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Biomedical subjects

G Ertl

Publications and source records attributed to G Ertl.

246 records · Page 14Linked to original sources
PubMedDate not supplied

Effect of experimentally induced atrial fibrillation on coronary circulation in dogs.

The influence of atrial fibrillation on coronary circulation was studied in 21 anesthetized open-chest dogs. Atrial fibrillation was induced either by local application of acetylcholine (10% in normal saline) on the left atrial appendage or by electric stimulation (2-7 volts, 2 ms, 50 Hz). When atrial fibrillation was induced (n = 10), mean aortic pressure fell and heart rate rose significantly; coronary blood flow (CBF) remained unchanged (78 +/- 6 vs. 75 +/- 5 ml/min X 100 g) while coronary vascular resistance (CVR) (1.16 +/- 0.05 vs. 0.87 +/- 0.07 [m Hg X min X 100 gl/ml [RU], p less than 0.0001) and sinus oxygen saturation (26 +/- 2 vs. 22 +/- 1%, p less than 0.05) decreased. Following the application of carbochromen (5 mg/kg in 3 min i.v.) resulting in maximal coronary dilatation, atrial fibrillation resulted in a reduction in CBF (311 +/- 48 vs. 205 +/- 30 ml/min X 100 g, p less than 0.01) and coronary sinus oxygen saturation (65 +/- 6 vs. 42 +/- 6%, p less than 0.01), while CVR (0.27 +/- 0.03 vs. 0.37 +/- 0.04 RU, p less than 0.0001) was 38 +/- 8% (p less than 0.0005) higher during atrial fibrillation than at sinus rhythm. When hearts were paced to a rate which was identical to the average heart rate at atrial fibrillation (n = 11), CBF (92 vs. 125 +/- 14 ml/min X 100 g, p less than 0.001) and sinus oxygen saturation (24 +/- 2 vs. 30 +/- 2%, p less than 0.0025) were higher and CVR (1.16 +/- 0.11 vs. 0.97 +/- 0.10 RU, p less than 0.0005) lower than during atrial fibrillation; during maximal coronary dilatation by carbochromen, pacing also resulted in a higher CBF (233 +/- 24 vs. 168 +/- 16 ml/min X 100 g, p less than 0.0005) and sinus oxygen saturation (70 +/- 3 vs. 57 +/- 2%, p less than 0.0005), while CVR (0.25 +/- 0.02 vs. 0.46 +/- 0.02 RU, p less than 0.0005) was lower than during atrial fibrillation. Thus atrial fibrillation results in a decrease in coronary vascular resistance but an increase in coronary oxygen extraction. When heart rate is controlled, the vasoconstrictor effect of atrial fibrillation becomes unmasked. Coronary vasoconstriction during atrial fibrillation appears to be greater during maximal coronary dilatation than during control.

Animals↗
PubMedDate not supplied

Interactions between coronary occlusion and the renin-angiotensin system in the dog.

Studies were carried out in 39 barbiturate-anesthetized dogs to determine whether the renin-angiotensin system is important in control of hemodynamics and coronary flow during myocardial ischemia. Plasma renin activity (PRA) was 2.2 +/- 0.4 ng x ml-l x hr-1 immediately before coronary artery occlusion (CAO) and increased to 3.8 +/- 0.5 (p less than .005) 15 minutes after CAO. In nephrectomized dogs, PRA was 0.76 +/- 0.14 ng x ml-l x hr-1 two hours after nephrectomy and remained unchanged after CAO. In contrast, hemodynamic changes following CAO were similar between nephrectomized and intact dogs: mean arterial pressure fell from 126 +/- 4 pre CAO to 116 +/- 4 mm Hg post CAO (p less than 0.005) in nephrectomized dogs and from 130 +/- 11 to 120 +/- 11 mm Hg (p less than 0.005) in intact dogs. Left atrial pressure rose from 5.4 +/- 0.9 pre CAO to 7.7 +/- 0.9 mm Hg (p less than 0.005) post CAO in nephrectomized from 5.4 +/- 0.9 pre CAO to 7.7 +/- 0.9 mm Hg (p less than 0.005) post CAO in nephrectomized dogs and 6.3 +/- 1.3 to 9.0 +/- 1.8 mm Hg (p less than 0.005) in intact dogs. Heart rate remained unchanged in both groups. In sham-operated dogs without CAO, neither the angiotensin II blocker Saralasin nor the converting enzyme inhibitor Captopril had significant effects on systemic (SVR) and coronary (CVR) vascular resistances. In contrast, in dogs with CAO, these drugs reduced CVR from 1.28 +/- 0.13 mm Hg x ml-1 x min x 100 g heart weight (resistance units = RU) to 0.85 +/- 0.08 RU (p less than 0.05) (Saralasin) 15 minutes after treatment and from 1.17 +/- 0.09 to 0.88 +/- 0.08 RU (p less than 0.025), (Captopril) respectively. However, only Captopril reduced SVR, from 10.7 +/- 1.13 to 8.2 +/- 0.8 RU (p less than 0.025). Both Captopril and Saralasin induced a significant increase in collateral blood flow. Nephrectomy, two hours prior to CAO, significant increase in collateral blood flow. Nephrectomy, two hours prior to CAO, significantly reduced the effect of Captopril on CVR and collateral blood flow while the effect on SVR persisted. Thus the reduction in CVR appears to be an effect of inhibition of the renin-angiotensin system; this system participates in control of CVR during CAO and may limit coronary collateral blood flow.

