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Biomedical subjects

G Christensen

Publications and source records attributed to G Christensen.

At least 73 records · Page 4Linked to original sources
PubMed1993

Complementation in situ of the yeast plasma membrane H(+)-ATPase gene pma1 by an H(+)-ATPase gene from a heterologous species.

In plants and fungi, the transport of solutes across the plasma membrane (pm) is driven by a proton pump (H(+)-ATPase) that produces an electric potential and a pH gradient. We expressed AHA2, a member of the Arabidopsis thaliana pm H(+)-ATPase gene family, in yeast cells in which transcription of the endogenous pm H(+)-ATPase gene (pma1) had been turned off. AHA2 was expressed mainly in intracellular membranes and only supported very slow growth of transformed yeast cells. Removal of the last 92 C-terminal amino acids from the plant H(+)-ATPase produced an enzyme with 2-3-fold higher specific ATPase activity than the wild-type plant enzyme. Surprisingly, the truncated H(+)-ATPase was now targetted to the yeast pm and fully supported normal yeast growth.

Arabidopsis↗
PubMed1993

Optimalization of the detection of NAD dependent Pasteurellaceae from the respiratory tract of slaughterhouse pigs.

NAD dependent members of the family Pasteurellaceae were cultured from the nasal cavity, surface and cut surface of the tonsils, and from the apical and caudal lobes of the lungs of 303 slaughterhouse pigs from 5 different herds in order to obtain information on the ecology of these bacteria. The specimens were plated on two different selective agar media using a special dilution technique that resulted in a good separation of individual colonies. Bacteriological results were compared with serological and pathological findings. The bacteriological examination demonstrated that NAD dependent Pasteurellaceae belonging to the taxa previously described could be isolated from the surface and cut surface of the tonsils, and from lungs with and without gross pathologic lesions. Haemophilus parasuis was detected mainly from the nasal cavity, and Actinobacillus pleuropneumoniae mainly from the surface and cut surface of the tonsils (42%). From two herds, 19% and 24% respectively of the animals without antibodies against A. pleuropneumoniae serotypes 1 and 2 harboured the bacteria mainly in the tonsils. This may reflect a very recent infection or may suggest that A. pleuropneumoniae can colonize the tonsils without inducing a serologic reaction. Serological and bacteriological evidence of more than one serotype in the same herd indicates that natural infection with one serotype does not necessarily protect against another.

Actinobacillus pleuropneumoniae↗
PubMed1993

Cardiovascular and renal effects of atrial natriuretic factor.

Atrial natriuretic factor (ANF) reduces cardiac output and systemic arterial blood pressure. The reduction in systemic arterial blood pressure is not caused by dilation of arterial resistance vessels, since total peripheral vascular resistance often increases during infusion of ANF. The reduction in cardiac output with subsequent hypotension can be explained by a decrease in venous return. The decrease in venous return is not due to pooling of blood in the capacitance vessels, since ANF reduces venous compliance. Reduced venous return during infusion of ANF can be explained by a reduction in circulating blood volume and an increase in resistance to venous return. The reduction in circulating blood volume is due to increased urine output and to a shift of circulating fluid into the interstitial space. The increase in renal sodium and water excretion is mediated by an increase in glomerular filtration rate and reduced sodium and chloride reabsorption in the collecting ducts. ANF also inhibits the renin-angiotensin-aldosterone system. The plasma level of ANF may be a parameter for the severity of heart diseases with increased preload. In congestive heart failure and supraventricular tachycardia, the increase in plasma ANF concentration may augment sodium excretion, but anti-natriuretic factors, such as reduction in renal perfusion pressure, may override the natriuretic effect of ANF. Reduced sodium excretion during mechanical ventilation with positive end-expiratory pressure (PEEP) is partly due to a decrease in ANF secretion.

Animals↗
PubMed1993

Alterations in plasma endothelin during passage through the left heart chambers before and after brief myocardial ischaemia.

