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Biomedical subjects

G Kaczmarczyk

Publications and source records attributed to G Kaczmarczyk.

At least 55 records · Page 3Linked to original sources
PubMed1982

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.

Animals↗
PubMed1981

Left atrial distension and intrarenal blood flow distribution in conscious dogs.

Measurements were made with radioactive microspheres of the distribution of renal blood flow in conscious dogs during left atrial distension. Urine volume, sodium excretion, mean arterial blood pressure and heart rate increased during the 60 min period of left atrial distension (increase in left atrial pressure by about 1.0 kPa). Total renal blood flow and cardiac output (electromagnetic flowmeters) did not change. The perfusion rates of four renal zones did not change. Striated muscle blood flow (M. psoas) fell markedly.--Stimulation of left atrial receptors in conscious dogs is followed by an increase in renal and skeletal muscle resistance. The diuresis and natriuresis during left atrial distension is not accompanied by a detectable redistribution of renal cortical blood flow.

Animals↗
PubMed1981

The role of the cardiac nerves in regulation of sodium excretion in conscious dogs.

Conscious, chronically instrumented dogs, maintained on a high sodium intake, were used to investigate whether surgical cardiac denervation impairs the natriuresis associated with left atrial pressure increase produced in three ways: during an increase in left atrial pressure by means of a reversible mitral stenosis (protocol 1); after an i.v. saline load (1.0 ml 0.9% saline min-1 . kg-1 over 60 min) (protocol 2); after an oral saline load (14.5 mmol Na . kg-1 given with the food as isotonic solution) (protocol 3). During a reversible mitral stenosis, in intact dogs, urine volume and sodium excretion increased markedly (from 34--145 microliters . min-1 . kg-1 and from 3--12 mumol . min-1 . kg-1); mean arterial pressure increased by an average of 2 kPa (15 mm Hg) and heart rate by 53 b/min; plasma renin activity fell from 0.37--0.21 ng AI . ml-1 . h-1 . Cardiac denervation eliminated these effects of left atrial distension except for a small increase in heart rate (12 b/min). This indicates that the natriuresis and diuresis during left atrial distension resulted from stimulation of receptors located in the left atrium. In contrast, during protocol 2 and 3, the same amounts of sodium and water were excreted in the cardiac denervated dogs as compared to the intact dogs. A comparable decrease in plasma renin activity also was observed. -- Apparently the presence of the cardiac nerves is not a prerequisite for maintenance of sodium and water homeostasis.

Animals↗
PubMed1980

Atrial natriuresis under the condition of a constant renal perfusion pressure: experiments on conscious dogs.

An experimental elevation of left atrial pressure (eLAP) by means of a reversible mitral stenosis is accompanied with an increase in sodium excretion (UNaV) and arterial blood pressure (by about 20 mm Hg, 2.7 kPa), and by a decrease in plasma renin activity. It is well established that an increase in renal perfusion pressure (Pren) can augment UNaV. Therefore the present study was undertaken to examine whether the eLAP-induced natriuresis was caused by the increased Pren. -Four female beagle dogs were kept under controlled environmental conditions. They received a sodium rich diet (14.5 mmol/Na/kg/d). The dogs were chronically instrumented: purse string around the mitral annulus, catheter in the left atrium, carotid loop, pneumatic cuff above the renal arteries, pressure transducer below the renal arteries. Pren was kept constant by means of a digital servofeedback control circuit. The dogs served as their own controls (13 experiments without and 15 experiments with a controlled renal perfusion pressure were performed). After eLAP(+1.0 kPa), UNaV rose from 4.1 +/- 2.6 to 10.3 +/- 3.9 mumol Na/min/kg. If Pren was kept constant, the corresponding values were 4.2 +/- 2.8 and 9.3 +/- 2.9 mumol/min/kg. These data clearly indicate that the atrial natriuresis is not mediated by an augmentation of renal perfusion pressure. Therefore these results support the hypothesis that atrial natriuresis probably is due to en eLAP-induced suppression of the renin-angiotensin-system or other natriuretic mechanisms.

Animals↗
PubMed1978

No relation between atrial natriuresis and renal blood flow in conscious dogs.

Conscious dogs were used to study whether changes in total renal hemodynamics are responsible for diuresis and natriuresis during an experimental increase in left atrial pressure (LAP). To ensure a controlled dietary sodium intake, the dogs (n = 8) were chronically kept on a high or a low sodium intake diet (HSI; LSI). After the dogs had completely recovered from surgery (carotid loop, thoracotomy, flank incision), LAP was increased by about 10 cm H2O for 60 min by tightening a purse string around the mitral annulus (51 expts.). Mean urine volume (V) increased in both groups to a comparable degree. Mean sodium excretion increased somewhat more in HSI dogs, but remained elevated in LSI dogs after the LAP increase. Renal blood flow (electromagnetic flow transducer) and inulin clearance did not change. Renal vascular resistance (RVR) increased by about 20% (HSI) and 15% (LSI). --When the induced LAP INCREASE WAS TERMINATED, V decreased. RVR decreased in HSI dogs by about -11% and in LSI dogs by about -6% below control values. --It is concluded that volume regulatory mechanisms induced by an experimental LAP increase operate independently of changes in total renal blood flow.

