妊娠期肾绞痛的诊疗分析

目的 提高妊娠期肾绞痛的诊断与治疗水平。方法 结合国内外文献,对48例首诊为妊娠期肾绞痛患者的临床资料进行回顾性分析。结果 B超发现肾积水伴输尿管结石21例,其中1例双侧输尿管结石;B超发现肾积水但未发现输尿管结石27例,其中1例首诊误诊为妊娠期肾绞痛,妊娠晚期剖宫产证实为右卵巢畸胎瘤不完全蒂扭转并卵巢部分坏死行卵巢部分切除术。35例行保守治疗有效;1例肾积水进展者、1例双输尿管结石伴双肾积水者、1例肾积脓者及9例顽固性肾绞痛者行Double J(D-J)管置入术;1例重度肾积水者行经皮肾造瘘(Percutaneous Nephrostomy, PCN)术。47例安全顺利分娩或剖宫产,1例早产。结论 妊娠期肾绞痛的诊断具有挑战性,须严格排除其他急腹症。保守治疗对大部分患者有效,但需随访肾积水进展;保守治疗无效时,D-J管置入术是一种安全、简单、有效的治疗方法。     

Distinct regulations by calcium of cyclic GMP levels and catecholamine secretion in isolated bovine adrenal chromaffin cells

The effects of various calcium-dependent secretagogues on cyclic GMP levels and catecholamine (CA) secretion were measured in a preparation of bovine adrenal chromaffin cells. The secretory effect of acetylcholine (ACh; 8--10 fold stimulation) was mimicked by nicotine but not muscarine. Three--five fold stimulations of cyclic GMP levels were also obtained with ACh and muscarine but not nicotine. High concentration of K+, and the ionophore A23187, also elevated cyclic GMP levels. However, secretion produced by veratridine, ouabain, and the ionophore X537A was not accompanied by any rise in cyclic GMP levels. Removal of extracellular calcium significantly decreased both basal levels of CA secretion and of cyclic GMP and completely abolished their stimulation by ACh. The half-maximal effects of calcium on the cholinergic stimulations of cyclic GMP levels and of CA secretion were observed at 0.2 and 2.5 mM, respectively. Substitution of Ca2+ by Sr2+ was more effective in maintaining the cyclic GMP response than the secretory response. The calcium channel blockers Co2+, Mg2+ and Ni2+ inhibited the cholinergic stimulation of cyclic GMP more than that of CA release. On the other hand, the organic calcium channel blockers, verapamil and methoxyverapamil (D--600) were more effective antagonists of the secretory response. These data indicate that the cholinergic stimulations of CA secretion and of cyclic GMP levels in bovine adrenal chromaffin cells are regulated by calcium via two distinct mechanisms.     

Effect of afterload reduction on plasma volume during acute heart failure

Previous investigations in our unit indicated that acute cardiogenic pulmonary edema is associated not only with an increase in left ventricular end-diastolic pressure and pulmonary arterial wedge pressure but also with a relative increase in colloid osmotic (oncotic) pressure and peripheral hemoglobin concentration. This combination of changes suggested that acute congestive heart failure with pulmonary edema, unlike chronic congestive heart failure, is associated with a contraction of intravascular blood volume. In this study, plasma volume changes were measured before and during the treatment of acute cardiogenic pulmonary edema in 14 patients with arteriosclerotic heart disease. The plasma volume measurement in all 14 patients before the initiation of treatment was either normal or decreased. After treatment with the alpha adrenergic blocking agent phentolamine, the plasma volume increased rather than decreased when measured 4 and 12 hours after the initiation of treatment. During this time colloid osmotic pressure and peripheral hemoglobin concentration progressively decreased. These findings suggest that acute cardiogenic pulmonary edema is associated with the extravasation of large quantities of plasma water from the intravascular compartment into the interstitial compartment and contraction of the intravascular plasma volume. The treatment of acute cardiogenic pulmonary edema is associated with the return of hypo-oncotic fluid from the interstitial compartment back into the intravascular compartment with expansion of plasma volume and reduction of colloid osmotic pressure and hemoglobin concentration.     

Atherosclerotic ulcerative disease and associated aneurysms of the coronary arteries.