OBJECTIVE: Although the lung can both produce and extract endothelin, its role in regulating plasma endothelin is not settled. Whether the endocardium is able to affect plasma endothelin is also unknown. The first aim of this study was to examine if endothelin concentration in plasma changes when passing through the pulmonary circulation or the left heart chambers. A marked decrease in endothelin concentration has been shown to occur in the aortic arch during early reperfusion following a 10 min mid left anterior descending coronary artery occlusion. A second aim was therefore to investigate whether this decrease was due to removal of endothelin in the pulmonary circulation or through the left heart chambers. METHODS: In seven open chest, pentobarbitone anaesthetised pigs blood was obtained from the pulmonary artery, the left atrium, and the aortic arch at control conditions and at 10 and 20 min reperfusion following a 10 min coronary occlusion. Endothelin measurements were performed using an endothelin 1-21 specific [125I] assay system (RPA 555). RESULTS: At control conditions there was no difference in endothelin concentration in blood obtained from the pulmonary artery [3.9 (2.7-5.2) fmol.ml-1, median (95% confidence interval)] and the left atrium [3.8 (2.8-5.8) fmol.ml-1], whereas there was a significantly higher endothelin concentration in the aortic arch [4.9 (3.8-7.2) fmol.ml-1]. At 10 min reperfusion following the 10 min coronary occlusion there was still no difference in endothelin concentration between the pulmonary artery [4.3 (2.8-6.0) fmol.ml-1] and the left atrium [4.1 (2.7-5.7) fmol.ml-1]. However, in contrast to the increase observed before myocardial ischaemia, the endothelin concentration was significantly reduced in the aortic arch [2.8 (2.4-4.4) fmol.ml-1] compared to the left atrium. At 20 min reperfusion, all endothelin concentrations had returned to preischaemic values. CONCLUSIONS: These findings suggest a role for the left heart chambers in regulating the endothelin concentration in blood entering the aorta.

Animals↗
PubMed1993

Release of endothelin from the porcine heart after short term coronary artery occlusion.

OBJECTIVE: Endothelin is increased in plasma following myocardial infarction. Whether brief periods of myocardial ischaemia not leading to myocardial infarction increase plasma endothelin is not known. Thus, the present study was designed to examine cardiac endothelin balance in association with a 10 min coronary artery occlusion followed by reperfusion. METHODS: Venous blood was selectively sampled from the transiently ischaemic myocardium using a shunt between the anterior interventricular vein and the right atrium in eight pentobarbitone anaesthetised pigs. Flow in the shunt was measured with a Doppler flow probe. Arterial blood was drawn from the aortic arch. Plasma endothelin was measured using an Endothelin 1-21 specific [125I] assay system. This assay system has no cross reactivity with big endothlin. RESULTS: A net cardiac endothelin uptake of 0.7(0.3-1.4) fmol.min-1 x g-1 (median, 95% confidence interval) in the control period shifted to a net release during the first 10 min of reperfusion. The release reached a maximum of 2.8(0.4-6.0) fmol.min-1 x g-1 after 1.5 min of reperfusion. Cardiac venous endothelin concentration increased from 3.4(2.5-4.8) to 4.4(3.6-6.9) and 4.4(3.6-6.6) fmol.ml-1 at 1.5 and 5 min of reperfusion, respectively (p < 0.001 for both). Arterial endothelin concentration decreased from 4.8(3.9-6.1) to 2.7(2.4-4.3) fmol.ml-1 at 10 min of reperfusion (p < 0.001). CONCLUSION: Endothelin is released from the heart for several minutes during reperfusion following a brief coronary artery occlusion.

Animals↗
PubMed1993

Endothelin is released from the porcine coronary circulation after short-term ischemia.

Endothelin (ET) is increased in plasma after myocardial infarction. Whether brief periods of myocardial ischemia not leading to myocardial infarction also increase plasma ET is not known. The purpose of the present study was to examine cardiac ET balance in association with a 10-min LAD occlusion followed by reperfusion. Venous blood was selectively sampled from the transiently ischemic myocardium using a shunt between the anterior interventricular vein and the right atrium in eight pentobarbital-anesthetized pigs. Flow in the shunt was measured with a Doppler flow probe. Arterial blood was drawn from the aortic arch. Plasma ET was measured using an ET [1-21]-specific 125I assay system. This assay system has no cross-reactivity with big ET. A net cardiac ET uptake of 0.7 (0.3-1.4) fmol min-1 g-1 (median, 95% confidence interval) in the control period shifted to a net release during the first 10 min of reperfusion. The release reached a maximum of 2.8 (0.4-6.0) fmol min-1 g-1 after 1.5 min of reperfusion. Cardiac venous ET concentration increased from 3.4 (2.5-4.8) to 4.4 (3.6-6.9) and 4.4 (3.6-6.6) fmol ml-1 at 1.5 and 5 min of reperfusion, respectively (p < 0.001 for both). Arterial ET concentration decreased from 4.8 (3.9-6.1) to 2.7 (2.4-4.3) fmol ml-1 at 10 min of reperfusion (p < 0.001). ET is released from the porcine heart for several minutes during reperfusion after a brief coronary artery occlusion.

Animals↗
PubMed1993

Atrial natriuretic factor (ANF) does not affect ion transport in human intestine but does in porcine intestine.

