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Biomedical subjects

K Grong

Publications and source records attributed to K Grong.

At least 19 recordsLinked to original sources
PubMed1998

Effect of gastric secretion on penetration of N-3H-methyl-N-nitro-N-nitrosoguanidine into gastric mucosa of rats.

Clinical conditions with low gastric acid secretion have been associated with increased risk of gastric cancer. There has also been concern about gastric acid inhibition and N-nitroso compound formation in the stomach. This study investigates the effect of gastric acid secretion on the penetration of N-3H-methyl-N-nitro-N-nitrosoguanidine, an N-nitroso compound and gastric carcinogen, into the gastric mucosa of rats. Gastric acid secretion was stimulated by pentagastrin (40 microg/kg/hr) and inhibited by omeprazole (40 micromol/kg) before mucosal exposure to N-3H-methyl-N-nitro-N-nitrosoguanidine. Penetration of the carcinogen was evaluated by light microscopic identification of cells in the S-phase labeled with N-3H-methyl-N-nitro-N-nitrosoguanidine. This population of double-labeled cells is considered at risk from N-methyl-N-nitro-N-nitrosoguanidine-induced carcinogenesis. The percentage of double-labeled cells was significantly higher in antrum than in corpus mucosa (P < 0.0001). Stimulation or inhibition of gastric acid secretion did not affect the penetration of N-3H-methyl-N-nitro-N-nitrosoguanidine in antrum or corpus mucosa. We conclude that modulation of gastric acid secretion does not affect the penetration of the carcinogen into the gastric mucosa nor does it explain the different penetration of the carcinogen into corpus and antrum mucosa.

Animals↗
PubMed1997

Glutathione and N-acetylcysteine reduce gastric mucosal blood flow in rats.

Glutathione has been studied as a possible mediator in gastric mucosal protection and healing, but its extracellular function is not fully understood. This study evaluates blood flow changes in normal gastric mucosa secondary to glutathione modulation under stable central hemodynamic conditions. Thiol substances were quantified by reverse-phase ion-pair liquid chromatography and fluorescence detection. Central hemodynamics remained stable when glutathione and N-acetylcysteine were administered in a dose of 0.5 mmol/kg. Higher doses than 0.5 mmol/kg of glutathione and N-acetylcysteine caused unstable hemodynamics. Glutathione (0.5 mmol/kg intravenously) and N-acetylcysteine (0.5 mmol/kg intravenously) reduced corpus mucosal blood flow by 28% and 26% (P < 0.0005), respectively, and glutathione reduced antral mucosa blood flow by 22% (P < 0.01). L-Buthionine-[S,R]-sulfoximine (2 mmol/kg intravenously) did not effect gastric mucosal blood flow. Cysteine content in mucosa and plasma increased while mucosal glutathione levels were largely unchanged after administration of reduced glutathione and N-acetylcysteine. Plasma glutathione only increased after injection of glutathione. L-Buthionine-[S,R]-sulfoximine reduced the glutathione level in both plasma and mucosa. We conclude that glutathione and N-acetylcysteine reduce gastric mucosal blood flow and that the effect may be related to increased cysteine levels in plasma or mucosa.

Acetylcysteine↗
PubMed1997

Small intestinal perforation and peritonitis after abdominal suction lipoplasty.

Suction lipoplasty for abdominal contouring in nonoperated patients is considered a safe procedure with a low incidence of local and systemic complications. Suction lipoplasty combined with a full abdominoplasty is, however, still controversial with a higher rate of local complications. A 56-year-old woman with a history of four laparotomies and two abdominoplasties was hospitalized with abdominal pain and signs of peritonitis after an ambulatory suction lipoplasty. During laparotomy for peritonitis the abdominal wall was found to be stiff and fibrotic, with massive adhesions to the intestine. Two small intestinal perforations caused soiling into the peritoneum. The perforated intestinal segment was resected and the postoperative history was uneventful. Both recent and former laparotomies in the lower abdomen represent a possible risk when suction lipoplasty is performed. An ultrasonographic or computed tomographic scan of the abdominal wall would identify or rule out any underlying fascial defect or hernia.

Abdominal Muscles↗
PubMed1997

Acute erosions of the gastric mucosa in burned rats: effect of sucralfate.

