Biomedical subjects

K Grong

Publications and source records attributed to K Grong.

At least 55 records · Page 3Linked to original sources

PubMed1992

Postjunctional alpha-adrenergic stimulation of inotropy in hypoperfused myocardium outside an acute infarct.

The functional significance of myocardial postjunctional alpha-adrenergic support of inotropy in the vicinity of an acute regional ischemic zone was addressed in pentobarbital-anesthetized, beta-adrenergic blocked cats with circumflex coronary artery occlusion. Regional myocardial performance was measured by ultrasonic crystals in the anterior wall perfused by the left anterior descending coronary artery (LAD) before and during postjunctional alpha-adrenergic antagonism (SK&F 104078 2 mg/kg). A group with unrestricted flow in the LAD (control group) was compared with a group perfused below the autoregulatory pressure range (stenosis group). End-systolic pressure-length relations during dynamic after-load elevation were calculated for assessment of regional contractility. Regional myocardial blood flow (RMBF) was measured by radioactive microspheres. SK&F 104078 did not alter regional myocardial shortening or the slope of end-systolic pressure-length relations in the control group. In the stenosis group, however, alpha-adrenergic antagonism produced significant deterioration of shortening as well as consistent reduction of the slope of the end-systolic pressure-length relations (p < 0.05). As a reflection of reduced demands for perfusion, impairment of midmyocardial and endocardial blood flow occurred in the stenosis group (p < 0.05). These findings imply a negative inotropic effect of SK&F 104078 in metabolically vasodilated myocardium in the vicinity of an acute ischemic region.

Adrenergic alpha-Agonists↗

PubMed1992

Alpha-adrenergic vasoconstriction in normal and hypoperfused myocardium during sympathetic nerve stimulation.

Coronary vasoconstriction mediated by postjunctional alpha 1- and alpha 2-adrenergic receptors was studied in normally perfused (control group) and left coronary hypoperfused (stenosis group) hearts of vagotomized, beta-blocked (propranolol) cats. Cardiac sympathetic nerve stimulation was combined with alpha 1- and subsequent alpha 2-adrenergic antagonism (doxazosin and SK&F 104078). Coronary perfusion pressure and heart rate were kept constant within groups; regional myocardial blood flow and cardiac output were obtained by means of microspheres with concomitant measurement of left ventricular myocardial oxygen consumption (MVO2). alpha 1-Adrenergic antagonism alone did not significantly alter blood flow in any wall layer in either group. Subsequent alpha 2-adrenergic antagonism increased epicardial as well as composite transmural flow in the stenosis group (P < 0.025). The inverse correlation between coronary resistance and MVO2 vanished in the stenosis group following alpha 1- and alpha 2-adrenergic antagonism. Maximal first derivative of the left ventricular pressure-time relation (dP/dt) and cardiac output were reduced simultaneously (P < 0.001). Hence, the significance of alpha 1- and alpha 2-adrenergic stimulation of inotropy and cardiac performance are augmented by myocardial hypoperfusion. Furthermore, alpha 2-adrenergic receptors are responsible for epicardial vasoconstriction in hypoperfused myocardium.

Adrenergic alpha-Agonists↗

PubMed1992

Effect of afterload and beta-adrenergic blockade on nonischemic myocardial contraction pattern.

We studied how changes in afterload affect regional contraction in the anterior wall of the left ventricular after circumflex coronary arterial (CFX) occlusion and subsequent beta-adrenergic blockade in pentobarbital sodium-anesthetized cats. Regional function was determined by orthogonal sonomicrometry. CFX occlusion produced nonuniform hyperkinesis in the nonischemic anterior wall; shortening of circumferential segments increased from 10.1 to 14.1% (P < 0.001), whereas shortening of longitudinal segments increased from 3.0 to 9.6% (P < 0.001). Hyperkinesis of longitudinal segments was influenced neither by changes in afterload over a pressure range of +/- 30 mmHg nor by beta-adrenergic blockade, indicating that hyperkinesis of longitudinal segments does not rely on increased inotropic state or resistance to ventricular emptying. Hyperkinesis of longitudinal segments occurred at end-diastolic lengths equal to preocclusion conditions, whereas hyperkinesis of circumferential segments was dependent on activation of the Frank-Starling mechanism. Furthermore, shortening of circumferential segments decreased with increments in afterload, particularly after CFX occlusion and subsequent beta-adrenergic blockade. In conclusion, CFX occlusion alters the contraction pattern of the nonischemic anterior wall. The postocclusion contraction is sensitive to increased afterload in the cardiac minor axis direction. These initial alterations may well direct the following remodeling process in infarcted hearts.

