Indwelling Arterial Catheter Research Articles

Control of rectal gland secretion by blood acid–base status in the intact dogfish shark (Squalus acanthias)

In order to address the possible role of blood acid-base status in controlling the rectal gland, dogfish were fitted with indwelling arterial catheters for blood sampling and rectal gland catheters for secretion collection. In intact, unanaesthetized animals, isosmotic volume loading with 500 mmol L-1 NaCl at a rate of 15 mL kg-1 h-1 produced a brisk, stable rectal gland secretion flow of about 4 mL kg-1 h-1. Secretion composition (500 mmol L-1 Na+ and Cl-; 5 mmol L-1 K+; <1 mmol L-1 Ca2+, Mg2+, SO(4)2-, or phosphate) was almost identical to that of the infusate with a pH of about 7.2, HCO3- mmol L-1<1 mmol L-1 and a PCO2 (1 Torr) close to PaCO2. Experimental treatments superimposed on the infusion caused the expected disturbances in systemic acid-base status: respiratory acidosis by exposure to high environmental PCO2, metabolic acidosis by infusion of HCl, and metabolic alkalosis by infusion of NaHCO3. Secretion flow decreased markedly with acidosis and increased with alkalosis, in a linear relationship with extracellular pH. Secretion composition did not change, apart from alterations in its acid-base status, and made negligible contribution to overall acid-base balance. An adaptive control of rectal gland secretion by systemic acid-base status is postulated-stimulation by the "alkaline tide" accompanying the volume load of feeding and inhibition by the metabolic acidosis accompanying the volume contraction of exercise.

Oscillometric blood pressure measurement used for calibration of the arterial tonometry method contributes significantly to error

We have investigated the accuracy of the Colin tonometry module, a non-invasive alternative to intra-arterial blood pressure (BP) measurement. The claims of previous publications range between good agreement to significant discrepancies between the Colin tonometry and intra-arterial methods. The Colin method relies on calibration of the tonometry module using an oscillometric method. Our aim was to look at the effect of this calibration on the accuracy. Ten conscious patients who already had an indwelling arterial catheter were studied. The Colin monitor was set to perform ten calibration cycles first with the oscillometric cuff on the same arm as the tonometry module and secondly on the opposite arm. Simultaneous recording of BP wave forms from the intra-arterial BP transducer and the Colin monitor allowed comparison of beat-by-beat systolic, diastolic and mean BP. There was considerable inter- and intra-patient variation. In the worst case, the error range was 41 mmHg over ten calibrations. Analysis of variance showed that contra- and ipsilateral calibrations gave a significantly different bias while the multiple calibrations accounted for a significant proportion of the variability in systolic BP error. The Colin Tonometry method is not accurate enough to be used with confidence in clinical practice. The main reason for this is its reliance on an oscillometric method for calibration of the tonometry module. Single BP measurements, using either manual or semiautomatic instruments may vary considerably from the 'true' BP due to short-term perturbations of BP.

Comparative analysis of haematological, haemostatic, and inflammatory parameters in canine venous and arterial blood samples

The objective of the present study was to validate the use of blood collected from an indwelling arterial catheter for analysis of haematological, coagulation and inflammatory parameters in canines compared to venous blood collected directly from the jugular vein. Blood samples were collected from 11 dogs. Agreement between sampling methods was found for neutrophil and monocyte counts, prothrombin time, activated partial thromboplastin time, antithrombin, protein C, factor VIII and C-reactive protein, whereas a statistically significant difference was found for white blood cells, lymphocyte, erythrocyte and platelet counts, haemoglobin, haematocrit, fibrinogen and thrombin time (TT). In conclusion, it is necessary to be aware that results from a complete blood count obtained from canine venous and arterial blood samples may not be comparable. Values for haemostatic parameters from arterial and venous blood samples, with the exception of fibrinogen and TT, were however statistically identical.

