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Biomedical subjects

O S Better

Publications and source records attributed to O S Better.

At least 19 recordsLinked to original sources
PubMed1992

Effect of hypertonicity on contractility of isolated working rat left ventricle.

OBJECTIVE: The aim was to evaluate the effect of hypertonic perfusate on isolated left ventricular mechanical and energetic characteristics. METHODS: An isolated working rat heart model was perfused with a hyponatraemic Krebs-Heinseleit bicarbonate buffer (240 mOsmol.litre-1). To this buffer was added increasing amounts of mannitol to achieve 280, 320, and 360 mOsmol.litre-1 perfusates. RESULTS: Left ventricular peak pressure, maximum time derivative of left ventricular pressure (dP/dtmax), and end systolic pressure were all increased to a maximum value at 280 or 320 mOsmol.litre-1 perfusate tonicity. A similar response was evident with cardiac output, which changed from 33.7(SEM 0.6) to 43.5(0.8) ml.min-1 following changing the perfusate tonicity from 240 to 280 mOsmol.litre-1 (p less than or equal to 0.003). However, increasing perfusate tonicity further decreased cardiac output to 36.5(1.3) ml.min-1 at 360 mOsmol.litre-1. Maximal left ventricular elastance remained unchanged during perfusion with increasing perfusate tonicities. CONCLUSIONS: Changing perfusate osmolality using mannitol has a positive inotropic effect at low osmolalities and a negative inotropic effect at perfusate osmolality greater than 320 mOsm.litre-1.

Animals↗
PubMed1992

Muscle microcirculatory impairment following acute compartment syndrome in the dog.

Visualization of the intramuscular microcirculation during and after compartmental syndrome was studied by microangiograms and histologic cross sections. A marked reduction in the circulation of the endomysial capillary network was found during compartment tamponade, whereas the perimysium arteriolar system was patent. Revascularization took place by formation of distorted blood vessels accompanied by intramuscular hematomas in muscles 7 and 14 days after the compartment insult. The cross sections show massive fibroblastic activity around blood vessels that caused concealed intramuscular pressure-ischemic contracture resulting in the foci of myofibrillar necrosis seen within normal muscle tissue. The muscle located in the tamponaded compartment profusely bleeds when it is touched, even though its viability is in doubt. The explanation for this clinical observation might be the abnormal intramuscular revascularization that was found in this work.

Acute Disease↗
PubMed1992

Sodium modulates inotropic response to hyperosmolarity in isolated working rat heart.

The present study was designed to examine the effects of acute changes in perfusate Na+ concentrations and osmolarities on left ventricular (LV) mechanics in the isolated working rat heart model. Specifically, we separated the effect of isosmotic perfusates with different Na+ concentrations on LV mechanics. After a control period during which the hearts were perfused in a working mode with a control solution of Krebs-Henseleit bicarbonate buffer (Na+ of 136 meq/l, Ca2+ of 2.6 mM, and osmolarity of 300 mosM), the hearts were subjected to different perfusates (Na+ of 96-156 meq/l and osmolarity of 240-380 mosM, using different mannitol concentrations) in a semirandom order. Peak LV pressure (PLVP), maximal time derivative of LV pressure (dP/dtmax), and cardiac output (CO) were recorded. Increasing Na+ concentrations from 96 to 156 meq/l, using isosmotic perfusates, decreased PLVP, dP/dtmax, and CO in a dose-dependent manner. The dose-dependent behavior was evident for tonicities of 240, 280, 320, and 360 but not for 380 mosM. Increasing Na+ concentration from 96 to 136 meq/l at constant perfusate tonicity (320 mosM) decreased dP/dtmax from 6,753 +/- 133 to 5,602 +/- 418 mmHg/s (P < 0.001). Rearranging the same results to examine the effect of perfusate tonicity with iso-Na+ concentration demonstrated that increasing perfusate osmolarity had a dose-dependent effect on PLVP, dP/dtmax, and CO. At a constant Na+ concentration of 116 meq/l, increasing perfusate osmolarity from 240 to 320 mosM increased dP/dtmax from 6,116 +/- 132 to 7,274 +/- 594 mmHg/s (P < 0.01). Further increase in perfusate tonicity to 380 mosM decreased dP/dtmax to 2,338 +/- 398 mmHg/s (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effect of atrial natriuretic factor on renal cGMP production in rats with adriamycin-induced nephrotic syndrome.

