Angiotensin-converting enzyme inhibition and blood pressure response during total intravenous anaesthesia for minor surgery.

BACKGROUND: This study investigates whether long-term treatment with an angiotensin-converting enzyme inhibitor (ACEI) impairs the haemodynamic regulation during total intravenous anaesthesia (TIVA) for minor surgery. METHODS: In a prospective, two-armed observational study, 36 patients undergoing TIVA for minor surgery were studied. Seventeen were taking ACEIs regularly but no other antihypertensive medication (ACEI group); 19 patients without any cardiovascular medication served as controls (non-ACEI group). Haemodynamic variables were measured every minute during induction and every 5 min during surgery. The plasma levels of renin, angiotensin II, vasopressin and catecholamines were measured before and 18 min after the induction of anaesthesia. RESULTS: The mean arterial pressure decreased to the same extent in both the groups during the induction of TIVA. There were also no differences between the groups regarding the heart rate, systolic and diastolic arterial pressure, as well as the use of vasoconstrictors, and fluids during induction and throughout surgery. In the ACEI group, the plasma renin concentration was higher at baseline and after the induction of anaesthesia presumably due to the interruption of the negative renin-angiotensin feedback loop (P<0.05). Angiotensin II increased only in the non-ACEI group (6.2 ± 2.2 before vs. 9.6 ± 3.5 pg/ml after induction; P<0.05). In both groups, the plasma norepinephrine concentration decreased after the induction of TIVA (P<0.05). Plasma vasopressin and plasma epinephrine concentrations did not change in either group. CONCLUSION: Long-term ACEI treatment does not further aggravate the blood pressure decrease under TIVA during minor surgery, provided the induction procedure is slow, the patient is kept well hydrated and vasoconstrictors are promptly applied.

Correlation of exhaled nitric oxide with nitrogen oxides and selected cytokines in induced sputum of chronic obstructive pulmonary disease patients.

Assessment of exhaled nitric oxide (eNO) in patients with chronic obstructive pulmonary disease (COPD) provides seemingly conflicting results and the relationships between eNO and other sputum inflammatory mediators are relatively weakly recognized. In the present study we measured eNO in 63 subjects (14 non-smoking healthy controls and 49 COPD stable patients--15 patients at stage 0, 9 patients at stage 1, 16 patients at stage 2, and 9 patients at stage 3). Additionally, concentrations of cytokines (IL-8, TNF-alpha, TGF-beta1, GM-CSF, Eotaxin) and nitrogen oxides (as nitrite or nitrate) (NOs) were measured in induced sputum in these patients. We found that there were no significant differences between the means of either eNO or NOs levels in COPD patients (stage 0-2) and controls. The only significant difference was noted for NOs between the COPD stage 3 patients and controls (9.0+/-1.7 microM vs. 21.1+/-4.8 microM). There was no significant correlation between eNO and sputum NOs. No relationships existed between eNO and the examined cytokine levels, except for a single negative correlation with GM-CSF (r=-0.38, P=0.02). In contrast, NOs correlated positively with IL-8 levels (r=0.51, P<0.01) and IL-8 levels correlated negatively (r=-0.47, P<0.01) with FEV1. We conclude that exhaled NO, sputum NOs, and other sputum cytokines offer separate and additive information about the pathophysiological condition in COPD.

Relationship between baroreflex sensitivity, renin suppression and natriuresis in salt-sensitive rabbits.

This study determined the influence of baroreflex sensitivity (BRS) on the rate of urinary sodium excretion and plasma renin activity (PRA) in response to a saline infusion in conscious male rabbits specifically bred for high (Group I; n = 7) and low (Group II; n = 10) BRS and in seven control animals. Only Group II showed significant increases in blood pressure on a chronic high-salt intake. After ensuring that each animal was in sodium balance, a (0.7-0.9%) saline infusion of 3-4 ml/kg per h for 90 min (25% daily sodium intake for each rabbit) was given and urine collected at 15-min intervals via a bladder catheter. No differences were found in control urine volumes, urinary sodium or PRA. Group I excreted over 50% of the sodium load and Group II less than 20% within 90 min. PRA fell by more than 30% within 30 min in six Group I rabbits but decreased by less than 30% or increased in Group II. In the control animals, sodium excretion rates and PRA suppression were also much greater in those with high BRS. A highly significant correlation (r = 0.808, P less than 0.01) was found between the per cent of the sodium load excreted and BRS. It is suggested that the delayed sodium excretion and blood pressure elevation in salt-sensitive subjects may be due to a genetic impairment in baroreflex control of renal sympathetic nerve activity.