Arterial thromboembolic complications in critically ill children

Purpose To evaluate incidence and characteristics of arterial thromboembolic complications in critically ill children. Materials and Methods Hospital records of all consecutive patients with arterial thromboembolic events (ATEs) occurring in the pediatric intensive care unit (PICU) from January 1997 to August 2001 were reviewed. Data collected included demographics and location, treatment modalities and outcome of ATEs. Results Fifty-four ATEs in 51 children (median age, 14 days) were identified, reflecting an incidence of 1.2% of all PICU patients. Arterial thromboembolic events were located in peripheral arteries in 52 (96%) cases and were associated with indwelling arterial catheters (n = 26) or cardiac catheterization (n = 26). The remaining 2 ATEs were located in the left ventricle and cerebral arteries, respectively. Therapy consisted of heparin (n = 51), thrombolysis (n = 22), oral anticoagulation (n = 12), and aspirin (n = 34). Complete resolution was noted in 33 (70%), partial resolution in 10 (21%), and no resolution in 4 (8.5%) cases. Bleeding complications occurred in 1 patient treated with heparin and in 12 (54%) of the 22 patients receiving thrombolytic therapy. Conclusions Arterial thromboembolic events are frequent complications of PICU, particularly affecting neonates, and mostly associated with catheters. Studies to determine safe and effective prophylactic and treatment modalities of ATEs in children are required.

Influence of elevated renin substrate on angiotensin II and arterial blood pressure in conscious mice

The present experiments were performed to determine the influence of intravenous administration of renin substrate on plasma angiotensin II levels and mean arterial blood pressure in conscious C57BL/6J mice. Mice with chronic indwelling femoral arterial and venous catheters were acutely or chronically administered intravenous doses of a synthetic peptide corresponding to the 14 amino acids on the N-terminal of angiotensinogen. A dose-dependent increase in arterial blood pressure was observed as the intravenous bolus dose of the renin substrate was increased from 0.18 to 180 nmol kg(-1) with a maximal increase in pressure of 40 +/- 3 mmHg achieved following administration of the 18 nmol kg(-1) bolus (n = 11). Additional experiments demonstrated that a sustained intravenous infusion of the renin substrate led to a long-term increase in arterial blood pressure. The continuous infusion of renin substrate at 0.05 nmol kg(-1) min(-1) for 3 days did not alter arterial blood pressure from the control level of 119 +/- 5 mmHg (n = 5); however, arterial blood pressure significantly increased to 129 +/- 6 mmHg with an infusion rate of 0.5 nmol kg(-1) min(-1) and further increased to 141 +/- 3 mmHg when the renin substrate infusion was increased to 5.0 nmol kg(-1) min(-1). Finally, the infusion of renin substrate at 5.0 nmol kg(-1) min(-1) resulted in a significant increase in plasma angiotensin II concentration from 34 +/- 6 pg ml(-1) in vehicle-infused mice to 288 +/- 109 pg ml(-1). These results demonstrate that modulation of the circulating level of angiotensinogen can alter the plasma angiotensin II level and arterial blood pressure in normal animals.

The renal medullary circulation and nitric oxide in hyperinsulinemic-hypertensive rats

1. Insulin resistance may play a role in hypertensive patients. The renal medullary blood flow (MBF) is thought to be an important component of blood pressure and sodium balance. Nitric oxide (NO) activity within the renal medulla is the primary characterized factor in the maintenance of MBF and plays an important role in the pressure-natriuresis response. Because MBF, which is strongly influenced by the NO system, is thought to be an important component of blood pressure and sodium balance, we focused on MBF in hypertension being secondary in the development of insulin resistance. This study was designed to test the hypotheses that the MBF will be decreased and to determine the gene expression of three nitric oxide synthases (eNOS, nNOS, iNOS) in obese zucker rats (OZ). 2. 8–9 weeks male OZ and lean zucker rats (LZ) were divided into two group: Group1; OZ (n=7). Group2; LZ (n=7). Renal hemodynamic study; Each rat was instrumented with indwelling arterial and venous catheters. The tip of the arterial catheter was advanced to just below the level of left renal artery to permit continuous measurement of renal arterial pressure (RAP). For measurement of changes in renal cortical blood flow (CBF) and MBF in rats by laser-Doppler flowmetry, the optical fibers were implanted 2mm beneath the surface of the renal cortex to measure the net flux of red blood cells in the cortex and 6mm deep to monitor changes in the outer medulla. The RAP was adjusted from 160 to 80 mmHg with the use of balloon cuff. Gene expression study; We developed real-time RT-PCR that allows to absolutely quantify the gene expression of eNOS, nNOS, and iNOS in cortex and medulla of rat kidney using the standard curve and delta CT methods. 3. MAP was significantly increased in OZ. MBF was also significantly lower in OZ across a wide range of RAP without the significant change of CBF. The mRNA expression of eNOS and nNOS in renal medulla, which were significantly increased to a greater extent compared in renal cortex, were decreased in OZ compared in LZ. 4. MBF plays an important role in the development of hypertension in OZ. It seems reasonable to suppose that an impaired NO system could contribute to reduced MBF and sodium excretion, which would result in the development of hypertension in insulin resistance.