The aim of this study was to test whether atrial natriuretic factor (ANF) exerts any effect on human intestinal ion transport, and the porcine intestine was used as a positive control of ANF's effects. Tissues from human proximal (n = 6) and distal (n = 6) colons, and from distal ileum (n = 6) were mounted in Ussing chambers, and short circuit current (Isc) was measured subsequent to serosal application of ANF (10(-6) M), 8-Br-cyclic guanosine monophosphate (8-Br-cGMP) (10(-4) M), and theophylline (10(-2) M). ANF did not affect Isc whereas 8-Br-cGMP increased Isc by 28 (8-53), 16 (3-36), and 16 (5-41) microA cm-2 in the distal colon (DC), proximal colon (PC) and distal ileum (DI), respectively. Likewise, transepithelial potential difference (PD) became more negative by 5.0 (0.6-8.9), 2.5 (0.4-4.0) and 0.9 (0.3-2.3) mV in DC, PC, and DI, respectively, subsequent to addition of 8-Br-cGMP. Isc and PD were further increased by theophylline. Additional radio-isotope flux studies in human colon revealed that ANF did not affect electroneutral sodium and chloride transport either. For comparison, ANF (10(-6) M) was administered to large intestinal tissues from young pigs in which ANF induced a significant increase in Isc which was comparable to the 8-Br-cGMP response in humans. The porcine Isc response was partly inhibited by chloride-free solution on the serosal side, by serosal application of bumetanide (10(-4) M) and BaCl2 (10(-3) M), and mucosal application of the chloride-channel blocker diphenylamine-2-carboxylate (DPC) (10(-3) M). Mucosal amiloride (10(-5) M) pre-treatment reduced baseline Isc but did not affect the porcine intestinal Isc response to ANF. In vitro radio-autography demonstrated specific binding sites for ANF in porcine distal colon, whereas no apparent labelling was observed in human distal colon. These findings suggest that the lack of effect of ANF on sodium and chloride transport in human distal ileum and colon is probably due to lack of ANF receptors. In the porcine intestine, however, the Isc response induced by ANF seems to involve stimulation of electrogenic chloride secretion, whereas electrogenic sodium absorption seems unaffected.

Adolescent↗
PubMed1993

Inhibitory effect of endothelin on renin release in dog kidneys.

To investigate the effect of endothelin on renin release, experiments were performed in barbiturate-anaesthetized dogs with denervated kidneys. Intrarenal infusion of endothelin (1 ng min-1 kg-1 body wt) reduced renal blood flow (RBF) from 145 +/- 10 ml min-1 to 98 +/- 9 ml min-1 without altering renin release (1 +/- 1 microgram angiotensin I (AI) min-1). Renin release was then increased either by renal arterial constriction or ureteral occlusion. When renal arterial pressure was reduced to 50 mmHg, renin release averaged 79 +/- 20 micrograms AI min-1 in six dogs and fell significantly to 24 +/- 6 micrograms AI min-1 during endothelin infusion. During ureteral occlusion the inhibitory effect of endothelin on renin release either during inhibition of beta-adrenergic activity with propranolol or after inhibiting prostaglandin synthesis by indomethacin during intrarenal infusion of isoproterenol was examined. After propranolol administration ureteral occlusion increased renin release from 5 +/- 2 micrograms AI min-1 to 38 +/- 12 micrograms AI min-1 in six dogs. Subsequent intrarenal endothelin infusion (1 ng min-1 kg-1 body wt) during maintained ureteral occlusion reduced renin release to 10 +/- 3 micrograms AI min-1. In six other dogs prostaglandin synthesis was inhibited by indomethacin. Subsequent infusion of isoproterenol (0.2 microgram min-1 kg-1 body wt) to stimulate beta-adrenoceptor activity increased renin release from 13 +/- 4 micrograms AI min-1 to 68 +/- 8 micrograms AI min-1 during ureteral occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1993

Effect on renin release of inhibiting renal nitric oxide synthesis in anaesthetized dogs.

Nitric oxide plays an important role in the regulation of basal renal blood flow. This study was performed to examine whether selective inhibition of renal nitric oxide synthesis affects renin release in vivo. Accordingly, in six barbiturate-anaesthetized dogs renin release was examined before and after intrarenal infusion of the selective inhibitor of nitric oxide synthesis, NG-nitro-L-arginine (NOARG). NOARG was infused into the renal artery to yield a renal arterial blood concentration of 0.4 mumol ml-1. NOARG did not change systemic arterial blood pressure and glomerular filtration rate, but reduced basal renal blood flow by 26 +/- 2%. Urine flow, sodium and potassium excretion were reduced after inhibition of renal nitric oxide synthesis. Basal renin release (3 +/- 2 micrograms AI min-1) was not altered by NOARG infusion (1 +/- 1 micrograms AI min-1). To stimulate renin release the renal artery was constricted to a renal perfusion pressure of 50 mmHg. At this perfusion pressure infusion of NOARG reduced renin release significantly from 48 +/- 11 micrograms AI min-1 to 14 +/- 4 micrograms AI min-1. In conclusion, inhibition of renal nitric oxide synthesis reduces basal renal blood flow and reduces renin release stimulated by renal arterial constriction. These findings indicate that renal nitric oxide modulates both renal blood flow and renin release in vivo.