Inhaled nitric oxide does not change transpulmonary angiotensin II formation in patients with acute respiratory distress syndrome.

STUDY OBJECTIVE: To investigate the effect of short-term inhalation of nitric oxide (NO) on transpulmonary angiotensin II formation in patients with severe ARDS. DESIGN: Prospective, clinical study. SETTING: Anesthesiology ICU of a university hospital. PATIENTS: Ten ARDS patients who responded to inhalation of 100 ppm NO by decreasing their pulmonary vascular resistance (PVR) by at least 20 dyne x s x cm(-5) were included in the study. INTERVENTIONS AND MEASUREMENTS: In addition to standard treatment, the patients inhaled 0, 1, and 100 ppm NO in 20-min intervals. Fraction of inspired oxygen was 1.0. Hemodynamics were measured and recorded online. Mixed venous (pulmonary arterial catheter) and arterial (arterial catheter) blood samples were taken simultaneously for hormonal analyses at the end of each inhalation period. RESULTS: Pulmonary arterial pressure decreased from 33+/-2 mm Hg (0 ppm NO, mean+/-SEM) to 29+/-2 mm Hg (1 ppm NO, p<0.05), and to 27+/-2 mm Hg (100 ppm NO, p<0.05, vs 0 ppm). PVR decreased from 298+/-56 (0 ppm NO) to 243+/-45 dyne x s x cm(-5) (1 ppm NO, not significant [NS]), and to 197+/-34 dyne x s x cm(-5) (100 ppm NO, p<0.05, vs 0 ppm). Arterial oxygen pressure increased from 174+/-23 mm Hg (0 ppm NO) to 205+/-26 mm Hg (1 ppm NO, NS), and to 245+/-25 mm Hg (100 ppm NO, p <0.05, vs 0 ppm). Mean plasma angiotensin II concentrations were 85+/-20 (arterial) and 57+/-13 pg/mL (mixed venous) during 0 ppm NO and did not change during inhalation of 1 and 100 ppm NO. Mean transpulmonary plasma angiotensin II concentration gradient (=difference between arterial and mixed venous blood values) was 28+/-8 pg/mL (range, 0 to 69) during 0 ppm NO and did not change during inhalation of 1 and 100 ppm NO. Mean transpulmonary angiotensin II formation (transpulmonary angiotensin II gradient multiplied with the cardiac index) was 117+/-39 ng/min/m2 (range, 0 to 414) during 0 ppm NO and did not change during inhalation of 1 and 100 ppm NO. Mean arterial plasma cyclic guanosine monophosphate concentration was 11+/-2 pmol/mL (0 ppm NO), did not change during 1 ppm NO, and increased to 58+/-8 pmol/mL (100 ppm NO, p<0.05). Arterial plasma concentrations of aldosterone (142+/-47 pg/mL), atrial natriuretic peptide (114+/-34 pg/mL), angiotensin-converting enzyme (30+/-5 U/L), and plasma renin activity (94+/-26 ng/mL/h of angiotensin I) did not change. CONCLUSION: The decrease of PVR by short-term NO inhalation in ARDS patients was not accompanied by changes in transpulmonary angiotensin II formation. Our results do not support any relationship between transpulmonary angiotensin II formation and the decrease in PVR induced by inhaled NO.

Angiotensin II formation and endothelin clearance in ARDS patients in supine and prone positions.