Antioxidant Treatment Prevents Renal Damage and Dysfunction and Reduces Arterial Pressure in Salt-Sensitive Hypertension

The goal of this study was to test the hypothesis that oxidative stress in Dahl salt-sensitive (SS) rats on a high-sodium intake contributes to the progression of renal damage, the decreases in renal hemodynamics, and the development of hypertension. We specifically studied whether antioxidant therapy, using vitamins C and E, could help prevent renal damage and glomerular filtration rate (GFR) and renal plasma flow reductions and attenuate the increases in arterial pressure. Thirty-three 7- to 8-week old Dahl SS/Rapp strain rats were placed on either a high-sodium (8%) or a low-sodium (0.3%) diet with or without vitamin E (111 IU/d) in the food and 98 mg/d vitamin C in the drinking water for 5 weeks. Rats were equipped with indwelling arterial and venous catheters at day 21. By day 35 in the rats with high-sodium diet, vitamin C and E treatment significantly decreased renal cortical and medullary O2*- release, mean arterial pressure, urinary protein excretion, glomerular necrosis, and renal tubulointerstitial damage. At this time, GFR significantly decreased in the high-sodium diet group (1.6+/-0.2 mL/min) when compared with either the high-sodium plus vitamins C and E (2.9+/-0.2 mL/min) or the low-sodium diet group (2.9+/-0.3 mL/min). In SS rats on high-sodium diet, renal plasma flow decreased 40%, and this reduced flow was restored by vitamin treatment. In Dahl salt-sensitive hypertension, increased oxidative stress plays an important role in the renal damage, decreases in renal hemodynamics, and increases in arterial pressure that occur. Antioxidant treatment with vitamins C and E improves renal dysfunction, lessens renal injury, and decreases arterial pressure in Dahl salt-sensitive hypertension.

Non-invasive measurement of systolic blood pressure on the arm utilising photoplethysmography: development of the methodology

Photoplethysmography (PPG) can be used to measure systolic blood pressure at the brachial artery. With a specially designed probe, positioned in the most distal position beneath a pressure cuff on the upper arm, this is possible. The distance between the light source (880 nm) and the photodetector was 20 mm. A test was performed on neuro-intensive care patients by determining blood pressure from the PPG curves, and, when it was compared with systolic blood pressure obtained from inserted indwelling arterial catheters, a correlation factor of r = 0.95 was achieved. The difference between blood pressure obtained using PPG and invasive blood pressure measurement was 3.9 +/- 9.1 mmHg (mean +/- SD), n = 19. The depth to the brachial artery was 13.9 +/- 4.1 mm (mean +/- SD), n = 18. A digital PPG system utilising pulsating light was also developed.