The effect of intragastric sucralfate on development of gastric erosions in burns was studied in 20 rats anaesthetised with midazolam/fentanyl/fluanisone. Gastric blood flow was measured by radioactive microspheres immediately before, and 20, 40, and 120 minutes after the rats had been burned. Significantly fewer erosions were found in the 10 rats treated with sucralfate (less than 2% of the gastric mucosal surface was affected) compared with the controls (16% of the mucosa affected). There was no difference in the rate of gastric blood flow in any part of the stomach between the rats treated with sucralfate and the controls. We conclude that sucralfate is effective in preventing gastric erosions in burned rats, but that other mechanisms of action than increase gastric blood flow are responsible for its protective effect.

Animals↗
PubMed1997

Carvedilol retards sudden loss of contraction during early regional myocardial ischemia in feline hearts.

The purpose of our study was to investigate whether loss of myocardial contraction immediately after coronary occlusion was nonuniform, and if pretreatment with carvedilol, a vasodilating nonselective beta-adrenoceptor antagonist, could retard loss of contraction after coronary artery occlusion. Feline hearts were subjected to acute regional ischemia by total occlusion of the left anterior descending coronary artery. The animals were either treated with vehicle (control group) or with carvedilol 1 mg/kg i.v. before left anterior descending coronary artery occlusion (n = 9 in each group). Regional contraction in the left anterior descending coronary artery perfused region of the heart was studied by cross-oriented sonomicrometry. In control animals, circumferential (subepicardial) contraction ceased after 10 sec, whereas longitudinal (subendocardial) contraction ceased immediately after left anterior descending coronary artery occlusion. Loss of contraction in animals treated with carvedilol was significantly slower compared to controls. Circumferential contraction ceased between 30 sec and 1 min, whereas longitudinal contraction ceased after 20 sec. In conclusion, loss of contraction during the first seconds after coronary occlusion was nonuniform, with most rapid dysfunction in the subendocardium. Pretreatment with carvedilol retarded loss of contraction in both axes.

Adrenergic beta-Antagonists↗
PubMed1996

Carvedilol improves function and reduces infarct size in the feline myocardium by protecting against lethal reperfusion injury.

This study examined the effect of carvedilol, a vasodilating beta-adrenoceptor antagonist and antioxidant, on lethal reperfusion injury in feline hearts subjected to 40 min of regional ischemia and 180 min of reperfusion. 30 open chest anaesthetized cats were randomized into three groups. A control (n = 10) was compared with a group given carvedilol before coronary artery occlusions (n = 10) and a group given carvedilol immediately before and during early reperfusion (n = 10). Regional myocardial function was measured by sonomicrometry. Infarct size was determined by staining the left ventricle with triphenyl tetrazolium chloride. Myocardial blood flow was measured by radiolabeled microspheres. Tissue levels of glutathione were measured after reperfusion. Infarct size was significantly reduced compared to control both when carvedilol was given before ischemia (0.2 +/- 0.1 vs. 17.6 +/- 3.6%, P < 0.05). and when given immediately before reperfusion (3.7 +/- 1.3 vs. 17.6 +/- 3.6%, P < 0.05). Regional shortening improved significantly and the incidence of ventricular fibrillation during early reperfusion was reduced in both groups treated with carvedilol compared to control. Oxidized glutathione did not differ between groups in the post-ischaemic myocardium. This study supports that lethal reperfusion injury is a significant phenomenon. Furthermore, carvedilol reduces infarct size and reperfusion arrhythmias, and improves post-ischaemic regional myocardial function by protecting against both ischaemic and lethal reperfusion injury. The present study does not answer whether it is the non-selective beta- or alpha 1-receptor antagonism, the antiarrhythmic or the antioxidant actions of carvedilol that is responsible for the protective effect.

Adrenergic beta-Antagonists↗
PubMed1996

Peroxisomal fatty acid oxidation capacity is more resistant to ischaemic and reperfusion injury than mitochondrial fatty acid oxidation capacity in feline hearts.