OBJECTIVE: In patients with acute respiratory distress syndrome (ARDS), the prone position may enhance oxygenation by changing ventilation/perfusion ratio. In this study, we investigated whether the prone position affects the net balance between pulmonary endothelin (ET-1) and angiotensin II (Ang II) production and clearance, two metabolic functions of lung endothelial cells. SETTING: Anaesthesiological intensive care unit of a university hospital. PATIENTS: Ten ARDS patients (Murray score > 2.5) were studied in both the supine position (SP) and the prone position (PP). MEASUREMENTS AND DESIGN: Blood samples were taken simultaneously from the patient in SP for assessment of mixed venous and arterial ET-1 and Ang II concentrations, and plasma renin concentration (PRC). This was repeated after 60 min in SP, immediately after turning the patient into PP, and 60 min thereafter. Net arterial/mixed venous ET-1 clearances and net Ang II formations were calculated. RESULTS: arterial oxygen tension increased from SP to PP by an average of 60 mmHg, about 20%. Arterial ET-1 concentrations of ARDS patients were 1.57 +/- 1.1 pg/ml (mean +/- SD) and within the range of healthy persons. Net ET-1 clearances were negative in SP, indicating pulmonary release of ET-1, and did not change in PP. Arterial Ang II concentrations (73 +/- 56 pg/ml) as well as PRC (126 +/- 85 pg/ml) were markedly elevated. Net transpulmonary Ang II formation did not change. CONCLUSION: Acute changes of oxygenation in ARDS patients by positioning do not induce any short-term effects on pulmonary ET-1 net clearance or Ang II net formation.

Evidence that the renin decrease during hypoxia is adenosine mediated in conscious dogs.

This study investigated whether adenosine mediates the decrease in plasma renin activity (PRA) during acute hypoxia. Eight chronically tracheotomized, conscious beagle dogs were kept under standardized environmental conditions and received a low-sodium diet (0.5 mmol.kg body wt(-1).day(-1)). During the experiments, the dogs were breathing spontaneously via a ventilator circuit: first hour, normoxia (21% inspiratory concentration of O(2)); second and third hours, hypoxia (10% inspiratory concentration of O(2)). Each of the eight dogs was studied twice in randomized order in control and theophylline experiments. In theophylline experiments, theophylline, an A(1)-receptor antagonist, was infused intravenously during hypoxia (loading dose: 3 mg/kg within 30 min, maintenance: 0.5 mg. kg(-1). h(-1)). In theophylline experiments, PRA (5.9 +/- 0.8 ng ANG I. ml(-1). h(-1)) and ANG II plasma concentration (15.9 +/- 2.3 pg/ml) did not decrease during hypoxia, whereas plasma aldosterone concentration decreased from 277 +/- 63 to 132 +/- 23 pg/ml (P < 0.05). In control experiments, PRA decreased from 6.8 +/- 0.8 during normoxia to 3.0 +/- 0.5 ng ANG I. ml(-1). h(-1) during hypoxia, ANG II decreased from 13.3 +/- 1.9 to 7.3 +/- 1.9 pg/ml, and plasma aldosterone concentration decreased from 316 +/- 50 to 70 +/- 13 pg/ml (P < 0.05). Thus infusion of the adenosine receptor antagonist theophylline inhibited the suppression of the renin-angiotensin system during acute hypoxia. The decrease in aldosterone occurred independently and is apparently directly related to hypoxia. In conclusion, it is likely that adenosine mediates the decrease in PRA during acute hypoxia in conscious dogs.

Acute hypoxic pulmonary vasoconstriction in conscious dogs decreases renin and is unaffected by losartan.

Acute hypoxic pulmonary vasoconstriction (HPV) may be mediated by vasoactive peptides. We studied eight conscious, chronically tracheostomized dogs kept on a standardized dietary sodium intake. Normoxia (40 min) was followed by hypoxia (40 min, breathing 10% oxygen, arterial oxygen pressures 36 +/- 1 Torr) during both control (Con) and losartan experiments (Los; iv infusion of 100 microg. min-1. kg-1 losartan). During hypoxia, minute ventilation (by 0.9 l/min in Con, by 1.3 l/min in Los), cardiac output (by 0.36 l/min in Con, by 0.30 l/min in Los), heart rate (by 11 beats/min in Con, by 30 beats/min in Los), pulmonary artery pressure (by 9 mmHg in both protocols), and pulmonary vascular resistance (by 280 and 254 dyn. s. cm-5 in Con and Los, respectively) increased. Mean arterial pressure and systemic vascular resistance did not change. In Con, PRA decreased from 4.2 +/- 0.7 to 2.5 +/- 0.5 ng ANG I. ml-1. h-1, and plasma ANG II decreased from 11.9 +/- 3.0 to 8.2 +/- 2.1 pg/ml. The renin-angiotensin system is inhibited during acute hypoxia despite sympathetic activation. Under these conditions, ANG II AT1-receptor antagonism does not attenuate HPV.