Animals↗
PubMedDate not supplied

Alpha-receptor constriction induced by atrial fibrillation during maximal coronary dilatation.

The mechanism of coronary vasoconstriction induced by atrial fibrillation during maximal coronary dilatation was studied in 19 chloralose-urethane anesthetized dogs. Maximal coronary dilatation was achieved by carbochromene (5 mg/kg i.v.) or dipyridamole (0.2 mg/kg i.v.). Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Atrial fibrillation was compared with rhythmic atrial pacing at similar heart rates (207 +/- 12 vs. 204 +/- 12 beats/min). During maximal coronary dilatation, coronary resistance was 0.38 +/- 0.05 mm Hg X min X 100 g/ml (RU) at sinus rhythm, 0.41 +/- 0.06 RU at atrial pacing, and 0.52 +/- 0.07 RU at atrial fibrillation, that was significantly (p less than 0.005) higher than during sinus rhythm and atrial pacing. Accordingly, coronary oxygen extraction was 14 +/- 1% at sinus rhythm, 17 +/- 1% at atrial pacing (p less than 0.005 vs. sinus rhythm) and 27 +/- 2% at atrial fibrillation (p less than 0.001 vs sinus rhythm and atrial pacing). Beta-adrenoceptor blockade with propranolol (1 mg/kg i.v.) did not prevent this coronary vasoconstrictive effect. Following alpha-blockade with phenoxybenzamine (10 mg/kg i.v.), however, coronary resistance was 0.52 +/- 0.08 RU during sinus rhythm, 0.54 +/- 0.10 RU during atrial pacing and 0.57 +/- 0.09 RU during atrial fibrillation. The data suggest coronary vasoconstriction induced by atrial fibrillation mediated by an alpha-adrenoceptor mechanism.

Animals↗
PubMedDate not supplied

On the range of alpha-adrenergic regulation of coronary vascular resistance.

In order to obtain an estimate of the range of alpha-adrenergic resistance regulation in the coronary vascular system, the following studies were performed: in 15 anesthetized dogs the circumflex coronary artery was cannulated and perfused with above-normal constant pressure to that coronary venous oxygen tension never fell below 40 mmHg. Thus, it was possible to eliminate the influence of the metabolic factor regulating coronary resistance. Furthermore, 15 isolated isovolumetrically working guinea-pig hearts were perfused according to the Langendorff method. Stimulation, resp. blockade, of alpha-receptors was achieved by administering xylometazoline, resp. phentolamine. Xylometazoline increased coronary resistance in both the isolated and the in-situ heart. Administering maximum doses to the anesthetized dog led to an increase in resistance to about 200%. This is equivalent to a reduction of conductance to about 50%. Phentolamine produced no significant effects in the isolated heart. Maximum dosage administered to the heart in situ led to a resistance decrease to about 60%, equivalent to an elevation of conductance to about 170%. If we let control values of coronary resistance and conductance be equal to 100%, our experiments showed alpha-adrenergic regulation of coronary resistance to range from about 60% to 200% and conductance to range from about 50% to 170%.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Alpha-adrenergic vasoconstriction in arterial and arteriolar sections of the canine coronary circulation.

Using a method which allowed the in-situ measurement of segmental coronary vascular resistances, the reaction of arterial and arteriolar sections of the coronary vascular system to alpha-receptor stimulation was studied i anaesthetized dogs. The left coronary artery was cannulated, and the perfusion pressure was kept constant. Allowance was made for extravascular and metabolic influences of alpha-stimulation on coronary vascular resistances. On an average, submaximal alpha-stimulation with xylometazoline increased the arterial resistance by about 60% and the arteriolar resistance by about 90%. The cannulation of the left coronary artery increased the sympathetic reactivity of the arterioles. Moreover, xylometazoline increased the extravascular component of the coronary vascular resistance by about 4%. Thus it can be assumed that under normal in-vivo conditions alpha-receptor vasoconstriction might be less different in coronary arteries and arterioles. Since the arterial resistance ranges from 20% to 50% of total coronary resistance, a sympathetic vasoconstriction of this vascular section might lead even to a critical limitation of coronary blood flow. On the other hand, a predominant constriction in arterioles leads to an increase in peripheral coronary pressure, i.e. to a "reverse coronary steal phenomenon".