We investigated ischaemic and postischaemic mitochondrial and peroxisomal fatty acid oxidation capacity, ATP levels and regional function in 40 anaesthetized open chest cats subjected to 10 or 40 min of regional myocardial ischaemia with or without 3 h of reperfusion (n = 10 in each situation). Following 10 min of ischaemia, the mitochondrial fatty acid oxidation capacity measured in tissue extracts from ischaemic tissue (nmol min-1 mg protein-1) was reduced in both subepi- and subendocardium, but was normalized in reperfused tissue extracts from both wall layers (0.29 +/- 0.03 and 0.30 +/- 0.04 vs. 0.57 +/- 0.05 and 0.59 +/- 0.05. P < 0.05). Peroxisomal fatty acid oxidation capacity in tissue extracts was unaffected by ischaemia and reperfusion. ATP levels and regional function measured in the LAD region was partly restored transmurally. After 40 min of LAD occlusion, mitochondrial fatty acid oxidation capacity was reduced, with higher activity in subepi- than in subendocardium (0.27 +/- 0.05 vs. 0.19 +/- 0.04. P < 0.05). Reperfusion did not restore mitochondrial fatty acid oxidation capacity. Peroxisomal fatty acid oxidation capacity was increased in the ischaemic subendocardium compared with levels in non-ischaemic subendocardium (0.53 +/- 0.02 vs. 0.45 +/- 0.03, P < 0.05), with normalization at the end of reperfusion. ATP levels were non-uniformly reduced during ischaemia and not repleted during reperfusion. Regional function recovered in circumferential segments but not in longitudinal segments following 40 min of ischaemia. In conclusion fatty acid oxidation enzymes seem to be more resistant to ischaemia in peroxisomes than in mitochondria. Mitochondrial fatty acid oxidation is fully reversible following shortlasting ischaemia, but remains depressed following prolonged ischaemia and reperfusion.

Adenine Nucleotides↗
PubMed1996

High afterload during 10 min of regional ischaemia affects diastolic creep but not systolic function in reperfused (stunned) myocardium.

The effect of afterload during regional ischaemia on myocardial stunning was studied in 15 pentobarbital anaesthetized cats. 10 min occlusion of the left anterior descending artery (LAD) was followed by 60 min of reperfusion. Afterload was decreased by intravenous infusion of nitroglycerine 3-8 micrograms kg-1 min-1 in group I (n = 8); left ventricular peak systolic pressure (LVSP) 84 +/- 4 mmHg (mean +/- SEM) during coronary artery occlusion. In group II (n = 7) LVSP was increased to 188 +/- 10 mmHg by inflating an intraaortic balloon during coronary artery occlusion. Regional function in the LAD perfused region was evaluated by cross-oriented sonomicrometry. Myocardial tissue blood flow was evaluated by radio-labelled microspheres. Afterload alterations did not affect regional systolic shortening (10.8 +/- 2.0% vs. 11.0 +/- 1.5% in group I and II, respectively, after 60 min of reperfusion). However, increased end-diastolic dimensions (diastolic creep) in both the circumferential and longitudinal segments were markedly more pronounced in the high afterload group (group II). Also important, the markedly increased myocardial tissue blood flow during reperfusion in group II as compared with group I (2.30 +/- 0.18 vs. 1.34 +/- 0.08 mL min-1 g-1 and 2.58 +/- 0.23 vs. 1.49 +/- 0.07 mL min-1 g-1 in subepicardial and subendocardial layers in the LAD perfused region) suggests that increased diastolic creep increased metabolic demands. This study indicates that passive stretching of the ischaemic area during coronary artery occlusion is an important mechanism behind diastolic creep.

Animals↗
PubMed1996

Carvedilol protects against lethal reperfusion injury through antiadrenergic mechanisms.