Pharmacokinetics of Famotidine in Infants

Although famotidine pharmacokinetics are similar in adults and children older than 1 year of age, they differ in neonates owing to developmental immaturity in renal function. Little is currently known about the pharmacokinetics of famotidine in infants aged between 1 month and 1 year, a period when renal function is maturing. To characterise the pharmacokinetics of famotidine in infants. This was a two-part multicentre study with both single dose (Part I, open-label) and multiple dose (Part II, randomised) arms. Thirty-six infants (20 females and 16 males) who required treatment with famotidine and who had an indwelling arterial or venous catheter for reasons unrelated to the study. Infants in Part I were administered a single dose of famotidine 0.5 mg/kg; the dose was intravenous or oral according to the judgement of the attending physician. Infants receiving 0.5 mg/kg intravenously were divided into two groups by age, and pharmacokinetic parameters in infants 0-3 months and >3 to 12 months of age were compared. Infants in Part II were randomised to one of the following treatments: 0.25 mg/kg/dose intravenously or 0.5 mg/kg/dose orally on day 1 and subsequent days, or 0.25 mg/kg/dose intravenously or 0.5 mg/kg/dose orally on day 1 followed by doses of either 0.5 mg/kg/dose intravenously or 1 mg/kg/dose orally on subsequent days. From day 2 onwards, age-adjusted dose administration regimens (once daily in infants <3 months of age and every 12 hours in infants >3 months of age) were used; the total number of famotidine doses ranged from 3 to 11 and the total number of days of dose administration ranged from two to eight. In infants <3 months of age, plasma and renal clearance of famotidine were decreased compared with infants >3 months of age. Pharmacokinetic parameters for the older infants (i.e. those >3 months) were similar to those previously reported for children and adults. Approximate dose-proportionality, no accumulation on multiple dosing and an estimated bioavailability similar to adult values were also observed. A short course of famotidine therapy in infants appears generally well tolerated, and the characteristics of famotidine pharmacokinetics during the first year of life are explained to a great degree by the development of renal function, the primary route of elimination for this drug.

Glucocorticoid receptors are involved in the regulation of pulsatile urea excretion in toadfish

The objectives of this study were to characterize the pattern of pulsatile urea excretion in the gulf toadfish in the wake of exogenous cortisol loading and to determine the receptors involved in the regulation of this mechanism. Toadfish were fitted with indwelling arterial catheters and were infused with isosmotic NaCl for 48 h after which fish were treated with cortisol alone, cortisol + peanut oil, cortisol + RU486 (a glucocorticoid receptor antagonist) or cortisol + spironolactone (a mineralocorticoid receptor antagonist). Upon cortisol loading, fish treated with cortisol alone, cortisol + oil or cortisol + spironolactone experienced a two- to threefold reduction in pulsatile urea excretion. This reduction was due to a decrease in urea pulse size with no effect on pulse frequency compared to values measured during the control NaCl infusion period. In addition, these fish showed an increase in plasma urea concentrations upon treatment. These apparent effects of cortisol treatment were abolished in fish treated with cortisol + RU486. In contrast, these fish showed an increase in pulsatile urea excretion mediated by a twofold increase in pulse size with no change in frequency. Likewise, fish treated with cortisol + RU486 showed a significant decrease in plasma urea concentrations over the course of the experiment. The findings of this study indicate that high levels of cortisol reduce pulsatile urea excretion by decreasing pulse size. In addition, it appears that glucocorticoid receptors and not mineralocorticoid receptors are involved in the regulation of the toadfish pulsatile urea excretion mechanism.

Physiological effects of dietary cadmium acclimation and waterborne cadmium challenge in rainbow trout: respiratory, ionoregulatory, and stress parameters

