Effects of shortening the steeplechase phase (phase B) of a 3-day-event

Thirty-four horses competing in the Endurance Test of a 3-day-event were divided into 3 groups: horses in Group 1 (n = 15) competing in a 3.5 min steeplechase phase; horses in Group 2 (n = 13) in a 3 min steeplechase phase (Phase B) and horses in Group 3 (n = 6) in a 2.5 min steeplechase phase. The shortening of Phase B was associated with a lengthening of Phase C so that the total distance of the event for all horses was 14,940 m. Bodyweight (BW) was measured and total body water (TBW) and water loss estimated. Blood samples were collected from the horses prior to the Endurance Test, at the end of Phase B, the 4 km marker on Phase C (C4K), the end of Phase C, and 20 min after the completion of Phase D for measurement of packed cell volume (PCV), total plasma protein [TPP], lactate, ionised calcium, pH, sodium, potassium, chloride, total calcium and glucose concentrations, and aspartate aminotransferase, creatine kinase and lactate dehydrogenase activities. Mean +/- s.d. ambient environmental temperature during the Endurance Test was 25.3 +/- 1 degrees C (range 20.3 degrees C-29.7 degrees C). Mean relative humidity was 43.8 +/- 2.4% (range 39%-48.6%) and the average 'comfort index' (CI) was 121. There were no significant differences between the groups competing in the Endurance Test, despite the shorter Phase B. However, there were significant decreases in BW, TBW, net exchangeable cations, chloride, ionised calcium, and pH. The sodium and total calcium concentrations remained at near pre-event values. The PCV, TPP, lactate, potassium, glucose, aspartate aminotransferase, and lactate dehydrogenase activity increased during the Endurance Test, when compared to pre-event values. Horses competing in this competition experienced significant fluid and electrolyte losses, reduced glomerular filtration, increased glycogenolysis and had significant leakage of enzymes from working muscles during competition. These changes could not be reduced by shortening Phase B and lengthening Phase C.     

Regulation of catch muscle by twitchin phosphorylation: effects on force, ATPase, and shortening

Recent experiments on permeabilized anterior byssus retractor muscle (ABRM) of Mytilus edulis have shown that phosphorylation of twitchin releases catch force at pCa > 8 and decreases force at suprabasal but submaximum [Ca2+]. Twitchin phosphorylation decreases force with no detectable change in ATPase activity, and thus increases the energy cost of force maintenance at subsaturating [Ca2+]. Similarly, twitchin phosphorylation causes no change in unloaded shortening velocity (Vo) at any [Ca2+], but when compared at equal submaximum forces, there is a higher Vo when twitchin is phosphorylated. During calcium activation, the force-maintaining structure controlled by twitchin phosphorylation adjusts to a 30% Lo release to maintain force at the shorter length. The data suggest that during both catch and calcium-mediated submaximum contractions, twitchin phosphorylation removes a structure that maintains force with a very low ATPase, but which can slowly cycle during submaximum calcium activation. A quantitative cross-bridge model of catch is presented that is based on modifications of the Hai and Murphy (1988. Am. J. Physiol. 254:C99-C106) latch bridge model for regulation of mammalian smooth muscle.     

Acid-base balance in chronic peritoneal dialysis patients

Endogenous acid production has never been measured directly in dialysis patients and an empiric formula is used to estimate acid production from their protein catabolic rate. We have studied acid-base balance in 19 stable CAPD patients attending the peritoneal dialysis clinic of Mount Sinai Hospital. They obtained a 24 hour collection of peritoneal dialysis fluid and urine while consuming their usual diet and performing their usual activities. Total alkali gain was calculated from net GI alkali absorption plus urinary net acid excretion plus alkali gain from dialysate, while total acid production was measured directly from the urinary and dialysate excretions of sulfate and organic anions. Net GI alkali absorption was estimated from the difference between cations (Na + K+Ca + Mg) and anions (Cl + 1.8P) in the 24 hour dialysate and urine collections minus the daily total amount of lactate infused. All of our patients had a normal or high serum bicarbonate concentration, which was stable with time. Total alkali gain was virtually identical to total acid production (54.2 vs. 52.4 mEq/day) which suggests that these patients were in neutral acid-base balance. Net GI alkali absorption (22.7 mEq/day) was one of the same range as that of chronic renal failure patients not on dialysis and represented almost one half of the total daily alkali gain. The daily acid production of 52.4 mEq/day was numerically equal to 84% of the protein catabolic rate expressed as g/day, which is similar to the predicted value of 77% of PCR reported in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)     

Renal effects of angiotensin converting enzyme inhibitors in heart failure: a clinician's guide to minimizing azotemia and diuretic-induced electrolyte imbalances

Angiotensin converting enzyme (ACE) inhibitors have proved to be valuable, life-saving medications in the management of heart failure. While reducing myocardial oxygen consumption, they increase cardiac output and thus renal plasma flow. Despite reports in the literature of adverse effects of these drugs on renal function, the risks of functional deterioration are predictable in patient populations and remediable. Patients at greatest risk of declining renal function during therapy with ACE inhibitors are those in whom maintenance of renal function is dependent on angiotensin II. Reducing the dose of the concomitant diuretic, liberalizing the dietary intake of sodium, and increasing the dose of the ACE inhibitor usually restores renal function to baseline. In patients with severe renal insufficiency, reducing the dose of the ACE inhibitor might be necessary to preserve the glomerular filtration rate.     

酸碱滴定法快速测定硼铁中硼

试样以过氧化钠熔融分解后,用热水浸取,加热煮沸除尽H2O2,定容后过滤铁等干扰元素沉淀与硼分离,滤液中铝元素影响硼的分析,加碳酸钙沉淀分离,以对硝基酚为指示剂,用盐酸滴定至中性。加入甘油与硼酸生成酸性较强的甘油硼酸,以酚酞为指示剂,用氢氧化钠标准溶液滴定硼酸,取得了满意的结果。     

萃余水相中环烷酸的容量法测定

研究了用磺化煤油萃取分离富集溶解在萃余水相中的环烷酸 ,然后用 KOH-乙醇标准溶液滴定测定萃余水相中环烷酸的质量浓度 ,籍此建立了一种简便、准确、快速、实用的环烷酸分析方法。本方法与分光光度法比较 ,分析结果相吻合 ,相对误差 <± 5%。     

酸碱滴定法快速测定硅锰铝合金中硅

利用氟硅酸钾溶解于沸水中生成氢氟酸的原理。试样以硝酸、氢氟酸溶解，硅转化为硅氟酸，加入硝酸钾生成氟硅酸钾沉淀。经过滤、洗涤沉淀中的游离酸后，溶解于中性沸水中，生成氢氟酸，以溴麝香草酚蓝为指示剂，用氢氧化钠标准溶液滴定游离出的氢氟酸，借此测定硅锰铝合金中硅含量，其相对标准偏差小于0．0796％。