We examined the effect of carvedilol as compared with that of a combination of propranolol and doxazosin on lethal reperfusion injury in 21 feline hearts subjected to 40-min regional ischemia and 180-min reperfusion. A control group (n = 7) was compared with one group given carvedilol, a nonselective beta - and alpha 1-adrenoceptor blocker and antioxidant (n = 7) and another group given nonselective beta - and alpha 1-adrenoceptor blockade with propranolol and doxazosin (n = 7) during initial reperfusion. Infarct size (IS: percent of area at risk, AAR) determined by staining the myocardium with triphenyl tetrazolium chloride (TTC), was reduced both in the carvedilol-treated group (median 1.8%, p < 0.05) and in the group given propranolol/doxazosin (median 6.5%, p < 0.05) as compared with controls (median 14.4%). Treatment with carvedilol reduced IS more than did treatment with propranolol/doxazosin (p < 0.05). Longitudinal segment shortening measured with sonomicrometry, improved in both treatment groups as compared with control (p < 0.05), but to a greater extent in the group treated with carvedilol. In circumferential segments, only carvedilol significantly improved segment shortening. The incidence of ventricular fibrillation (VF) after reperfusion was reduced in both treatment groups as compared with control. Oxidized glutathione and thiobarbituric acid-reactive substances (TBARS) measured at the end of reperfusion did not differ between groups. Carvedilol protected against lethal reperfusion injury mainly through blockade of adrenoceptors.

Adrenergic Antagonists↗
PubMed1995

Endogenous adenosine attenuates myocardial stunning by antiadrenergic effects exerted during ischemia and not during reperfusion.

The effect of adenosine receptor blockade and adrenergic blockade on myocardial stunning [left anterior descending coronary artery (LAD) occluded for 10 min and reperfused for 180 min] was studied in 38 open-chest cats. A control group (Control) was compared with two other groups in which adenosine receptors were blocked by 8-phenyltheophylline (7.5 mg/kg) before reperfusion (8-PT-R) or before ischemia (8-PT-I). Group A, in which adrenergic receptors were blocked (doxazosin 200 micrograms/kg + propranolol 1 mg/kg), was compared with group A + 8-PT-I, in which both adenosine and adrenergic receptors were blocked before coronary artery occlusion. Regional systolic function assessed by sonomicrometry in the LAD perfused area recovered less in 8-PT-I (55 +/- 5% recovery) as compared with Control (87 +/- 9%) and 8-PT-R (89 +/- 8%), which indicates that adenosine receptor blockade during ischemia increases stunning. Functional recovery was similar in Control, group A (96 +/- 5%), and group A + 8-PT-I (87 +/- 5%), which demonstrates that if adrenergic receptors are blocked, adenosine receptor blockade during ischemia does not increase stunning. These results may indicate that the cardioprotective effects of endogenous adenosine are mediated through antiadrenergic effects exerted during coronary artery occlusion.

Adenosine↗
PubMed1995

Non-uniform recovery of segment shortening during reperfusion following regional myocardial ischaemia despite uniform recovery of ATP.

OBJECTIVE: This study focused on transmural postischaemic recovery of ATP and regional contractile function related to reversible and irreversible tissue injury. METHODS: Fifty anaesthetised open-chest cats were randomised into two groups. Groups I: 10 min of LAD occlusion (n = 10) and 10 min of LAD occlusion followed by 180 min of reperfusion (n = 15). Group II: 40 min of LAD occlusion (n = 10) and 40 min of LAD occlusion followed by 180 min of reperfusion (n = 15). Histochemical staining (TTC) was performed in hearts from 5 additional cats subjected to 40 min of LAD occlusion and 180 min of reperfusion. Regional function was measured by sonomicrometry in the circumferential (CIRC) and longitudinal (LONG) axis of the anterior left ventricular midwall. Myocardial blood flow was measured with radiolabelled microspheres. Adenine nucleotides in the subepi- and subendocardium were measured with high-pressure liquid chromatography after LAD occlusion and after reperfusion. RESULTS: Ten minutes of ischaemia induced a transmurally uniform ATP depletion. Repletion of ATP following reperfusion was transmurally uniform. Recovery of regional shortening was non-uniform with better recovery in CIRC (76 +/- 8% vs. LONG; 46 +/- 10%, P < 0.05). Forty minutes of ischaemia induced a more severe ATP depletion in the subendocardium compared to the subepicardium. A slight recovery of ATP following reperfusion was transmurally uniform. Recovery of function was present only in CIRC (48 +/- 6%). Tissue blood flow showed a transmurally homogenous flow restriction during ischaemia and uniform recovery following reperfusion. TTC staining demonstrated predominantly subendocardial infarctions following 40 min of regional ischaemia. CONCLUSIONS: Postischaemic recovery of regional function is non-uniform and independent of ATP repletion and collateral blood flow during ischaemia. Absence of functional recovery in LONG is associated with development of infarction.