A suite of respiratory, acid–base, ionoregulatory, hematological, and stress parameters were examined in adult rainbow trout ( Oncorhynchus mykiss) after chronic exposure to a sublethal level of dietary Cd (500 mg/kg diet) for 45 days and during a subsequent challenge to waterborne Cd (10 μg/L) for 72 h. Blood sampling via an indwelling arterial catheter revealed that dietary Cd had no major effects on blood gases, acid–base balance, and plasma ions (Ca 2+, Mg 2+, K +, Na +, and Cl −) in trout. The most notable effects were an increase in hematocrit (49%) and hemoglobin (74%), and a decrease in the plasma total ammonia (43%) and glucose (49%) of the dietary Cd-exposed fish relative to the nonexposed controls. Dietary Cd resulted in a 26-fold increase of plasma Cd level over 45 days (∼24 ng/mL). The fish exposed to dietary Cd showed acclimation with increased protection against the effects of waterborne Cd on arterial blood P aCO2 and pH, plasma ions, and stress indices. After waterborne Cd challenge, nonacclimated fish, but not Cd-acclimated fish, exhibited respiratory acidosis. Plasma Ca 2+ levels declined from the prechallenge level, but the effect was more pronounced in nonacclimated fish (44%) than in Cd-acclimated fish (14%) by 72 h. Plasma K + was elevated only in the nonacclimated fish. Similarly, waterborne Cd caused an elevation of all four traditional stress parameters (plasma total ammonia, cortisol, glucose, and lactate) only in the nonacclimated fish. Thus, chronic exposure to dietary Cd protects rainbow trout against physiological stress caused by waterborne Cd and both dietary and waterborne Cd should be considered in determining the extent of Cd toxicity to fish.

Effects of Intra-Operative Glucose Control on the Development of Surgical Site Infection in Cardiac Surgery Patients

OBJECTIVE: To assess the effects of timing and glucose control on the development of post-operative surgical site infections in cardiac surgery patients. METHODS: The cardiothoracic team at Rochester General Hospital instituted a program to standardize cardiac care by initiation of a standardized intra-operative insulin protocol. The objective was to maintain glucose levels below 200mg/dL. A distinct data-collection tool was designed to measure and record glucose levels pre-, intra-, and post-operatively. Blood glucose readings were determined by a Chiron ABG chemistry analyzer and obtained via an indwelling arterial catheter and documented at 30-minute intervals. Glucose levels were recorded on all patients regardless of diabetic history. RESULTS: A total of 1880 patients from 2000 to 2002 were entered into the database. In the univariate analysis, pre-operative and early intra-operative glucose levels of 200 or more were not associated with an increased risk of infection. However, of the 61 patients who developed a surgical-site infection (chest or leg), 38 had glucose levels above 200 after bypass. Of the 1819 non-infected patients, 566 had glucose levels above 200 during the same timeframe. A Fisher's Exact test was performed to evaluate the association of elevated blood sugars in the post bypass and late surgical phase and the development of a surgical site infection. This relationship was statistically significant (p=0.0001). CONCLUSIONS: Although further evaluation is necessary, preliminary results suggest that tight glucose control is especially critical during the latter part of surgery and in the early recovery phase of cardiac surgery.

Efficacy and cardiovascular tolerability of extended dialysis in critically ill patients: a randomized controlled study

Background: Extended dialysis is an increasingly used modality of renal replacement therapy that theoretically offers advantages of both intermittent and continuous therapies in the intensive care unit (ICU). Methods: We randomly treated 39 ventilated critically ill patients with oliguric acute renal failure with either continuous venovenous hemofiltration (CVVH; n = 19; age, 50.1 ± 3.2 years; Acute Physiology and Chronic Health Assessment II [APACHE II] score, 32.3 ± 1.2; 79% sepsis) and a substitution fluid rate of at least 30 mL/kg/h for 24 hours or with extended dialysis for 12 hours (n = 20; age, 50.8 ± 3.6 years; APACHE II score, 33.6 ± 1.0; 85% sepsis). The latter was performed using an easy-to-handle, single-pass, batch dialysis system. All hemodynamic parameters were monitored invasively by means of an indwelling arterial catheter. Results: Average mean arterial blood pressure, heart rate, cardiac output, systemic vascular resistance, and catecholamine dose were not significantly different in both therapies. Urea reduction rate was similar with extended dialysis compared with CVVH therapy (53% ± 2% versus 52% ± 3%; P = not significant) despite an average rate of substitution fluid with the latter of 3.2 ± 0.1 L/h. This was corroborated by the finding of similar amounts of urea eliminated in the collected spent total hemofiltration and dialysis fluid. Correction of acidosis was accomplished faster with extended dialysis than CVVH, and the amount of heparin used was significantly lower with extended dialysis (P < 0.01). Conclusion: Extended dialysis combines excellent detoxification with cardiovascular tolerability, even in severely ill patients in the ICU. The technically simple dialysis system used offers flexibility of treatment time.

