PubMed · 4452162
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A Valík. 1974. [Acetonemic vomiting].. https://pubmed.ncbi.nlm.nih.gov/4452162/
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BACKGROUND: We previously demonstrated that coronary arteriolar dilation in response to acidosis is mediated by the opening of ATP-sensitive potassium (KATP) channels. However, the signal transduction involved in the KATP-channel activation during acidosis has not been elucidated. A recent study in cardiac myocytes implied that pertussis toxin (PTX)-sensitive G proteins may be involved in the signal transduction for KATP-channel activation. However, it remains unclear whether this transduction process also occurs in the vascular tissue and, in particular, whether it exerts functional dilation in response to acidosis. METHODS AND RESULTS: To examine the signaling pathway for acidosis-induced dilation, porcine coronary arterioles were isolated, cannulated, and pressurized for in vitro study. The GTPase activity in reconstituted G proteins was examined at different levels of pH. Extravascular acidosis (pH 7.3 to 7.0) produced a graded dilation of coronary arterioles. This dilation was not affected by removal of endothelium but was significantly attenuated after inhibition of KATP channels and G proteins by glibenclamide and PTX, respectively. Glibenclamide and PTX attenuated the acidosis-induced arteriolar dilation to the same extent, and combined administration of both inhibitors did not further inhibit the vasodilation. These results indicated that both inhibitors act on the same vasodilatory pathway. Furthermore, vasodilation of coronary arterioles to the KATP-channel opener pinacidil and to the endothelium-independent vasodilator sodium nitroprusside was not affected by PTX. Because PTX inhibited acidosis-induced vasodilation without inhibiting KATP-channel function, it is suggested that PTX inhibits the vasodilatory pathway upstream from KATP channels. GTPase activity in reconstituted G proteins was significantly enhanced by a reduction in pH, indicating that G proteins were directly activated by acidosis. CONCLUSIONS: On the basis of these findings, we conclude that acidosis-induced coronary arteriolar dilation is mediated by the opening of smooth muscle KATP channels through the activation of PTX-sensitive G proteins.
The objectives of urinary diversion are expanding from merely preserving kidney functions to enabling the patient to have a good quality of life while maintaining an acceptable certain body image. During the new era of continent urinary diversion the psychological drawbacks of noncontinent skin stoma in young adolescents cannot be overlooked. Ureterosigmoidostomy has been the technique of choice for continent urinary diversion in bladder extrophy patients when bladder reconstruction is not feasible or has failed. Although it provides a good daytime continence it is associated with a high rate of nighttime incontinence and delayed complications of pyelonephritis and hyperchloremic acidosis. We managed five male bladder extrophy patients with noncontinent skin stoma (sigmoid colon conduit in three and ileal conduit in two) including two patients who had previously had complicated classic ureterosigmoidostomy. They underwent urinary undiversion to the valved and augmented rectum (three patients) and the valved S-shaped rectosigmoid pouch (two patients) with some modifications. The conduit was used in the construction, and the ureters were implanted behind an isolated intussusception ileal nipple valve. Tube cecostomy and total parenteral nutrition was used for 7 to 10 days instead of a temporary defunctioning transverse colostomy. With a mean follow-up of 19.8 months (range 9-36 months) all the patients are fully continent during the day and night, with an emptying intervals of 3 to 6 hours. Follow-up intravenous pyelography and renal scans revealed improvement or stabilization of the function and configuration of the upper tracts in all renal units. No prophylactic alkali therapy was given. No clinical evidence of acidosis or symptomatic urinary tract infection was observed. Modified ureterosigmoidostomy is a good alternative for continent urinary undiversion even in those who have previously had complicated classic ureterosigmoidostomy. Our modification of using tube cecostomy and parenteral nutrition instead of a temporary transverse colostomy warrants attention; it made the technique simpler and more attractive.
OBJECTIVES: The study's objectives were to verify a threshold value for fetal arterial oxygen saturation as the critical boundary for fetal compromise during labor and to investigate a method of predicting acidosis caused by hypoxemia. STUDY DESIGN: In a multicenter study involving 3 German obstetric centers, a total of 400 deliveries were monitored by fetal pulse oximetry (Nellcor-Puritan-Bennett Model N-400 Oxygen Saturation Monitor and FS-14 Sensor; Nellcor, Inc, Pleasanton, Calif). The durations of low (</=30%), medium (31%-60%), and high (>60%) fetal arterial oxygen saturations during the measurement were compared between neonates with a pH <7.15 versus >/=7.15 and a base excess <-12 mmol/L versus >-12 mmol/L in the umbilical artery post partum and in neonates with an Apgar score <7 versus >/=7 by Mann-Whitney U test. In 121 of the pulse oximetry measurements the durations of low, medium, and high fetal arterial oxygen saturations were measured from one fetal scalp blood sampling to the next and correlated with the change of scalp blood pH between samplings. Multiple regression analysis was performed to estimate the expected change of pH between 2 fetal scalp blood samplings, and receiver operating characteristic analysis was done to define a minimum duration of low fetal arterial oxygen saturation values to exclude or predict a significant decline of pH. RESULTS: Neonates with a 1-minute Apgar score <7 differed from those with 1-minute Apgar score >/=7 significantly in the duration of low fetal arterial oxygen saturation but not in the durations of medium and high fetal arterial oxygen saturations. The duration of low fetal arterial oxygen saturation had been significantly longer in children with pH <7.15 or base excess <-12 mmol/L in the umbilical artery compared with those with a pH >/=7.15 or base excess >/=-12 mmol/L. The duration of high fetal arterial oxygen saturation was significantly shorter for children with a pH <7.15 or base excess <12 mmol/L than for those with a pH >/=7.15 or base excess >/=12 mmol/L. There was no difference in the groups with respect to the duration of medium fetal arterial oxygen saturation values. The duration of low fetal arterial oxygen saturation proved to be the best predictor of a decline of scalp pH between 2 fetal scalp blood samples. The pH declined significantly with a longer duration of low fetal arterial oxygen saturation (0.02 per 10 minutes). No decrease of pH by more than 0.05 was observed unless fetal arterial oxygen saturation had remained at </=30% for >/=10 minutes. CONCLUSION: An arterial oxygen saturation of 30% was confirmed as the critical boundary for fetal compromise during labor. The development of acidosis seems to be predictable by the duration of hypoxemia, as indicated by fetal arterial oxygen saturation </=30%.