Inferior vena caval pressure increase contributes to sodium and water retention during PEEP in awake dogs.

UNLABELLED: This study compared the hemodynamic, renal, and hormonal effects of an experimentally induced increase in inferior vena caval pressure (IVCP) [to the same extent as during controlled mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP)] with those of CMV with PEEP. Six volume-expanded conscious chronically tracheotomized dogs were studied under three conditions: CONTROL: 4 h of spontaneous breathing at 4 cmH2O continuous positive airway pressure (CPAP); CMV: CPAP for the 1st and 4th h and CMV with PEEP for the 2nd and 3rd h, resulting in a mean airway pressure of 20 cmH2O; and Increased IVCP: 4 h of CPAP, with IVCP increased during the 2nd and 3rd h by inflation of a chronically implanted cuff. Urine volume, sodium excretion, and fractional sodium excretion decreased during the 2nd and 3rd h of CMV and during increased IVCP compared with CONTROL. Glomerular filtration rate, mean arterial pressure, and antidiuretic hormone, atrial natriuretic peptide, and aldosterone plasma concentrations were not affected by CMV or Increased IVCP. Plasma renin activity decreased during CONTROL and Increased IVCP conditions but remained elevated during the 2nd and 3rd h of CMV. We conclude that, in conscious extracellular volume-expanded dogs, IVCP elevation contributes considerably to the water- and sodium-retaining effect of short-term CMV with PEEP.

ACE inhibition facilitates sodium and water excretion during PEEP in conscious volume-expanded dogs.

Increased activity of the renin-angiotensin system may be involved in sodium and water retention during controlled mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP). We therefore evaluated renal, hemodynamic, and hormonal effects of an acute angiotensin-converting enzyme inhibition (ACEI) during PEEP and extracellular volume expansion in five trained chronically tracheotomized dogs. Three protocols were performed: control, 4 h spontaneous breathing with continuous positive mean airway pressure (Paw) of 4 cmH2O (CPAP 4); CMV 20, CPAP for 1st h, CMV with 20 cmH2O Paw for 2 h (2nd and 3rd h), and 1 h of CPAP (4th h); and CMV20-ACEI, ACEI (Ramipril, 2 mg/kg body wt) followed by the same protocol as in CMV 20. During control, sodium excretion (UNaV) and urine volume (V) increased continuously to 56.2 +/- 2.7 (SE) mumol.min-1.kg body wt-1 and 482 +/- 23 microliters.min-1.kg body wt-1, respectively. UNaV and V increased less during PEEP in CMV 20 and CMV 20-ACEI. However, significantly more sodium and water were retained in CMV 20 than in CMV 20-ACEI (2.3 +/- 0.3 vs. 1.0 +/- 0.3 mmol/kg body wt, and 20 +/- 3 vs. 11 +/- 2 ml/kg body wt) because of a decrease of glomerular filtration rate and fractional UNaV in CMV 20. Heart rate did not change in control, CMV 20, or CMV 20-ACEI. Mean arterial pressure increased during control by 13 mmHg, did not change during CMV 20, and was decreased by 7 mmHg in CMV 20-ACEI.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic peptide ameliorates hypoxic pulmonary vasoconstriction without influencing systemic circulation.