Betamethasone in the last week of pregnancy causes fetal growth retardation but not adult hypertension in rats.

We tested the hypotheses that (1) maternal betamethasone (betaM) treatment over the range of clinical doses for prevention of prematurity-related pathologies from day 15 to 21 of rat gestation would produce growth retardation, and (2) the lowest betaM dose to produce growth retardation would result in hypertension in adult offspring. In experiment 1, pregnant Sprague-Dawley rats were administered betaM (0, 50, 100, 200, 400, or 600 microg/kg per day, subcutaneously) on days 15-21 of pregnancy and necropsied on day 21.5, with fetal lung and placental weights recorded. In experiment 2, two more groups of rats (0 or 100 microg/kg per day, subcutaneously) were allowed to deliver, and offspring were instrumented at 100 +/- 4 days of postnatal life with indwelling left carotid arterial catheters. After 48 hours of recovery, blood pressure was recorded continuously for 24 hours. In experiment 1, all newborn rats treated with betaM, and their placentas, except those receiving 50 microg/kg per day, were growth retarded in comparison with controls (P <.05). All treated lungs were smaller than those of controls (P <.05). In experiment 2, no differences were found in the mean arterial blood pressure of adult offspring given the lowest effective dose of betaM (100 microg/kg per day) compared with controls (114.2 +/- 5.3 mmHg versus 114.6 +/- 3.4 mmHg, respectively). These data suggest that glucocorticoids given in the last week of rat pregnancy in the lowest human clinical dose do not cause hypertension and somatic growth retardation. However, the presence of lung growth restriction at this dose argues for more studies on the efficacy of even lower concentrations for their ability to improve lung and other organ and tissue function while avoiding unwanted side effects.

Beta-endorphin concentration after administration of sucrose in preterm infants.

Sucrose is an effective analgesic for procedural pain in preterm infants. It has been hypothesized that its analgesic effects are mediated by the release of endogenous opioid neurotransmitters such as beta-endorphin. To determine whether intraoral administration of sucrose was associated with an increase in serum beta-endorphin concentrations in preterm infants with a gestation period less than 29 weeks who were not exposed to a painful stimulus. We performed a prospective open-label study in preterm infants admitted to 2 tertiary neonatal intensive care units. Each infant received a single dose of 30% sucrose intraorally during a 1- to 2-minute period. A blood sample was obtained using an indwelling arterial catheter to determine beta-endorphin concentration immediately before and 2 to 5 minutes after the commencement of sucrose administration. We enrolled 11 preterm infants with a mean +/- SD gestational age of 27.2 +/- 0.9 weeks and a mean +/- SD birth weight of 1018 +/- 238 g (1.02 +/- 0.24 kg) at a mean +/- SD postnatal age of 3.0 +/- 2.5 days. The mean +/- SD beta-endorphin concentration before and after sucrose administration was 60.4 +/- 30.5 pg/mL and 57.4 +/- 22.4 pg/mL, respectively (P =.45). No adverse events were observed during the study procedures. Intraoral administration of sucrose in preterm infants did not lead to an increase in serum beta-endorphin concentrations at a point in time when the analgesic effects of sucrose were presumed to be present.

Splanchnic free fatty acid kinetics.

These studies were conducted to assess the relationship between visceral adipose tissue free fatty acid (FFA) release and splanchnic FFA release. Steady-state splanchnic bed palmitate ([9,10-(3)H]palmitate) kinetics were determined from 14 sampling intervals from eight dogs with chronic indwelling arterial, portal vein, and hepatic vein catheters. We tested a model designed to predict the proportion of FFAs delivered to the liver from visceral fat by use of hepatic vein data. The model predicted that 15 +/- 2% of hepatic palmitate delivery originated from visceral lipolysis, which was greater (P = 0.004) than the 11 +/- 2% actually observed. There was a good relationship (r(2) = 0.63) between the predicted and observed hepatic palmitate delivery values, but the model overestimated visceral FFA release more at lower than at higher palmitate concentrations. The discrepancy could be due to differential uptake of FFAs arriving from the arterial vs. the portal vein or to release of FFAs in the hepatic circulatory bed. Splanchnic FFA release measured using hepatic vein samples was strongly related to visceral adipose tissue FFA release into the portal vein. This finding suggests that splanchnic FFA release is a good indicator of visceral adipose tissue lipolysis.