Adriamycin-induced nephrotic syndrome in the rat is associated with a blunted natriuretic response to infusion of atrial natriuretic factor. To study the mechanism of renal hyporesponsiveness to the peptide in rats with experimental nephrosis, we evaluated the effects of the hormone on renal production of cGMP, the second messenger of the hormone. Baseline GFR and sodium excretion were lower in nephrotic as compared with normal controls. Infusion of synthetic rat atrial natriuretic factor (10 micrograms/kg/h) increased fractional sodium excretion by 7.3 +/- 2.4% in control rats but only by 1.4 +/- 0.5% in adriamycin-treated rats (P less than 0.05). However, the increments in urinary nucleotide excretion rate (UcGMP x V/GFR), in response to atrial natriuretic factor infusion, were comparable in control and nephrotic rats (control, 114.7 +/- 16.1 pmol/mL; adriamycin, 95.5 +/- 12.0 pmol/mL; P was not significant). The in vitro generation of cGMP in response to incremental doses of the hormone (10(-11) to 10(-6) M + 1 mM 3-isobutyl methyl xanthine) was of similar magnitude in isolated glomeruli derived from control (2.4 +/- 0.25 to 9.1 +/- 1.0 pmol/mg of protein) and nephrotic rats (2.9 +/- 0.2 to 10.3 +/- 1.0 pmol/mg of protein) and was not impaired in suspensions of medullary tissue derived from nephrotic rats (control, 8.4 +/- 0.6 to 14.2 +/- 1.2 pmol/mg of protein; adriamycin, 7.3 +/- 0.7 to 22.0 +/- 2.4 pmol/mg of protein).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Hypertonic mannitol ameliorates intracompartmental tamponade in model compartment syndrome in the dog.

Acute compartment syndrome (ACS) is a devastating complication of rhabdomyolysis caused by muscle tamponade secondary to increased intracompartmental pressure (Pi). ACS requires emergency surgical decompression when Pi greater than 30 mmHg (normal less than 4.0 mmHg) and clinical signs exist. The present study was undertaken to examine whether mannitol which has been used extensively for prevention of acute renal failure in rhabdomyiolysis may also improve muscular hemodynamics in ACS. ACS was produced in dogs by injecting dog plasma into the anterolateral compartment of the hind limb. The Pi was directly monitored. Control dogs received saline, whereas experimental dogs received intravenously 20% mannitol (0.15 ml/min/kg) over a period of 1 h. The initial Pi was set arbitrarily at 100 mm Hg. Following the establishment of ACS, the spontaneous mean decrease in Pi in the control group was 40% of initial value over 60 min (n = 5) versus a decrease of 65%/60 min in the experimental (mannitol) group (n = 7, p less than 0.01). The net mean decompressive effect of mannitol treatments was approximately 28 mm Hg (mean control Pi minus mean experimental Pi at time 60 min). Extrapolated to man with ACS, such a decrease in Pi induced by mannitol theoretically could relieve compartmental tamponade noninvasively.

Angiography↗
PubMed1991

Acid-base balance and acute renal failure.

In several models of acute renal failure (ARF) in animals, acidosis has been found to worsen the renal failure, whereas alkalosis may ameliorate it. Most evidence points to a reduction in the degree of tubular obstruction by casts as the explanation for the beneficial effects of bicarbonate administration. However, alkalinization of the urine is effective only in some experimental conditions but not in others. The reason for these differences is not known but may relate to the nature of the obstructing casts. Alkalinization of the urine could decrease cast formation in Bence-Jones protein and hemoglobinuric ARF by increasing the negative charge on these molecules, thereby diminishing precipitation with anionic Tamm-Horsfall protein. In contrast, release of tubular cell contents into the urine, as occurs in renal ischemia, could lead to complex casts not responsive to alterations in urine pH. In aminoglycoside ARF, the beneficial effects of urine alkalinization may be due primarily to reduced uptake of the antibiotic by tubular epithelium, resulting in less cellular damage. Because tubular obstruction reduces net filtration pressure, new approaches to therapy which include efforts to raise net glomerular filtration pressure may improve the therapeutic efficacy of alkali administration.

Acid-Base Imbalance↗
PubMed1990

[Crush syndrome].

Explore the source record for details and available documents.

Crush Syndrome↗
PubMed1990

The crush syndrome revisited (1940-1990).

This article reviews the local and systemic effects of crush injury. Within minutes to hours after extrication of survivors trapped under fallen masonry (and immediately following decompression of limbs), a massive volume of extracellular fluid is lost into the injured muscles, leading to circulatory failure. Solutes leaking out of damaged muscles cause a spectrum of metabolic disturbances. Chief among them are hyperkalemia and hypocalcemia which, synergistically, have a lethal cardiotoxic potential, particularly in hypotensive patients. Early volume replacement, preferably already started at the rescue site, may combat shock and correct the hyperkalemia. If urine flow is established, this regimen should be followed by a forced solute-alkaline diuresis for the prevention of myoglobinuric and uricosuric acute renal failure, which is a common and ominous late complication of crush injury. Preparation for future catastrophes occurring particularly in remote regions where an 'epidemic' of crush syndrome may be forecast, should include the setting up of a radio communications network to coordinate rescue and salvage operations and the forwarding of intravenous fluid bags and lines to the disaster site. Also, it is advisable to prepare artificial kidney devices which do not require pumps and electricity and which utilize a low dialysate volume for emergency temporary use, until conventional definitive medical facilities and services have been reestablished.