Animals↗
PubMed1977

Left atrial pressure and sodium balance in conscious dogs on a low sodium intake.

10 conscious chronically prepared dogs were used. After recovery from thoracotomy (catheter into the left atrium, nylon purse string around the mitral annulus) they were kept chronically on a low sodium intake (less than 0.5 meq Na/kg bw daily). On 51 days left atrial pressure (LAP) was increased for 60 min about 10 cm H2O once daily by tightening the purse string (distension period: DP). During (DP) urine volume (V) increased about threefold, and sodium excretion (ENa) about sixfold. The amount of renal sodium loss on the days when LAP was increased exceeded the daily intake considerably. The application of DOCA (15 mg i.m.) did not diminish ENa during DP and 60 min therere increased by about 15 mm Hg. The data suggest that stimulation of intrathoracic receptors by a reversible mitral stenosis augments renal sodium excretion even in a state of a highly stimulated tubular sodium resorption.

Animals↗
PubMed1977

Left atrial pressure and postprandial diuresis in conscious dogs on a high sodium intake.

5 conscious, well trained, female dogs kept on a high sodium intake (14 meq Na/kg bw) were used to measure left atrial pressure (LAP), urine volume (V), sodium and potassium excretion (UNaV, UKV) as well as plasma osmolality (Posm) before and up to 180 min after food intake. The dogs were fitted with a catheter in the left atrium (thoracotomy). In all experiments (n=23) LAP increased postprandially (pp) above fasting controls. The mean peak increase ranged from 4 to 6 cm H2O and was observed as early as 61-80 and as late as 161-180 min pp. Increase in LAP was closely correlated to V which rose from 36+28 to 160+51/ul/min. kg. pp V was also correlated to pp UNa V, which increased from 4.8 +/- 3.3 to 34.O+/-8.5/ueq/min-kg. The pp increase in LAP and its close relation to pp V and pp UNav emphasize the assumption that intrathoracic receptors are involved in the regulation of body fluids.

Animals↗
PubMed1975

Postprandial changes of renal blood flow. Studies on conscious dogs on a high and low sodium intake.

Postprandial renal blood flow was studied in 14 conscious dogs on a chronic high and low sodium intake on 72 days after implantation of an electromagnetic flow transducer around the left renal artery. Fasting renal blood flow was 11.7 plus or minus 3.2 ml/min with kg on high socium intake (43 days) and 11.5 plus or minus 3.3 ml/min with kg on low sodium intake (29 days). During ingestion no change of renal blood flow occurred; mean arterial pressure rose transiently. During digestion renal blood flow increased always and was, like the fasting renal blood flow of dogs on a high sodium intake was 41 plus or minus 23%, and of dogs on a low sodium intake 35 plus or minus 15% referring to fasting controls; peak increase mostly occurred between 60 and90 min postprandially and was due to a decrease of renal vascular resistance. Renal blood flow also increased after augmentation of intravascular volume by an intravenous infusion; volume receptors may be involved.

Animals↗
PubMed1975

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.

Acid-Base Equilibrium↗
PubMedDate not supplied

Acute effects of angiotensin II on renal haemodynamics and excretion in conscious dogs.

The effects of a 60-min intravenous infusion of angiotensin II (A II; 4 or 20 ng A II/min/kg body weight) on renal blood flow (RBF; electromagnetic flow transducer, control value 19-25 ml/min/kg), glomerular filtration rate (GFR; control value 4.2-5.0 ml/min/kg), mean arterial blood pressure, sodium excretion, water excretion, and plasma A II and plasma aldosterone concentrations were examined in 6 chronically instrumented female conscious beagle dogs kept on three different dietary sodium intakes (SI): SI 0.5 or SI 2.5 mmol Na/kg/day or SI 4.5 mmol Na/kg/day plus an oral saline load prior to the experiment SI 4.5(+) dogs. Four nanograms A II decreased RBF and GFR in SI 4.5(+) dogs without changing the filtration fraction (FF%); in SI 0.5 dogs the RBF decreased, and the FF% increased. Twenty nanograms A II decreased RBF and increased FF% in all dietary protocols, less in SI 4.5(+) dogs. The mean arterial blood pressure increased in all dietary protocols by 10-15 mm Hg (4 ng A II) and 32-37 mm Hg (20 ng A II). Sodium and water excretions decreased by 32 and 46%, respectively, in SI 4.5(+) dogs at both doses of A II. The plasma aldosterone concentration increased in all but one protocol: 4 ng A II, SI 4.5(+) dogs. It is concluded that when A II plasma concentrations are most likely borderline to pathophysiological conditions (up to an average of 370 pg/ml), the GFR is less decreased than the RBF. This phenomenon also can be observed at lower plasma A II concentrations (average 200 pg/ml), when the renin-angiotensin system had been previously moderately activated.

Aldosterone↗