Biomedical subjects

S E Rynning

Publications and source records attributed to S E Rynning.

11 recordsLinked to original sources

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

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

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

Left ventricular hypertrophy and myocardial ischaemia in hypertension: the THAMES Study.

A multicentre epidemiological study to detect the prevalence of myocardial ischaemia in hypertensive left ventricular hypertrophy (LVH) was performed in 188 asymptomatic male hypertensives (131 treated). The mean age was 55 (range 40-82) years with blood pressure (BP) > or = 160/100 mmHg or a systolic BP > or = 180 mmHg. The participants were screened with echocardiography, and left ventricular hypertrophy (LVH), defined as LV mass index (LVMI) > or = 130 g.m-2, was found in 127 (68%), of whom 95 were on antihypertensive treatment. Patients with LVH underwent a maximal bicycle ergometer exercise test and significant ST depression, indicating possible stress-induced ischaemia, was found in 29 men (23%). These subjects were subjected to exercise thallium-201 scintigraphy, which was normal in 14 but showed reversible perfusion defects in 15. Thus, a high prevalence of LVH (70%) was detected in male hypertensives selected only on age and BP. In addition, although chest pain on exertion excluded patients from entry, a substantial portion had signs of ischaemia (23% on exercise ECG alone, and in 52% confirmed by thallium scan). The prevalence of these risk factors should be considered when evaluating hypertensive patients.

Adult↗

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↗

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↗

PubMed1991

[Severe hemorrhage in pancreatic pseudocyst].

Pseudocysts in the pancreas occur in 10% of patients with pancreatitis and may lead to serious complications, i.e. infection, obstruction of the bile duct, rupture, and hemorrhage. The last complication is highly lethal. Two patients are described, with differing modes of presentation and therapy. In one patient hemostasis was obtained by surgical packing followed by percutaneous embolization. In the other patient embolization failed and surgical resection was necessary.

Adult↗