Acute Kidney Injury↗
PubMed1990

Nonazotemic hyperkalemia with renal and extrarenal defects in potassium transport: association with high levels of digoxin-like immunoreactive factor.

We report a hypertensive patient with nonazotemic hyperkalemia caused by a combined disturbance in both the internal and external balance of potassium. During a follow-up of 30 months, exacerbations of hyperkalemia were observed, interposed with a return to the previous baseline. Two brief normokalemic periods were recorded. Blood pressure tended to be higher during hyperkalemic peaks. The following findings were detected: (1) hyperchloremic hyperkalemic acidosis with normal glomerular filtration rate, adequately elevated plasma aldosterone levels, and normovolemia; (2) a tubular defect in potassium excretion, refractory to intravenous sodium sulfate (nonreabsorbable anion) and mineralocorticoids; (3) impaired tissue uptake of potassium under insulin administration; (4) exaggerated hyperkalemia following beta-adrenergic blockade and blunted hypokalemic response to a beta-agonist; and (5) a defect in Na/K transport in erythrocytes detected in vitro, coexistent with an elevated level of free digoxin-like immunoreactive factor in serum. These results suggest that our patient had a generalized abnormality in potassium transport.

Acid-Base Equilibrium↗
PubMed1990

The mechanism of muscle injury in the crush syndrome: ischemic versus pressure-stretch myopathy.

Crush injuries are ubiquitous, common sequelae in victims of seismic, industrial and military catastrophes, and were considered to be mainly due to ischemia of the affected limbs. Our clinical experience suggests that early in the crush syndrome, interference with the circulation may occur but is rare. The predominant earliest lesion in the crush syndrome is postulated to be pressure-stretch myopathy, rather than ischemic myopathy. It is proposed that at the membrane level, stretch increases sarcoplasmic influx of Na, Cl, H2O and Ca down their electrochemical gradient. Energy-requiring cationic extrusion pumps work at maximal capacity, but are unable to cope with the increased load. This results in cell swelling and increase in cytosolic and mitochondrial calcium with activation of autolytic destructive processes and interference with cellular respiration. Extensive muscle swelling may cause late muscle tamponade and myoneural ischemic damage (compartmental syndrome). Thus, whereas prevalent theory suggests that the sarcolemmal cationic pump activity is attenuated in the crush syndrome due to early ischemia, we propose that the cationic extrusion pump is maximally activated as in the amphotericin B model. Because the cationic pump is maximally activated in the stretched muscle and in cells exposed to amphotericin, these models rapidly deplete their scarce ATP stores and are susceptible to hypoxia in the face of initially normal circulation.

Biological Transport, Active↗
PubMed1989

Portal hypertension ameliorates arterial hypertension in spontaneously hypertensive rats.

Systemic hemodynamic effects of portal hypertension in arterial hypertension and their relationship to serum bile acid levels were investigated using spontaneously hypertensive rats 2 and 15 weeks after partial portal vein ligation (SHR-PVL) or sham operation (SHR-SH) and normotensive controls. Mean arterial pressure in SHR-PVL at 2 weeks was decreased to normal due to a decrease in peripheral resistance. Mean arterial pressure and peripheral resistance in SHR-PVL at 15 weeks did not differ from SHR-SH. Resolution of this arterial hypotensive effect and systemic hyperdynamic circulation was associated with decreased portal-systemic shunting. Bile acid levels were increased in both SHR-PVL groups. These results suggest that an endogenous circulating vasodilator(s) associated with portal hypertension ameliorates the systemic vasoconstriction in SHR. Bile acids, while not direct mediators of these hemodynamic events, may be prototypic of this vasodilator. This arterial hypertensive model may aid further investigation of the mechanisms contributing to the hyperdynamic state in portal hypertension.

Animals↗
PubMed1989

Traumatic rhabdomyolysis ("crush syndrome")--updated 1989.

In rescue operations for people trapped under fallen debris, i.v. replenishment of the massive internal fluid volume losses should be started as soon as physical contact has been established with the injured person. This should be followed by induced alkaline-mannitol diuresis. This regimen will stabilize the impaired hemodynamics, prevent myoglobinuric and hyperuricosuric renal failure, and correct the hyperkalemia and metabolic acidosis often seen in rhabdomyolysis. This treatment is effective even in individuals rescued after 28 h. Local treatment of the crushed limbs should be conservative. A closed injury should not be converted into an open one unless distal arterial perfusion has been compromised.

Animals↗