the potentiation induced by d-cis diltiazem was significantly greater in all cases than that induced by l-cis diltiazem, which suggests that calcium channel blockade plays a role in these interactions. However, other mechanisms such as calcium antagonists-induced nicotinic receptor desensitization may also be involved.     

Modulation of Fas-mediated apoptosis of human thyroid epithelial cells by IgG from patients with Graves' disease (GD) and idiopathic myxoedema

The expression of two autoimmune thyroid diseases, GD and idiopathic myxoedema, is associated with antibodies to the thyroid-stimulating hormone (TSH) receptor. Thyroid stimulating antibodies (TSAb) in GD are TSH agonists and cause hyperthyroidism as well as goitre, whereas thyroid stimulation blocking antibodies (TSBAb) in idiopathic myxoedema are TSH antagonists and cause hypothyroidism and thyroid atrophy. We investigated the effect of antibodies to TSH receptor on Fas-mediated apoptosis of thyroid epithelial cells (thyrocytes). Human IgG was isolated from healthy donors, patients with GD and idiopathic myxoedema. Human thyrocytes were obtained from surgical specimens. Thyrocytes were cultured in the presence or absence of human IgG with or without interferon-gamma (IFN-γ) or IL-1β for a specified time. After incubation, we examined the level of cAMP in cultured supernatants and both Fas and Bcl-2 expression on thyrocytes. In addition, we examined anti-Fas-mediated apoptosis of thyrocytes. Fas expression on thyrocytes was significantly down-regulated by Graves' IgG and TSH, although idiopathic myxoedema IgG did not affect Fas expression on thyrocytes. Idiopathic myxoedema IgG abrogated the effect of TSH on both cAMP production and inhibition of Fas expression on thyrocytes. Treatment of thyrocytes with IL-1β or IFN-γ caused a marked augmentation of Fas expression on thyrocytes. The increase of Fas expression of thyrocytes induced by IL-1β or IFN-γ was significantly suppressed in the presence of TSH or Graves' IgG. Anti-Fas-induced apoptosis of thyrocytes was observed in thyrocytes treated with IL-1β or IFN-γ, but was markedly inhibited in the presence of TSH or Graves' IgG. Furthermore, idiopathic myxoedema IgG abrogated most of the inhibitory effect of TSH on Fas-mediated apoptosis of thyrocytes treated with IL-1β or IFN-γ. Bcl-2 expression of thyrocytes did not change after stimulation with TSH, Graves' IgG, idiopathic myxoedema IgG, IL-1β or IFN-γ. These results suggest that TSAb found in Graves' patients may be potentially involved in the development of goitre by inhibition of Fas-mediated apoptosis of thyrocytes. In addition, TSBAb inhibit the action of TSH and increase the sensitivity toward Fas-mediated apoptosis of thyrocytes, inducing thyroid atrophy seen in patients with idiopathic myxoedema.     

Autonomic Nervous System Function and Essential Hypertension: Individual Response Specificity With and Without Beta-Adrenergic Blockade

The aim of the present research was to study individual response specificity in 22 male patients having essential hypertension (HT) and to compare these patients with age-matched male normotensive controls (NT). Four stimuli, letter identification, mental arithmetic, cold pressor and isometric exercise, were administered while recordings were made of: systolic and diastolic blood pressures, heart rate, respiration, forearm and hand blood flows, and skin conductance level and fluctuations. After each session urine samples were collected and epinephrine and norepinephrine levels were analyzed. Twelve subjects in the HT group were given beta-adrenergic blocking agents and retested 1 to 21 months (X?= 12 months) after the first session. Each response was standardized, using NT as the reference group. Intraclass correlations were computed to evaluate whether HT males reacted with a more consistent hierarchy of responses than did NT. Intraclass correlations were significantly higher among the patients than in the control group, regardless of whether the blood pressure response was included or excluded in the computation of the intraclass correlations. Thus, we conclude that male HT patients show more individual response specificity than NT controls. Beta-adrenergic receptor antagonists reduced levels of cardiovascular activity and attenuated reactivity but did not affect amount of specificity. Thus, intraclass correlations provide unique and useful information, since they are not related to blood pressure reactivity or to urinary catecholamine levels, nor affected by beta-adrenergic blockade.