UNLABELLED: Hypoxic pulmonary vasoconstriction (HPV) is encountered during ascent to high altitude. Atrial natriuretic peptide (ANP) could be an option to treat HPV because of its natriuretic, diuretic, and vasodilatory properties. Data on effects of ANP on pulmonary and systemic circulation during HVP are conflicting, partly owing to anesthesia, surgical stress or uncontrolled dietary conditions. Therefore, ten conscious, chronically tracheotomized dogs were studied under standardized dietary conditions. The dogs were trained to breathe spontaneously at a ventilator circuit. PROTOCOL: 30min of normoxia [inspiratory oxygen fraction (F(i)O(2))=0.21] were followed by 30min of hypoxia without ANP infusion (Hypoxia I, F(i)O(2)=0.1). While maintaining hypoxia an intravenous infusion of atrial natriuretic peptide was started with 50ng x kg body wt(-1) x min(-1) for 30min (Hypoxia+ANP1=low dose), followed by 1000ng x kg body wt(-1) x min(-1) for 30min (Hypoxia+ANP2=high dose). Thereafter, ANP infusion was stopped and hypoxia maintained for a final 30min (Hypoxia II). Compared to normoxia, mean pulmonary arterial pressure (MPAP) (16+/-0.7 vs. 26+/-1.3mmHg) and pulmonary vascular resistance (PVR) (448+/-28 vs. 764+/-89dyn x s(-1) x cm(-5)) increased during Hypoxia I and decreased during Hypoxia+ANP 1 (MPAP 20+/-1mmHg, PVR 542+/-55dyn x s(-1) x cm(-5)) (P<0.05). The higher dose of ANP did not further decrease MPAP or PVR, but started to have a tendency to decrease mean arterial pressure and cardiac output. We conclude that low dose ANP is able to reduce HPV without affecting systemic circulation during acute hypoxia.

Nifedipine inhibits the hypoxia-induced decrease in plasma renin activity in conscious dogs.

Acute hypoxia induces a decrease in plasma renin activity (PRA), mediated, e.g., by an increase in adenosine concentration, calcium channel activity, or inhibition of ATP-sensitive potassium channels. The decrease in PRA results in a decrease in angiotensin II (AngII) and plasma aldosterone concentration (PAC). This study investigates whether these hypoxia-induced mechanisms can be inhibited by the L-type voltage-dependent calcium channel antagonist nifedipine. Eight conscious, chronically tracheotomized dogs received a low sodium diet (0.5 mmol Na x kg body wt(-1) x day(-1)). The dogs were studied twice in randomized order, either with nifedipine infusion (1.5 microg x kg body wt(-1) x min(-1), Nifedipine) or without (Control). The dogs were breathing spontaneously: first hour, normoxia [inspiratory oxygen fraction (FiO2)=0.21]; second and third hour hypoxia (FiO2=0.1). In Controls, PRA (6.8+/-0.8 vs. 3.0+/-0.5 ngAngI x ml(-1) x min(-1)), AngII (13.3+/-1.9 vs. 7.3+/-1.9 pg/ml), and PAC (316+/-50 vs. 69+/-12 pg/ml) decreased during hypoxia (P<0.05). In Nifedipine experiments, PRA (6.5+/-0.9 vs. 10.5+/-2.4 ngAngI x ml(-1) x min(-1)) and AngII (14+/-1.1 vs. 18+/-3.9 pg/ml) increased during hypoxia, whereas the decrease in PAC (292+/-81 vs. 153+/-41 pg/ml) was blunted (P<0.05). These results foster the idea that the hypoxia-induced decrease in PRA involves L-type calcium channel activity.

[A new method of ex vivo whole blood perfusion of isolated mammalian organs, exemplified by the kidney of swine]. / Eine neue Methode zur Ex-vivo-Vollblut-Perfusion isolierter Warmblüterorgane, dargestellt an der Niere von Schweinen.

A new method for the ex vivo perfusion of organs from large mammals is described. Gas exchange and dialysis are carried out simultaneously with a low-flux polysulfon dialysis module. The dialysate (e.g. Tyrode solution) is aerated with a mixture of oxygen and carbon dioxide to ensure gas exchange with the blood. Dialysis is carried out in a closed thermostatically controlled system. Monitoring of ultrafiltration is maintained by continuously weighing the blood reservoir and adjusting an afferent and efferent blood pump. Initial results obtained with isolated pig kidneys demonstrate the suitability of the new method for use as a model for the replacement of animal experiments. Theoretically, clinical application in the area of in vivo regional organ perfusion may also be possible.

Pulmonary-renal axis during positive-pressure ventilation.

Controlled mechanical ventilation with positive end-expiratory pressure (PEEP) is generally associated with decreases in urine volume and renal sodium excretion. The resulting positive sodium and water balance is an undesirable side effect of controlled mechanical ventilation with PEEP. The increase in intrathoracic pressure initiates a cascade of hemodynamic, neural, and hormonal changes which, in turn, stimulate the kidney to decrease the glomerular filtration rate and increase tubular reabsorption. The redundancy of these regulatory mechanisms makes it difficult to determine the involvement of only one or two single parameters as causative events of the phenomenon.

