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Biomedical subjects

R D Rink

Publications and source records attributed to R D Rink.

8 recordsLinked to original sources
PubMed1979

The effect of methylprednisolone on hepatic oxygen supply and plasma lactate and glucose in endotoxemia.

This study was designed to determine the effect of methylprednisolone on the profile of hepatic oxygen supply and selected blood parameters in fasted, male rats administered an LD85 dosage of E coli endotoxin intraperitoneally. Mortality rates within 24 hours were 85% in rats receiving endotoxin only, 9% in rats receiving a 30 mg/kg dosage of methylprednisolone intraarterially one hour subsequent to endotoxin insult, and 0% in methylprednisolone controls. Beginning with the fourth hour, untreated endotoxin rats had significantly higher heart rates and lower plasma glucose; by the sixth or eighth hour there was significantly greater hypocapnia, lower blood pH, and higher plasma lactate levels in comparison to endotoxic rats receiving methylprednisolone. In addition, mean hepatic pO2 between the sixth and seventh hours was 2.6 mm Hg in endotoxic rats, 10.6 mm Hg in endotoxic methylprednisolone rats, and 17.7 mm Hg in methylprednisolone controls. Methylprednisolone controls showed a steady increase of plasma glucose levels through eight hours but were otherwise stable. Maintenance of hepatic circulation is cited as the probable basis for differences of morbidity and mortality between treated and glucocorticoid-treated endotoxic rats.

Animals↗
PubMed1979

Hepatic cellular hypoxia in murine peritonitis.

Reduced oxygen consumption and lactic acidosis were observed frequently in patients with peritonitis. This study was designed to evaluate whether reduced oxygen consumption is secondary to deficient oxygen delivery or is a function of primary injury to mitochondria. Peritonitis was produced in rats by cecal ligation and perforation. Animals were killed at 2, 4, and 6 hours and agonally. Oxygen utilization was studied polarographically in isolated hepatic mitochondria with glutamate, pyruvate, and succinate substrates. State 3, state 4, respiratory control index (RCI), and ADP:O ratios were determined. Whole tissue and isolated mitochondrial ultrastructure were examined by electron microscopy. Systemic blood pressure and oxygenation were monitored. Hepatic tissue oxygenation was examined using a surface oxygen electrode. Peritonitis resulted in acceleration of state 3 respiratory rates and increased respiratory control indices at all time intervals. Maximal respiratory control was observed at 4 hours with all substrates. Whole tissue mitochondria demonstrated mild swelling and thinning of membranes and matrix. Experimental and control isolates showed similar orthodox-to-condensed conformational changes. Hepatic tissue oxygenation declined to less than 10% of control by 6 hours, while arterial Po2 was unchanged. The conclusions of this study are that lethal peritonitis results in (1) no primary injury to the hepatic mitochondria, (2) increased efficiency of hepatic mitochondrial oxygen utilization, and (3) reduced hepatic tissue oxygenation. The exact mechanisms of defective oxygen delivery require further study.

Animals↗
PubMed1978

The acute effects of nicotine, tobacco smoke and carbon monoxide on myocardial oxygen tension in the anaesthetized cat.

1 The acute effects of nicotine, tobacco smoke, and carbon monoxide on myocardial oxygen tension (MPo(2)) were estimated amperometrically in 33 anaesthetized open-chest cats with a glass-insulated 25 mum platinum cathode within a 22-gauge needle implanted in the left ventricular wall.2 MPo(2) was 1.6-60 mmHg (mean 23.5 mmHg) when arterial Po(2) was >80 mmHg. Sequential intravenous infusions of nicotine (2-3 mug/kg every 45 s) or intracheal puffs (3-5 ml) of tobacco smoke commonly produced transitory increases (25-35 mmHg) of arterial pressure and 4-6 mmHg increments of MPo(2). Intratracheal puffs (5 ml) of 5% carbon monoxide sufficient to increase carboxyhaemoglobin from 0.8 to 1.5% to 4-7% had no effect on arterial Po(2) or blood pressure but typically decreased MPo(2) by approximately 1-4 mmHg. Augmentation of MPo(2) often succeeded carbon monoxide administration.3 Arterial hypoxia (arterial Po(2) < 60 mmHg) reduced mean MPo(2) to 14.4 mmHg but anoxic levels were not observed. Pressor responses to nicotine and tobacco smoke were accompanied by small increases (usually 1-3 mmHg) of MPo(2). Puffs of 5% carbon monoxide had less effect than during normoxia. Locations of low MPo(2) (<10 mmHg) were unaffected as carboxyhaemoglobin was raised to 7-11% during hypoxaemia.4 It is concluded that nicotine and tobacco smoke cause augmentation of myocardial oxygen supply, even during moderate hypoxaemia. By contrast, smoking dosages of carbon monoxide have the potential of producing a small reduction of MPo(2) during normoxia, but the effect is negligible during moderate hypoxaemia.

Animals↗
PubMed1978

Hepatic oxygen supply and plasma lactate and glucose in endotoxic shock.

Hepatic oxygen supply and selected blood parameters were recorded in fasted male rates given 20--30 mg/kg Escherichia coli endotoxin intraperitoneally. Mortality was 70% within 24 hours. Measurements during the initial eight hours postendotoxin recorded no differences of hematocrit, systemic arterial pressure, or arterial pO2 between survivors and eventual nonsurvivors. However, by the sixth or eighth hour nonsurvivors showed significantly higher plasma lactate, lower plasma glucose and blood pH, and a greater degree of hypocapnea. In addition, a mean hepatic pO2 had decreased from 25.2 mm Hg during the control to 3.8 mm Hg after six hours. A decline of hepatic oxygen supply also occurred in surviving rats but was significantly less severe. Control rats showed a mild degree of respiratory alkalosis but were otherwise stable over eight hours. The relationship of hepatic oxygen supply to differences of plasma lactate and glucose is discussed. Failure of hepatic circulation is cited as the probable cause of extensive liver anoxia and related developments in nonsurviving endotoxic rats.

Acid-Base Equilibrium↗
PubMed1977

Role of colonic bacteria in the pathophysiology of fecal peritonitis.

This study was designed to clarify the role of colonic bacteria in the reactions accompanying fecal peritonitis. Rats were subjected to septic or nonseptic peritonitis induced by fresh fecal suspensions or suspensions pretreated with heat or antibiotic. Measurements during 8 hr in rats with septic peritonitis recorded bacteremia, hypoglycemia dn progressive hemoconcentration, lactacidemia, and hypocapnea. Mortality was 100% by 24 hr. Nonseptic peritonitis produced significantly lesser degrees of hemoconcentration and hypocapnea. Plasma lactate remained in control ranges while plasma glucose concentrations increased slightly. Mortality was 5% in 24 hr. Parameters in control rats were stable over 8 hr. Hepatic oxygen supply was estimated in each group by multiple platinum wire electrodes. Severe hepatic hypoxia was recorded by 6 hr in rats with septic peritonitis. By contrast, nonseptic peritonitis caused a comparatively mild degree of hypoxia. The pathophysiologic developments in septic rats appear to be largely the result of hypovolemia induced by colonic bacteria. Administration of a colloid solution was effective in preventing its development.

Animals↗