Plasma clearance of cadmium and zinc in non-acclimated and metal-acclimated trout

Adult rainbow trout were pre-exposed to a sublethal concentration of waterborne cadmium (Cd, 26.7 nmol/l) or waterborne zinc (Zn, 2294 nmol/l) for 30 days to induce acclimation. A single dose of radiolabeled Cd (64.4 nmol/kg) or Zn (183.8 nmol/kg) was injected into the vascular system of non-acclimated and Cd- or Zn-acclimated trout through indwelling arterial catheters. Subsequently, repetitive blood samples over 10 h and terminal tissue samples (liver, heart, bile, stomach, intestine, kidney, gills, muscle, and spleen) were taken to characterize the effect of metal acclimation on clearance kinetics in vivo. Plasma clearance of Cd in Cd-acclimated fish (0.726±0.015 and 0.477±0.012 ml/min per kg for total and newly accumulated Cd, respectively), was faster than that in non-acclimated trout (0.493±0.013 and 0.394±0.009 ml/min per kg). Unlike plasma Cd, the levels of Cd in red blood cells (RBCs) were 1.2–2.2 times higher in Cd-acclimated fish than in non-acclimated fish. At 10 h post-injection, the liver accumulated the highest proportion (∼22%) of the injected Cd dose in both non-acclimated and Cd-acclimated fish but did not account for the difference in plasma levels of Cd between two groups. Plasma clearance of Zn (∼0.23 ml/min per kg for new Zn) was substantially lower than Cd clearance. Pre-acclimation to waterborne Zn reduced the new Zn levels in RBCs, but did not affect the clearance of Zn from blood plasma or tissue burdens of Zn in fish. Bile concentrations of both Cd and Zn were elevated in acclimated fish, but total bile burden accounted for <1% of the injected metal dose. The results suggest that the detoxification process of injected plasma Cd is stimulated by pre-acclimation to waterborne Cd, and that Zn levels are homeostatically controlled in both non-acclimated and acclimated trout.

Historical Perspectives

“The experimental hypothesis, in short, must always be based on prior observation.”—Claude Bernard (1) Modern adult intensive care started in Denmark in 1952 in response to the high mortality from the respiratory complications seen with a devastating epidemic of poliomyelitis. Anesthetists and physiologists created a new discipline when they collaborated to make sequential measurements of cardiorespiratory variables, then aggressively corrected abnormal conditions. (2) When modern neonatal intensive care emerged a decade later, it followed the same philosophy. The start of modern neonatology was stimulated in large part by an expanding understanding of: 1) the circulatory and respiratory physiology of adaptation to extrauterine life, 2) how those adjustments could fail, and 3) the pathophysiology of hyaline membrane disease. (3)(4)(5)(6)(7)(8)(9)(10) (The monograph by Dawes (3) gives an excellent overview of the relevant animal research). This research had reached a point where it could be applied to clinical care if the necessary physiologic measurements could be made in newborns. To this end, investigators began to catheterize the umbilical arteries of newborns to measure blood gas tensions and pH, with several investigators also measuring aortic pressures. (9)(11)(12)(13) Such invasive techniques were highly controversial initially, but they gradually became the accepted methodology for monitoring the sick neonate. (12) The use of oxygen in preterm infants who had cardiorespiratory distress was an important component of this change in approach to the sick infant. The standard had been to use no more than 40% oxygen to prevent retrolental fibroplasia (retinopathy of prematurity). However, it was obvious that this approach would be insufficient to relieve hypoxia in some infants and would produce hyperoxia in others. Avery and Oppenheimer (13) observed an increase in deaths due to …

Oxidative stress in Dahl salt-sensitive hypertension.