Adrenergic beta-Antagonists↗

PubMed1992

Myocardial adenine nucleotide depletion within 1 h of acute coronary artery occlusion.

In anaesthetized open-chest casts with occlusion of the left anterior descending coronary artery (LAD), adenine nucleotides and degradation products were studied in small myocardial tissue samples (10-20 mg) with high-pressure liquid chromatography, and tissue blood flow was measured with radioactive microspheres 5, 10, 20, 40, and 60 min after LAD occlusion. There was a rapid and parallel decrease of myocardial ATP and accumulation of adenosine, inosine, hypoxanthine, and xanthine both in epicardial and endocardial half-layers of the ischaemic myocardium within the first 20 min of coronary occlusion. After 40 and 60 min, myocardial ATP content decreased and degradation products accumulated further in the endocardium but stabilized epicardially. Analysis of covariance showed that the slightly higher blood flow in ischaemic epicardial layers, did not explain the transmural difference in ATP content after 40 and 60 min. Adenosine decreased after 40 min of ischaemia in both wall layers reaching negligible amounts after 60 min. It is concluded that breakdown of energy stores is less severe in epicardial than in endocardial wall layers during the first hour after acute coronary occlusion in the cat heart. This transmural difference cannot be explained entirely by less severe epicardial ischaemia. Therefore, transmural heterogeneity in metabolic function during severe ischaemia may also be important.

Adenine Nucleotides↗

PubMed1991

[Cerebral air embolism after percutaneous lung puncture].

Cerebral air embolism is a rare but serious complication to percutaneous transthoracic fine needle aspiration of the lung. A case is described after puncture of a tumour in the right lung with a 0.6 mm needle. The patient developed paralysis of the upper and lower extremities on his left side, probably due to an air embolism in the right middle cerebral artery. He was fully restituted after early hyperbaric treatment with oxygen.

Aged↗

PubMed1991

Blood flow regulation during acute regional ischemia in feline hearts: importance of postjunctional alpha 1- and alpha 2-adrenoceptors.

Influence of postjunctional alpha 1- and subsequent alpha 2-adrenergic antagonism on myocardial blood flow was measured in a group of anesthetized cats with acute occlusion of the left anterior descending coronary artery (LAD) and a control group (n = 10 for both). The relatively selective postjunctional alpha 1-(doxazosin) and alpha 2-adrenergic (SK&F 104078) antagonists were applied after beta-adrenergic blockade (propranolol). Regional myocardial blood flow was obtained with radiolabeled microspheres. Major hemodynamic determinants for perfusion were kept constant both within and between groups by right atrial pacing and aortic obstruction. Mean coronary resistance in nonischemic myocardium was permanently lower in the occlusion group as compared with controls (p less than 0.01). Subsequent alpha 2-adrenergic antagonism reduced mean coronary resistance in controls only (p less than 0.05). Cardiac output (CO) and dP/dt was reduced in LAD-occluded hearts after alpha 2-adrenergic blockade (p less than 0.01, p less than 0.05). The study demonstrates the significance of postjunctional alpha 2-adrenergic-mediated vasoconstriction in well-perfused myocardium of control hearts, whereas such vasoconstriction was deteriorated in LAD-occluded hearts. A role for myocardial alpha 2-adrenoceptors for maintenance of global cardiac function in acute regional ischemia was also indicated.

Adrenergic alpha-Antagonists↗

PubMed1991

Tissue reaction to polypropylene mesh: a study of oedema, blood flow, and inflammation in the abdominal wall.

The purpose of the present work was to study the tissue reaction to polypropylene mesh (Marlex) implanted in three different layers of the abdominal wall, comparable to common clinical practices. The reaction to mesh was compared in terms of tissue oedema, blood flow, and histological appearance in rats. When mesh was placed between muscle layers, blood flow in the abdominal wall was high during the first 4 days after implantation but similar to flow in nonoperated rats 14 and 140 days after implantation. When mesh was placed under skin or on the peritoneum, there was no hyperaemia early after implantation, and flow rate was clearly lower than in non-operated controls 140 days after implantation. The operative procedure produced increased tissue water content, declining from the 1st to the 14th day after operation. Mesh induced additional oedema in adjacent muscle tissue irrespective of localization of the implant (p less than 0.01, vs. sham). Except when separated by peritoneum, mesh caused hyperaemia in muscle tissue in direct contact with mesh the 1st and the 4th day after implantation. After 14 and 140 days no mesh-induced hyperaemia was present. The inflammatory response to mesh was similar in the peritoneum and between muscles, less pronounced in the subcutis. It was characterized by the accumulation of macrophages and the formation of inflammatory granulation tissue in the subacute phase, later followed by the formation of fibrous tissue around mesh fibres. This study suggests that mesh implants should be placed in apposition to muscles in order to obtain well-vascularized healing.