The effect of anaesthesia on renal function.

Anaesthesia and surgical stress can affect renal function and body fluid regulation indirectly as well as directly. The indirect effects, through influences on haemodynamics, sympathetic activity and humoral regulation, are more pronounced than the direct ones. Inhalational anaesthetics generally reduce glomerular filtration rate and urine output, mainly by extra-renal effects that are attenuated by pre-operative hydration. Opioids, barbiturates and benzodiazepines also reduce glomerular filtration rate and urine output. The effects of regional anaesthesia seem to be less than those of general anaesthesia and are related to changes in systemic haemodynamics. These peri-operative alterations of renal function are usually transient and clinically insignificant. Mechanical ventilation decreases urine volume and sodium excretion to an extent that depends on the increase in intrathoracic pressure, though ADH release, unloading of baroreceptors and activation of the renin-angiotensin system may also be involved. The direct effects of anaesthesia which are dose- and agent-dependent include effects on autoregulation of renal blood flow, alteration in the effect of ADH, and effects on tubular transport of sodium and organic acids. The only proven direct toxic effect of any anaesthetic agent is the fluoride-related toxicity of methoxyflurane.

Sodium homeostasis in conscious dogs after chronic cardiac denervation.

The ability to regulate renal sodium excretion after an acute reduction of total body sodium by peritoneal dialysis (PD) and subsequent dietary sodium repletion was investigated in 12 [6 intact, 6 chronically cardiac denervated (CD)] conscious, chronically instrumented dogs. For 10 days, balance experiments were performed with daily measurements of mean arterial blood pressure (MABP), right atrial pressure (RAP), and heart rate (HR). The prepared diet contained 0.5 (days 1-3 after PD) or 2.5 mmol Na.kg body wt-1.day-1 (control day and days 4-9 after PD). Control values were all similar in both groups except higher fasting plasma renin activities (PRA) were observed in the CD dogs [2.6 +/- 0.4 vs. 1.0 +/- 0.2 ng angiotensin I (ANG I).ml-1.h-1; P less than 0.05]. Days 1-4 after PD, RAP fell in both groups by 2-3 cmH2O, and renal sodium excretion decreased abruptly. PRA increased to 22.8 +/- 4.1 (intact) and 29.9 +/- 4.9 ng ANG I.ml-1.h-1 (CD dogs) (day 3 after PD). Both groups continued to retain sodium, and when it was available again, PRA decreased. After the amount of sodium lost by PD was regained, the intact dogs remained in a balanced equilibrium. In the CD dogs, PRA was still above control, and they retained sodium in excess (+ 1.9 +/- 0.1 mmol/kg body wt). We conclude that the cardiac nerves are not essential for stimulating PRA and sodium retention after an acute sodium deficit. However, the inhibition of PRA and the rapid adjustment of sodium balance during sodium repletion is impaired after cardiac denervation.

Plasma renin activity during hypotensive responses to electrical stimulation carotid sinus nerves in conscious dogs.

1. The interaction of electrical stimulation of the carotid sinus nerves (carotid sinus nerve stimulation, CSNS) with mechanisms of renin release was studied in conscious and unrestrained resting beagle dogs receiving a standardized diet (sodium intake, 4.5 mmol/kg bodyweight (bw); water intake, 91 mL/kg bw). 2. By CSNS, mean arterial blood pressure (MAP) was lowered for periods of 20 min to levels between 101 +/- 4 and 56 +/- 5 mmHg. 3. In another group of conscious dogs, renal perfusion pressure (RPP) was lowered to 95 +/- 4 mmHg for periods of 20 min by partial suprarenal aortic occlusion in order to assess the influence of a reduced RPP on plasma renin activity (PRA) without concomitant CSNS. 4. During CSNS, PRA increased markedly (> 100%) only when MAP was reduced below 75 mmHg. 5. With aortic constriction and an RPP of 95 mmHg, the increase in PRA was 955%, which is more than three-fold higher than the increase in PRA during CSNS at MAP levels < 65 mmHg (314%). 6. The observed responses indirectly support the hypothesis that basal activity in efferent renal nerve discharge is present even at rest and can be inhibited by CSNS, and furthermore suggests that CSNS attenuated the pressure-dependent renin release.