Adenosine Triphosphate↗
PubMed1994

Blockade of adenosine receptors during ischaemia increases systolic dysfunction but does not affect diastolic creep in stunned myocardium.

The impact of adenosine receptor blockade on left ventricular systolic function and diastolic creep in stunned myocardium was studied in 20 sodium pentobarbital anaesthetized cats. A control group (n = 10) was compared with a group (n = 10) where adenosine receptors were blocked by 8-phenyltheophylline (7.5 mg.kg-1 i.v.) prior to a 10 min occlusion of the left anterior descending coronary artery. Regional function was assessed by sonomicrometry of the left ventricular anterior wall. Tissue blood flow and haemodynamic measurements were obtained at pre-occlusion, during occlusion, and after 30 and 60 min of reperfusion. Tissue blood flow in the LAD region was low and homogeneous during coronary occlusion in both groups. Systolic function assessed by regional shortening and inotropic parameters was significantly more reduced in the 8-PT treated group (P < 0.05). Diastolic creep and compliance assessed by the end-diastolic pressure-length relationship did not differ between groups. Thus, endogenous adenosine protects against systolic dysfunction, but appears to have no impact on diastolic creep in stunned myocardium. Furthermore, our results show that the protective effect of endogenous adenosine is not caused by increased collateral blood flow into the ischaemic area during coronary artery occlusion or by increased blood flow in the reperfusion period.

Adenosine↗
PubMed1994

Myocardial contraction patterns in non-ischaemic and ischaemic regions during acute coronary insufficiency.

The effect of coronary insufficiency on the myocardial contraction pattern was studied in 11 thoracotomized cats using apical long axis echocardiograms and cross-oriented segments in the anterior midwall. Myocardial tissue blood flow was studied using radiolabelled microspheres. After circumflex coronary artery occlusion, ejection shortening increased on average 17% for circumferential segments (P < 0.05) and 61% for longitudinal segments (P < 0.001). Hyperkinesis was also validated as augmented anterior endocardial wall motion and wall thickening. Circumflex occlusion increased end-systolic sphericity of the left ventricle (P < 0.05). Subsequent underperfusion of the left coronary artery, in two discrete steps, decreased subendocardial blood flow by, on average, 36% (P < 0.001) and 75% (P < 0.001) vs the post-occlusion value, while subepicardial flow did not change. While subendocardial blood flow decreased by 36%, systolic shortening of the global major axis decreased, by, on average, 77% (P < 0.001), shortening of the longitudinal segments by 36% (P < 0.001), and systolic shortening of the minor axis by 18% (P < 0.05), whereas shortening of midwall circumferential segments did not change. This study shows that changes in myocardial contraction in both non-ischaemic and ischaemic regions during coronary insufficiency are most pronounced in the direction of the cardiac major axis.

Acute Disease↗
PubMed1994

Gastric mucosal repair and release of HCO3- after damage by 2 M NaCl in cat: role of systemic acid base status.

To study the influence of acid base balance on gastric mucosal repair, NH4Cl or NaHCO3 was given intravenously to anesthetized cats after mucosal damage induced by intraluminal 2 M NaCl. Saline at pH 5 or 1 was perfused via an oral tube through the stomach lumen and evacuated via a pyloric tube to a chamber with pH and PCO2 electrodes. Luminal bicarbonate (HCO3-) was markedly increased early after damage in both acidotic and alkalotic animals. In alkalotic animals mucosal blood flow increased about twofold in response to mucosal damage, whereas the early hyperemic response was either completely attenuated or blunted in acidotic animals. HCO3- release was correlated to availability of HCO3- by blood in alkalotic animals with luminal pH 5. Alkalotic animals showed improved repair compared with acidotic animals, and mucosal restitution was correlated to availability of HCO3- by blood. We conclude that luminal leakage of HCO3- or plasma after mucosal damage depends on availability by blood and consumption of HCO3- within the mucosa and that blood borne HCO3- has a major influence on gastric mucosal repair.