Abdominal Muscles↗

PubMed1991

Ultrastructural changes at the border of the ischaemic zone within one hour of coronary artery occlusion.

The ultrastructure was studied by electron microscopy in myocytes obtained from the periphery of the ischaemic zone 10, 20, 40, and 60 min after occlusion of the left anterior descending coronary artery (LAD) in open chest anaesthetized cats. The morphology of this zone was compared to that of the normally perfused myocardium in the same hearts. Samples were collected from the border of the ischaemic tissue as defined by in vivo injection of fluorescein and verified by regional blood flow measurements with radiolabelled microspheres. After 10 min of LAD-occlusion, we observed swelling of the mitochondria in the border zone. The mitochondrial swelling remained stable for the first hour after LAD-occlusion. There was no difference in the fractional volume of lipid droplets between the normal and border zones after 10 min of ischaemia. The fractional volume of lipid droplets, however, was significantly reduced in the normal zone after 20 min of coronary artery occlusion, whereas it remained unchanged in the border zone. Up to 60 min after LAD-occlusion the fractional volumes of cytoplasm in the border zone were not different from the corresponding values in the normal zone, indicating that there was no cytoplasmic oedema in the border zone. However, a reduced fractional volume of myofibrils in the border zone after 20 min of LAD-occlusion, may indicate a slight cell swelling, probably due to the mitochondrial swelling. In the border zone there was a slight increase in the number of cells with sarcolemmal injuries after 10 min of LAD-occlusion. Cells with chromatin clumping and margination were found after 20 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1991

Early restoration of cardiac function in hearts with acute regional ischaemia. The importance of beta-adrenergic stimulation.

The effects of acute coronary artery occlusion in anaesthetized cats has been studied with regard to changes in cardiac function and regional myocardial blood flow. Occlusion of the left anterior decending coronary artery (LAD) is followed by a rapid reduction of peak systolic blood pressure (LVSP) and contractility (dP/dt) and increased left ventricular end-diastolic pressure (LVEDP). Five minutes after coronary occlusion heart rate, LVSP, and (dP/dt) was reduced and LVEDP increased. Global cardiac function measured by these variables was gradually restored to preocclusion values; LVSP after 10 min., heart rate and dP/dt after 20 min. After 40 and 60 min these variables were stable at preocclusion levels. LVEDP remained permanently elevated. In hearts with regional ischaemia and paced heart rate global cardiac function was mainly restored 20 min after coronary occlusion except for increased LVEDP, both in cats pretreated with non-selective beta-adrenergic blockade (propranolol) and in unblocked cats. In general, blood flow in non-ischaemic myocardium adjacent to the ischaemic region increased following coronary occlusion, although not significantly in the endocardium. The endocardial/epicardial blood flow ratio was stable in unblocked hearts and was reduced in beta-blocked hearts. In normally perfused myocardium remote from the ischaemic region, blood flow increased following occlusion both in beta-blocked and unblocked cats, most pronounced in the epicardium; the endo/epicardial blood flow ratio decreased.

Adaptation, Physiological↗

PubMed1990

Gradual reduction of coronary perfusion pressure in cats: changes in transmural distribution of blood flow.

We evaluated a model for regional myocardial hypoperfusion in cats with an extracorporeal shunt line to the left main coronary artery, and investigated the effects of reduced coronary perfusion pressure on the transmural distribution of left ventricular blood flow measured with radioactive microspheres. Shunt establishment did not alter cardiac function, myocardial tissue blood flow, or its transmural distribution. An artificial shunt stenosis, which clearly reduced coronary perfusion pressure without changing cardiac function, caused reduced endocardial blood flow, slight flow reduction in mid-myocardium, and no flow change in the epicardium. When a severe stenosis was applied, causing increased end-diastolic pressure and reduced shunt flow, endocardial and mid-myocardial flow further decreased whereas epicardial blood flow remained essentially unchanged. These results demonstrate a transmural profile of the coronary autoregulation capacity.

Animals↗

PubMed1990

Regional perfusion in hearts with acute coronary artery occlusion and subsequent beta 2- and alpha 1-adrenergic blockade.