The role of oxidative stress in the long-term regulation of arterial pressure, renal hemodynamics, and renal damage was studied in Dahl salt-sensitive rats. Twenty-eight Dahl S/Rapp strain rats, equipped with indwelling arterial and venous catheters, were subjected to a 3-week intravenous infusion of either low Na (0.9 mmol/d) or high Na (20.6 mmol/d) or the superoxide dismutase mimetic, 4-hydroxyl-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol), at 125 micromol x kg(-1) x h(-1) plus low Na or high Na. After 21 days, mean arterial pressure was 140+/-3 mm Hg in the high-Na group, 118+/-1 mm Hg (P<0.05) in the high-Na/Tempol group, and unchanged in the low-Na/Tempol and low-Na groups. Tempol did not change renal blood flow, glomerular filtration rate, or glomerular cross-sectional area in rats subjected to the high-Na intake but did decrease urinary protein excretion, the percentage of sclerotic glomeruli, and the kidney weight to body weight ratio. In 15 additional Dahl S rats subjected to high or low Na intake for 3 weeks, renal cortical and medullary O2*- release increased significantly in the high-Na group when compared with the low-Na group. Tempol decreased both renal cortical and medullary O2*- release in the high- and low-Na rats, but the decrease in O2*- release was greater in high-Na rats. The data suggest that oxidative stress contributes to Dahl salt-sensitive hypertension and the accompanying renal damage.

Digital ischaemia after ulnar artery cannulation

Editor—Arterial cannulation is frequently undertaken in major surgery and in intensive care. After failure to cannulate the radial artery at the wrist, cannulation of the ipsilateral ulnar artery has been performed uneventfully.1Slogoff S Keats AS Arlund C On the safety of radial artery cannulation.Anesthesiology. 1983; 59: 42-47Crossref PubMed Scopus (288) Google Scholar The presence of an indwelling arterial catheter may lead to ischaemic damage, which is sometimes permanent. We recently experienced this complication following ulnar artery catheterization. To our knowledge, this has not been reported previously. A 76-yr-old woman was admitted to our intensive care unit following laparotomy. After unsuccessful attempts to cannulate the left radial artery, a catheter was finally inserted into the left ulnar artery (Vygon Leader Flex 20G catheter, length 8 cm). We did not cannulate the right radial artery or the femoral arteries as these had been cannulated recently. Six days after cannulation, it was noticed that the tips of the left index, middle and little fingers had become cyanotic and cold (Fig. 1). The arterial catheter was removed immediately. The patient was given a bolus of heparin 5000 U i.v. followed by an i.v. infusion of heparin 1000 U h−1. The patient had not experienced any pain or neurological deficit in the hand. Circulation to the fingers gradually improved and eventually recovered fully. A number of factors may contribute to ischaemia following arterial cannulation. These include emboli originating from a proximal site,2Vender JS Watts DR Differential diagnosis of hand ischaemia in the presence of an arterial cannulation.Anesth Analg. 1982; 61: 465-468Crossref PubMed Scopus (8) Google Scholar prolonged cannulation, and severe local trauma.3Wyatt R Glaves I Cooper DJ Proximal skin necrosis after radial artery cannulation.Lancet. 1974; 1: 1135-1138Abstract PubMed Scopus (30) Google Scholar The other factors associated with increased risk of arterial occlusion are female sex, and low cardiac output.4Davis FM Stewart JM Radial artery cannulation. A prospective study in patients undergoing cardiothoracic surgery.Br J Anaesth. 1980; 52: 41-47Crossref PubMed Scopus (94) Google Scholar This incident shows that ulnar artery cannulation following failure to cannulate the ipsilateral radial artery may increase the risk of arterial insufficiency and should therefore be discouraged, unless any alternative is available. Before this procedure continuing blood flow through the radial artery should be demonstrated (e.g. by a reverse Allen's test, digital plethysmography, or Doppler studies. In this case, the risk was further augmented by the fact that the catheter was left in situ for 6 days. The patient's hand should be examined regularly if an arterial catheter has been inserted. If signs of arterial occlusion occur, the cannula should be removed promptly and appropriate anticoagulant treatment given without delay.