Method-specific reference intervals for serum anion gap and osmolality.

While it is known that treatment with insulin-like growth factor I (IGF-I) stimulates growth of the fetal kidney, nothing is known about the short term or long term effects of IGF-I on fetal renal function. To investigate the acute effects of IGF-I on fetal renal function and on the activity of the fetal renin-angiotensin system, studies were carried out in 12 chronically catheterized fetal sheep aged 120 +/- 1 days, before and during a 4 h I.V. infusion of IGF-I at 80 ug h-1. Seven control fetuses were infused over the same period with vehicle (0.1% bovine serum albumin in 0.15 M saline). IGF-I infusion increased plasma IGF-I concentrations by about 80%. There was a small fall in arterial PO2 (P < 0.01), arterial PCO2 increased (P < 0.05), plasma lactate levels increased (P < 0.01) and arterial pH fell (P < 0.05). Fractional bicarbonate reabsorption increased and bicarbonate excretion decreased (P < 0.05). Infusions of IGF-I had no sustained effect on fetal arterial pressure. Glomerular filtration rate (GFR) did not change significantly during IGF-I infusion, but renal blood flow (RBF) fell (P < 0.05). Therefore filtration fraction relative to control values increased (P < 0.05), suggesting that efferent arteriolar vasoconstriction had occurred. IGF-I infusion led to an antidiuresis (P < 0.01), a rise in urinary osmolality (P < 0.05) and a fall in free water clearance (P < 0.01). Since fetal PO2 fell, it is probable that these effects were mediated by arginine vasopressin. The excretion rates of sodium, chloride and phosphate were all reduced by 4 h of infusion (P < 0.05), because their fractional reabsorption rates were all increased (sodium, P < 0.01; chloride, P < 0.01; and phosphate, P < 0.05). Plasma renin concentration increased by 275 +/- 52% during infusion of IGF-I (P < 0.005). Plasma renin activity also increased (P < 0.005), while circulating angiotensinogen concentrations fell (P < 0.05). In the adult, IGF-I increases both RBF and GFR, enhances tubular reabsorption and stimulates the renin-angiotensin system. In the fetus, however, it decreased RBF and had no effect on GFR, but was associated with enhanced tubular function and intense stimulation of renin secretion. Some of these effects of IGF-I on fetal renal function may be involved in maturation of the kidney in preparation for life after birth.

Acid-Base Equilibrium↗

PubMed2001

Exercising skeletal muscle blood flow in humans responds to reduction in arterial oxyhaemoglobin, but not to altered free oxygen.

We hypothesised that reducing arterial oxyhaemoglobin (O2Hba) with carbon monoxide (CO) in both normoxia and hyperoxia, or acute hypoxia would cause similar compensatory increases in human skeletal muscle blood flow and vascular conductance during submaximal exercise, despite vast differences in arterial free oxygen partial pressure (Pa,O2). Seven healthy males completed four 5 min one-legged knee-extensor exercise bouts in the semi-supine position (30 +/- 3 W, mean +/- S.E.M.), separated by approximately 1 h of rest, under the following conditions: (a) normoxia (O2Hba = 195 ml l-1; Pa,O2 = 105 mmHg); (b) hypoxia (163 ml l-1; 47 mmHg); (c) CO + normoxia (18% COHba; 159 ml l-1; 119 mmHg); and (d) CO + hyperoxia (19% COHba; 158 ml l-1; 538 mmHg). CO + normoxia, CO + hyperoxia and systemic hypoxia resulted in a 29-44% higher leg blood flow and leg vascular conductance compared to normoxia (P < 0.05), without altering blood pH, blood acid-base balance or net leg lactate release. Leg blood flow and leg vascular conductance increased in association with reduced O2Hba (r2 = 0.92-0.95; P < 0.05), yet were unrelated to altered Pa,O2. This association was further substantiated in two subsequent studies with graded increases in COHba (n = 4) and NO synthase blockade (n = 2) in the presence of normal Pa,O2. The elevated leg blood flow with CO + normoxia and CO + hyperoxia allowed a approximately 17% greater O2 delivery (P < 0.05) to exercising muscles, compensating for the lower leg O2 extraction (61%) compared to normoxia and hypoxia (69%; P < 0.05), and thereby maintaining leg oxygen uptake constant. The compensatory increases in skeletal muscle blood flow and vascular conductance during exercise with both a CO load and systemic hypoxia are independent of pronounced alterations in Pa,O2 (47-538 mmHg), but are closely associated with reductions in O2Hba. These results suggest a pivotal role of O2 bound to haemoglobin in increasing skeletal muscle vasodilatation during exercise in humans.

Acid-Base Equilibrium↗

PubMed2001

Gastric air tonometry during laparoscopic cholecystectomy: a comparison of two PaCO2 levels.

PURPOSE: Pneumoperitoneum can cause disturbances in acid-base balance and splanchnic perfusion. We studied the effect of ventilation on acid-base balance and gastric mucosal tonometric values in patients undergoing laparoscopic cholecystectomy. METHODS: Twenty-four patients (ASA I-II) were randomly allocated into two groups. In the fixed ventilation group, ventilation was constant allowing free increase in PCO2, while in the constant CO2 group end-tidal PCO2 was fixed with ventilatory adjustment. Intraabdominal pressure was limited to 12 mmHg. Arterial acid-base balance, automated air tonometric variables and gastric mucosal to arterial PCO2 gap were determined frequently from anesthesia induction until three hours postoperatively. RESULTS: During pneumoperitoneum, in the fixed ventilation group arterial PCO2 changed from 5.0 +/- 0.2 to 6.6 +/- 0.4 kPa and pH from 7.43 +/- 0.03 to 7.33 +/- 0.04, tonometric PCO2 from 5.1 +/- 0.5 to 6.9 +/- 0.4 and pH from 7.44 +/- 0.04 to 7.33 +/- 0.04. In the constant CO2 group these variables remained at control levels (P < 0.01 between groups). The PCO2 gap remained unchanged without any differences between the groups. In the recovery room all measured variables were within normal range in both groups. CONCLUSION: Despite inter-group differences in arterial and tonometric PCO2 and pH values during CO2 pneumoperitoneum, the patients did not develop splanchnic hypoperfusion detectable by air tonometric method, as indicated by normal PCO2 gap in both groups throughout the study.

Acid-Base Equilibrium↗