Blockade of cardiac adrenoceptor subtypes, coronary or myocardial, might elicit compensatory interaction from remaining unblocked subtypes. An attempt to explore this interplay was made by studying regional myocardial blood flow alterations associated with beta 2-adrenergic blockade followed by alpha 1-adrenergic blockade in anaesthetized cats with acute coronary occlusion. In order to maintain constant needs for perfusion, atrial pacing was established and the aortic blood pressure was kept constant. In myocardium remote from the ischaemic region, beta 2-adrenergic blockade produced higher endocardial blood flow whereas no flow changes were observed close to the ischaemic region. With subsequent alpha 1-adrenergic blockade, blood flow increased endocardially in non-ischaemic regions, but remained unchanged in epicardial tissue. Control experiments without coronary ligation revealed no increase in left ventricular oxygen consumption during the experiments and support the theory that the observed blood flow increase in the coronary ligation group, following drug interventions, was not caused by increased cardiac work. This study indicates that combined beta 2- and alpha 1-adrenergic blockade alters the balance between receptor subtypes. Unopposed beta 1-mediated vasodilation is the most likely candidate to explain why endocardial flow was increased.

Adrenergic alpha-Antagonists↗

PubMed1990

Distribution of cardiac output during pentobarbital versus midazolam/fentanyl/fluanisone anaesthesia in the rat.

Differences in effects on central haemodynamics, organ blood flow, and serum corticosterone were studied in 11 rats anaesthetized with midazolam/fentanyl/fluanisone (MFF) and 11 other rats anaesthetized with sodium pentobarbital. Compared with pentobarbital, MFF reduced aortic blood pressure by 25%, increased heart rate by 20%, and increased cardiac output by 80%. Unlike most tissues, MFF produced a fivefold increase in blood flow to skeletal muscle, and decreased adrenal blood flow compared to pentobarbital anaesthesia. Initial serum corticosterone levels were lower in rats given MFF anaesthesia, indicating better stress protection. This study also indicates that MFF anaesthesia is preferable to pentobarbital because tissue perfusion generally was better preserved.

Anesthesia↗

PubMed1990

Early morphologic changes in cat heart muscle cells after acute coronary artery occlusion.

The left descending coronary artery (LAD) was occluded in 16 open-chest cats for 10, 20, 40, or 60 minutes (four cats in each group). In addition, four sham-operated cats served as controls. Specimens for electron microscopy were obtained from the normal and ischemic zones, guided by in vivo injection of fluorescein, and verified by blood flow measurements with microspheres. The ultrastructure of 2,400 heart muscle cells and nuclei was studied. Fractional volumes of main cell components, mitochondrial surface density, and mitochondrial surface: volume ratio were calculated in 480 micrographs. After 10 minutes of ischemia we observed signs of sarcolemmal fragility, mitochondrial swelling, and lipid droplet accumulation. After 20 minutes of ischemia sarcolemmal fragmentation, chromatin clumping or margination and a maximal cytoplasmic edema were evident. The fractional volume of mitochondria was equally increased in ischemic zones of all groups. In both normal and ischemic zones there was a tendency toward smaller fractional volumes of lipid droplets during ischemia. In the normal zone there was mild cytoplasmic edema and slight mitochondrial swelling 10 minutes after occlusion as compared with the sham group. The present study demonstrates that a large proportion of cardiac myocytes undergoes severe damage within 20 minutes of coronary occlusion.

Animals↗

PubMed1989

Does alpha 1-adrenergic blockade influence regional blood flow regulation in hearts with coronary artery occlusion?

The effects of selective alpha 1-adrenergic blockade with doxazosin on regional myocardial tissue blood flow was studied in anaesthetized cats with acute coronary artery occlusion. Reflex tachycardia was prevented by selective beta 1-adrenergic blockade with atenolol and coronary perfusion pressure was kept constant by partial stenosis of the descending aorta. Administration of atenolol reduced cardiac mechanical work-load by its negative inotropic and chronotropic effects, and reduced myocardial tissue blood flow in normally perfused myocardium. This reduction was most pronounced in the endocardial half-layer of the myocardium adjacent to the ischaemic region. Administration of doxazosin in this situation clearly reduced peak systolic and coronary perfusion pressure. But when coronary perfusion pressure was raised to pre-administration values, measurements of regional blood flow revealed no changes either in ischaemic or non-ischaemic myocardium. Also, there was no sign of redistribution of blood flow between endocardial and epicardial tissue in any area. This study, therefore, indicates that alpha 1-adrenoceptors play a minor role in the regulation of coronary blood flow in normal myocardium as well as ischaemic myocardium.

Animals↗

PubMed1989

Effects of verapamil on intracellular lipid accumulation in cat hearts with 3 h of regional-ischaemia.