Acid-Base Equilibrium↗
PubMed1994

Changes in myocardial contraction pattern during initial reperfusion.

The characteristics of hypercontraction during initial reperfusion were studied in 10 pentobarbitone-anesthetized cats. The left anterior descending coronary artery was occluded for 10 min followed by 1 h of reperfusion, and regional function was assessed by two cross-oriented pairs of sonomicrometers placed in the left ventricular anterior wall. At 1 min of reperfusion (hyperfunctional phase) there was an uniform contraction pattern with 90% recovery of ejection shortening in both circumferential and longitudinal segments. During initial hypercontraction, end-diastolic segment lengths remained unchanged, whereas end-systolic segment lengths decreased transiently. Inotropic stimulation during reperfusion in four additional animals also affected end-systolic lengths more than end-diastolic lengths. This suggests that the initial hyperfunctional phase is due to an inotropic stimulation of the stunned myocardium, most probably caused by intracellular Ca2+ overload. At 5 min of reperfusion a nonuniform contraction pattern had developed with 68% recovery of shortening in circumferential segments vs. 25% in longitudinal segments. The decreased performance in longitudinal segments was paralleled by a delayed start of contraction as well as a decreased velocity of contraction. Because longitudinal segment shortening is a sensitive parameter of subendocardial performance, our results indicate a brief transmural hypercontraction followed by increasing dysfunction (stunning) in the subendocardial layer.

Animals↗
PubMed1993

Gastric mucosal injury and associated changes in mucosal blood flow and gastric fluid secretion caused by dimethyl sulfoxide (DMSO) in rats.

Dimethyl sulfoxide applied intragastrically for 10 min in rats caused extensive mucosal damage. In concentrations of 5%, 10%, or 100%, dimethyl sulfoxide caused superficial damage to 33%, 36%, and 97%, respectively, of the corpus mucosa, and 28%, 44%, and 96%, respectively, of the antral mucosa. Concentrated dimethyl sulfoxide also caused damage to the pits and glands in some areas of the mucosa. The amount of fluid in the stomach increased by 0.24 ml, 0.48 ml, and 2.07 ml during application of 5%, 10%, and 100% dimethyl sulfoxide. The 10% dimethyl sulfoxide increased mucosal blood flow by 0.57 ml/min/g in the antrum, and 100% dimethyl sulfoxide increased mucosal blood flow by 2.21 ml/min/g in the antrum and by 1.17 ml/min/g in the corpus. We conclude that dimethyl sulfoxide is a gastric irritant, which should be considered when it is used as an oxygen radical scavenger, as a drug or carcinogen vehicle, or as oral medication in patients. The protective effect of intragastric dimethyl sulfoxide against stress and various drug-induced gastric injury may be due to "adaptive cytoprotection" rather than an oxyradical scavenger effect.

Analysis of Variance↗
PubMed1993

Non-uniform recovery of performance in stunned myocardium evaluated by two-dimensional sonomicrometry.

The objective of the present study was to assess the uniformity of contraction in reperfused myocardium. Regional function was measured by two pairs of piezo-electric crystals oriented in the circumferential and longitudinal axis of the left ventricular anterior midwall in 10 open-chest pentobarbitone-anaesthetized cats. The left anterior descending coronary artery was occluded for 10 min followed by 60 min of reperfusion. Myocardial blood flow was measured four times by radioactive labelled microspheres: at pre-occlusion, occlusion and after 30 and 60 min of reperfusion. There was a severe and transmural homogenous ischaemia during coronary occlusion. The recovery of ejection shortening was on average 76% at 30 min and 77% at 60 min of reperfusion in circumferential segments versus 25 and 44% in longitudinal segments (P < 0.05). Diastolic function was deranged in longitudinal segments; at 60 min of reperfusion the end diastolic pressure-length relation was still shifted rightwards in longitudinal segments, whereas it was normalized in circumferential segments. In conclusion, systolic and diastolic dysfunction in stunned myocardium were more severe in the longitudinal axis than in the circumferential axis of the feline heart. This indicates that stunning was more pronounced in longitudinally oriented sub-endocardial fibres which were reflected by the longitudinal segment, despite transmural homogenous ischaemia during coronary artery occlusion.

Animals↗