Animals↗
PubMedDate not supplied

Influence of the ischemic coronary bed on collateral blood flow.

The purpose of this study was to determine the influence of the resistance of the terminal vascular bed of an occluded coronary artery on collateral blood flow and collateral resistance. In 6 anesthetized dogs, left anterior descending coronary artery (LAD) was ligated, cannulated, and the terminal vascular bed was occluded by latex microspheres (diameter: 25 mu). Retrograde flow was measured using a new technique, which allowed control of outflow pressure of retrograde flow (PRF) at the LAD cannula. When retrograde flow was interrupted, pressure in the occluded vessel represented collateral perfusion pressure (CPP) within the border zone of the ischemic vessel. Collateral resistance was determined dividing the pressure difference across the collateral bed (CPP-PRF) by retrograde flow. Variation of PRF was used as a model for changes in resistance of the ischemic bed. Retrograde flow fell when PRF was increased from 11.0 +/- 3.0 ml X min-1 X 100 g-1 (PRF = 0) to 8.3 +/- 2.4 (p less than 0.01)(PRF = 24.6 +/- 6 mm Hg). For the same PRF range, collateral resistance fell from 9.68 +/- 2.96 to 8.30 +/- 2.50 mm Hg X ml-1 X min X 100 g (p less than 0.01). These results indicate that the vascular resistance of the terminal ischemic bed may considerably influence collateral blood flow and resistance.

Animals↗
PubMedDate not supplied

Chronic effects of ACE-inhibition (quinapril) and angiotensin-II-type-1 receptor blockade (losartan) on atrial natriuretic peptide in brain nuclei of rats with experimental myocardial infarction.

Alterations of the central nervous system may be important for imbalance of cardiovascular and fluid regulation in heart failure. The central renin-angiotensin and atrial natriuretic peptide (ANP) systems act as mutual antagonists. The effects of angiotensin converting enzyme (ACE) inhibition (quinapril, 6 mg/kg/day) and angiotensin II type 1 (AT1) receptor blockade (losartan, 10 mg/kg/day) on ANP levels in 18 selected, microdissected brain nuclei were determined in sham-operated rats and rats with left ventricular dysfunction 8 weeks after myocardial infarction (MI). Plasma ANP tended to increase in MI rats and was further increased by quinapril. ANP was decreased in 12 brain areas of MI rats. ANP concentration was also significantly decreased by quinapril in six brain nuclei including subfornical organ and organum vasculosum laminae terminalis (areas lacking blood-brain barrier), and by losartan in 16 brain nuclei outside and within the blood-brain barrier in sham operated rats. However, both quinapril and losartan prevented a further reduction of central ANP as a result of myocardial infarction. These data suggest that there are effects on central ANP that result from chronic left ventricular dysfunction as well as an ACE-inhibitor and AT1-antagonist. Mechanisms and consequences of central ANP depression remain unclear. They could, however, support systemic vasoconstriction and sodium and fluid retention.

Angiotensin Receptor Antagonists↗
PubMedDate not supplied

Effects of nifedipine and indomethacin on leukotriene C4- and D4-induced coronary constriction at normal and reduced coronary perfusion in dogs.

The effects of intracoronary leukotriene C4 (LTC4) and D4 (LTD4) (both 0.1 microgram/kg) were studied in 23 anesthetized open-chest dogs at normal (= mean aortic pressure) and reduced (51 +/- 2 and 32 +/- 2 mm Hg) coronary perfusion pressures. The left anterior descending coronary artery was cannulated and blood flow measured. Subendocardial fiber segment length was obtained with ultrasonic crystals. At normal coronary perfusion pressure, LTC4 and LTD4 reduced coronary blood flow from 81 +/- 6 and 78 +/- 7 ml/min per 100 g by 41 +/- 4% and 41 +/- 4% (both p less than 0.0005), respectively. However, segment length shortening was not depressed by LTC4 or LTD4. At reduced coronary perfusion pressure, LTC4 and LTD4 diminished coronary blood flow from 35 +/- 5 and 32 +/- 3 ml/min per 100 g, by 28 +/- 5% (p less than 0.0025) and 30 +/- 5% (p less than 0.005). Thus, reduction of coronary blood flow was less by both LTC4 (p less than 0.01) and LTD4 (p less than 0.05) at reduced rather than at normal coronary perfusion pressure. Segment length shortening was depressed by LTC4 from 6.5 +/- 1.2% to 2.4 +/- 1.6% (p less than 0.05) and by LTD4 from 5.6 +/- 1.4% to 3.1 +/- 0.9% (p less than 0.05), respectively. Indomethacin (5 mg/kg, i.v.) and nifedipine (10 micrograms/kg, i.v.) did not abolish the LT-induced coronary artery constriction. However, in animals pretreated with indomethacin or nifedipine, reduction of coronary blood flow by LTs was not attenuated at reduced coronary perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