In the regionally ischaemic heart lipid droplet accumulation is found in the ischaemic area and is most pronounced in the periphery. The purpose of the present study is to explore the potential effects of the calcium-channel-blocker verapamil on this accumulation. The drug is known to reduce the intensity of myocardial ischaemic injury. The myocardial ultrastructure was studied in anaesthetized open chest cats with 3 h of coronary artery occlusion. Biopsies were taken from the ischaemic, border and normally perfused myocardium defined in vivo injections of fluorescein and verified by blood flow measurements using radiolabelled microspheres. Arterial concentration of non esterified fatty acids (NEFA) was measured during the ischaemic period. A higher accumulation of lipid droplets was found in the central ischaemic myocardium of verapamil-treated cats than in control animals (p less than 0.05). The normally perfused and borderline areas were unaffected by verapamil as far as lipid accumulation was concerned and showed the same pattern as in the untreated group. The increased accumulation of lipid droplets in the ischaemic myocardium, after treatment with verapamil, may reflect a preserved metabolic activity in the ischaemic tissue or result from a higher supply of fatty acids due to increased perfusion of the central ischaemic tissue.

Animals↗

PubMed1988

Cellular morphometric changes in cat hearts subjected to three hours of regional ischaemia.

The left anterior descending coronary artery (LAD) was occluded for three hours in seven anaesthetized open chest cats. Seven cats served as sham operated controls. Biopsies were collected from the mid-myocardium of the normal, border and ischaemic zones as defined by fluorescein staining and verified by blood flow measurements with radiolabelled microspheres. In the sham operated hearts the biopsies were taken from the mid-myocardium of the lateral wall of the left ventricle. Fractional volumes of mitochondria, myofibrils and remaining cytoplasm as well as data on the outer mitochondrial membrane were obtained by standard point counting techniques. In the LAD occluded hearts we observed a morphologically distinct lateral border zone characterized by a greater swelling of the mitochondria than in the ischaemic zone. However, in this group a more marked oedema of the cytoplasm and a greater percentage of heavily damaged cells were observed in the ischaemic than in the border zone. The ischaemic zone also had the largest water content. Furthermore, cytoplasmic oedema occurred in the normal zone of the LAD occluded cats when compared with the sham operated controls. This indicates that LAD occlusion also affects the normally perfused parts of the heart.

Animals↗

PubMed1988

Effects of verapamil and timolol on cellular morphometric changes in cat hearts with regional ischaemia.

In twenty-one anaesthetized open chest cats the left anterior descending coronary artery (LAD) was occluded for three hours. Seven cats were pretreated with a bolus injection of Verapamil, followed by a continuous infusion of Verapamil during the ischaemic period. Seven cats were pretreated with a bolus injection of Timolol to a heart rate reduction of 20 beats/min or more and seven cats were given saline. In the latter two groups the cats received a continuous infusion of saline during the period of coronary occlusion. Biopsies were taken from the mid-myocardium of the normal, border and ischaemic zones, as defined by fluorescein staining, and verified by blood flow measurements with radiolabelled microspheres. Standard point counting techniques were used for calculations of fractional volumes of mitochondria, cytoplasm and myofibrils as well as of mitochondrial surface density and surface to volume ratio. We observed a cytoplasmic oedema in the border and ischaemic zones, that was not altered by medical treatment. In the border zone of the control cats there is greater mitochondrial swelling than in the ischaemic zone. This particular swelling is not seen in the treatment groups. However, in the normal and border zones of the verapamil group the mitochondria are smaller when compared with the respective zones in the two other groups, but increases relatively more in size in the border and ischaemic zones. Furthermore, we measured the water content, sarcomere length and per cent heavily damaged cells. These variables were not altered by Verapamil or Timolol in any zone when compared with the respective zones in the control group.

Animals↗

PubMed1987

Gastric epithelial restitution at low luminal pH during influence of pentagastrin or cimetidine in the cat.

This study examines restitution of the gastric surface epithelium at luminal pH 1 after damage to the gastric mucosa by instillation of 2 M NaCl for 10 min. After mucosal damage, potential difference decreased to zero and H+ back-diffusion increased. Gastric blood flow increased after exposure to 2 M NaCl, irrespective of the secretory state of mucosa. Neither pentagastrin nor cimetidine showed any protective effect against mucosal damage produced by 2 M NaCl. Ninety minutes after mucosal exposure to 2 M NaCl there was an almost complete restitution of the gastric surface epithelium in pentagastrin-stimulated and cimetidine-treated animals, whereas about 15% of the gastric surface still showed damage in animals in which acid secretion was not interfered with. These findings show that restitution of the surface epithelium, in vivo, is a rapid and resistant process even at a very low luminal pH. The secretory state of mucosa may have some influence on this process.

Animals↗