Abnormal cardiac muscle function has been reported in experimental diabetes mellitus from this laboratory. To examine left ventricular performance in diabetic patients without clinical evidence of myocardial ischemia or other cardiovascular disease, a noninvasive measurement of the systolic time intervals was carried out. Simultaneous recordings of the electrocardiogram, heart sounds, and carotid pulse were made in 25 diabetic subjects, 20 to 56 years of age, and compared with 37 normal subjects. The diabetic subjects had a shorter left ventricular ejection time, longer pre-ejection period, and a higher ratio of pre-ejection period/left ventricular ejection time (P < 0.001). The isovolumic time was prolonged (P < 0.001), while heart rate and arterial pressure were within normal limits. Abnormal function was independent of apparent duration and treatment by diet alone, insulin, or hypoglycemic agents. On the basis of available morphologic data in human and canine diabetes, an alteration of the myocardial interstitium may be the basis for this preclinical abnormality in diabetic patients.     

Macromolecular dispersion of human plasma low-density lipoproteins in hyperlipoproteinemia.

Low-density lipoprotein (LDL) has previously been reported to exist in either a polydisperse or a monodisperse state. Using the techniques of analytical velocity sedimentation and/or equilibrium density-gradient ultracentrifugation, the macromolecular dispersion of LDL has been investigated in 139 subjects classified by their lipoprotein phenotypes as follows: 63 normal, 25 type IIA, 6 type IIB, and 45 type IV. LDL polydispersion was found in 78% of subjects with hypertriglyceridemia (type IIB or IV phenotypes), while only 9% of normotriglyceridemic subjects had polydisperse LDL. A study of LDL dispersion in two families, one with hyperpreβ-lipoproteinemia and one with combined hyperlipoproteinemia, also demonstrated the frequent association of LDL polydispersity with increased plasma very low density lipoprotein (VLDL) concentrations. LDL polydispersion results from the presence of higher molecular weight, lipid-enriched lipoproteins of the LDL class. Among hyperlipoproteinemic subjects with a type IV phenotype and with polydisperse LDL, the concentrations of these higher molecular weight subspecies of LDL appear to increase with severity of the hyperlipemia. In 6 subjects, reduction of VLDL concentration resulted in a decrease in the concentration of the higher molecular weight LDL; however, LDL remained polydisperse. By contrast, approximately one-third of subjects with hypertriglyceridemia were observed to have monodisperse LDL, even in the presence of high VLDL concentrations. This observation raises the possibility of two separate populations of subjects with hypertriglyceridemia arising from increased VLDL concentration.     

Clinical and electrophysiologic assessment of oral flecainide acetate for recurrent ventricular tachycardia: Evidence for exacerbation of electrical instability

Four patients with recurrent, symptomatic ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents were given flecainide acetate to control arrhythmias. Ventricular stimulation studies were performed in all patients before and 1 to 2 weeks after initiation of oral flecainide therapy. Before flecainide, all patients had easily inducible VT that was morphologically identical to their spontaneously occurring arrhythmia. Flecainide increased the mean PR interval (from 0.17 to 0.23 second), mean QRS duration (from 0.08 to 0.12 second) and mean ventricular effective refractory period (from 235 to 270 ms). Mean corrected QT interval did not change (0.51 second).In 2 patients, VT could not be induced during follow-up stimulation studies. One patient has been treated successfully for 10 months, with no clinically apparent episodes of VT. One patient had recurrent nonsustained VT and was withdrawn from the study as a treatment failure after 6 months of therapy. Two patients had inducible, polymorphous VT that degenerated into ventricular fibrillation that required 2 countershocks before the successful restoration of sinus rhythm. One of these patients had VT stimulation by atrial pacing at a cycle length of 320 ms in the postflecainide electrophysiologic study. VT was not inducible by atrial pacing during this patient's preflecainide study.Thus, sustained oral flecainide administration may precipitate serious electrical instability in susceptible patients, and ventricular stimulation studies and other clinical variables may be useful in selecting patients with recurrent VT who may benefit or may be endangered by oral flecainide therapy.     

Plasma lipid alterations in leukemia and lymphoma

Plasma lipids and lipoproteins were studied at presentation in 25 patients with acute leukemia and non-Hodgkin's lymphoma. All patients demonstrated an abnormality in at least one plasma lipid fraction, and most exhibited a predictable pattern of lipid alterations that consisted of extremely low levels of high-density lipoprotein cholesterol (median [Xm] = 23), elevated triglyceride (Xm =165) and elevated very-low-density lipoprotein (Xm = 26). Patients restudied during remission demonstrated a return to normal values. The degree of lipid abnormality was directly related to the underlying tumor burden and particularly to the presence of bone marrow involvement. However, even patients with minimal tumor bulk demonstrated plasma lipid abnormalities. The results suggest that an abnormality in systemic lipid metabolism, possibly in triglyceride clearance, is present in these patients and that its incidence in this population is high.