Arterial blood gas tensions and acid-base status of Wistar rats during thiopental and halothane anesthesia.

Arterial blood gas tensions and acid-base status of spontaneously-breathing, unanesthetized Wister rats were compared with values obtained during 4 hr of thiopental and 6 hr of halothane (1%) anesthesia. During thiopental anesthesia, marked respiratory depression occurred (PaCO-2:57.0 plus or minus 10.0 MM Hg, PaO-2:70.4 plus or minus 11.2 MM Hg). Thirty-six percent of the rats died. During inhalation of room air and 1% halothane, PaO-2 decreased also, whereas PaO-2 did not change. Twenty-seven percent of the original number of rats died. Lowered arterial oxygen tension may have caused death; no rats died during inhalation of oxygen and 1% halothane. This technic insured sufficient analgesia for surgical procedures without marked alterations of the acid base status and is recommended for long-term anesthesia of small laboratory animals like rats.

Renal norepinephrine content decreases after chronic flow probe implantation.

Electromagnetic flow probes were chronically implanted around the left renal artery in 6 female beagle dogs. 3-10 months after implantation, renal cortex norepinephrine contents of right and left kidneys were compared (liquid chromatography). In 4 out of the 6 dogs investigated 3-6 months after implantation, the norepinephrine content of the left kidney was reduced by 27-72%. In 2 dogs investigated 7 and 10 months after implantation, the difference between left and right kidney was not significant. These findings should be taken into consideration when interpreting results from chronically instrumented kidneys.

Role of renal arterial pressure in the regulation of extracellular volume in conscious dogs.

1. This study in conscious dogs examined the quantitative effects of a reduction in the renal arterial pressure on the renal homeostatic responses to an acute extracellular fluid volume expansion. 2. Seven female beagle dogs were chronically instrumented with two aortic catheters, one central venous catheter and a suprarenal aortic cuff, and were kept under standardized conditions on a constant high dietary sodium intake (14.5 mmol of Na+ day-1 kg-1 body weight). 3. After a 60 min control period, 0.9% (w/v) NaCl was infused at a rate of 1 ml min-1 kg-1 body weight for 60 min (infusion period). Two different protocols were applied during the infusion period: renal arterial pressure was maintained at 102 +/- 1 mmHg by means of a servo-feedback control circuit (RAP-sc, 14 experiments) or was left free (RAP-f, 14 experiments). 4. During the infusion period, in the RAP-sc protocol as well as in the RAP-f protocol, the mean arterial pressure increased by 10 mmHg, the heart rate increased by 20 beats/min, the central venous pressure increased by 4 cmH2O and the glomerular filtration rate (control 5.1 +/- 0.3 ml min-1 kg-1 body weight, mean +/- SEM) increased by 1 ml min-1 kg-1. 5. Plasma renin activity [control 0.85 +/- 0.15 (RAP-f) and 1.08 +/- 0.23 (RAP-sc) pmol of angiotensin I h-1 ml-1] decreased similarly in both protocols.(ABSTRACT TRUNCATED AT 250 WORDS)

The control of sodium metabolism to maintain osmo- and volumehomeostasis.

Chronically instrumented female beagles were maintained in standardized environmental and dietary conditions allowing careful examination of the mechanisms governing sodium homeostasis. The experimental increase in left atrial pressure (obtained by a reversible mitral stenosis) is accompanied by an increase in sodium excretion (atrial natriuresis, AN). AN served as an experimental manoeuvre from which the mechanisms governing sodium homeostasis could be elucidated. The results allow the following conclusions: (1) The 'signals' arising from distension of the left atrium (e.g. expansion of the extracellular fluid volume) appear not to be a necessary prerequisite for the maintenance of sodium homeostasis. (2) The control mechanisms seem to be very sensitive to changes in total body sodium (TBS). A small reduction in TBS abolishes sodium eliminating processes e.g. saline diuresis, osmotic diuresis, AN. (3) It is probable that a natriuretic factor exists for sodium elimination. In summary, total body sodium appears to be controlled by a series of 'redundant' mechanisms which guarantee an appropriate strategy for the comfort and ultimate survival of the organism. At the moment it is impossible to quantitate the contributions made by the various mechanisms in the control of sodium metabolism.