Animals↗
PubMed1993

Significance of increased atrial pressure on stroke volume during atrial fibrillation in anaesthetized pigs.

During atrial fibrillation synchronized atrial contraction is lost and cardiac output declines. Concomitantly, atrial pressure increases. The significance of the increase in atrial pressure on stroke volume was examined before and after blood volume expansion. Atrial fibrillation was induced by rapid atrial pacing in seven anaesthetized, open-chest pigs. The increase in right atrial pressure subsequently was counteracted by an appropriate constriction of the inferior vena cava. To avoid the confounding effect of a rapid and irregular heart rate, ventricular rate was kept constant by separate His bundle pacing after complete atrioventricular block. When atrial fibrillation was induced, right and left atrial pressure at the top of the v-wave increased both during normovolaemia and during hypervolaemia. Concomitantly, stroke volume declined. When the increase in atrial pressure was prevented during atrial fibrillation, stroke volume declined further: by 35 (21-50) and 9 (2-17)% (difference: P = 0.01), during normo- and hypervolaemia, respectively. Thus, the increase in atrial pressure counteracts the decline in stroke volume after induction of atrial fibrillation and thereby represents an important compensatory mechanism. This mechanism is more important with normal blood volume than during hypervolaemia.

Animals↗
PubMed1993

Atrial contractile performance after cessation of atrial fibrillation.

Atrial fibrillation is associated with a fall in cardiac output, and cardioversion to sinus rhythm is frequently attempted. After cardioversion, atrial contractile performance might be depressed. It is, however, unclear whether or not atrial contractile performance is altered following atrial fibrillation periods lasting < 1 wk. Atrial contractile performance after short-term paroxysmal atrial fibrillation was examined in seven barbiturate-anesthetized, open-chest pigs paced at constant ventricular rate after complete atrioventricular block. Percent left atrial systolic shortening (systolic shortening of left atrial diameter in percent of atrial diameter at onset of atrial contraction, %LASS) increased from 100 to 116.2% (107.7-121.8) (median and 95% confidence interval) immediately after cessation of a fibrillation period of 1 min. A brief phase of atrial hypercontractility (%LASS significantly above control) was also demonstrated after fibrillation periods of 5 and 15 min. A subsequent phase of atrial hypocontractility (%LASS significantly below control) was recorded after atrial fibrillation periods of 5, 15, and 30 min. After the 30-min fibrillation period, atrial hypocontractility was most pronounced and reached a nadir of 86.8% (75.1-93.3).

Aged↗
PubMed1993

Effects of atrial fibrillation on left and right atrial dimensions, pressures, and compliances.

The effects of atrial fibrillation on left and right atrial dimensions, pressures, and compliances were examined in two groups of seven barbiturate-anesthetized open-chest pigs. Atrial diameters and pressures were recorded during atrioventricular (AV) pace and thereafter during atrial fibrillation. Both rhythms were studied with constant ventricular rate after complete AV block. Left atrial maximal diameter, which appeared at the end of the atrial filling phase, decreased from 32.4 (28.9-36.7; median and 95% confidence interval) to 31.3 (28.4-35.7) mm after induction of atrial fibrillation. The right atrial maximal diameter also decreased, although not significantly. Atrial pressure at the peak of the v wave rose from 7.0 (5.5-8.5) to 9.6 (8.3-11.2) mmHg in the left atrium and from 5.0 (4.3-5.6) to 7.3 (6.2-8.7) mmHg in the right atrium. Left and right atrial chamber stiffness constants increased from 0.25 (0.19-0.48) to 0.41 (0.28-0.66) mm-1 and from 0.21 (0.11-0.31) to 0.33 (0.30-0.39) mm-1, respectively. Instantaneous diastolic atrial compliance decreased in both atria after induction of atrial fibrillation. Thus, during atrial fibrillation with regular ventricular rate, changes in atrial diameter, pressure, and compliance take place.

Animals↗
PubMed1993

Release of atrial natriuretic factor.

The cardiac atria synthesize and store a hormone termed atrial natriuretic factor (ANF). ANF is released into the systemic circulation, and the circulating 28 amino acid peptide can be measured by radioimmunoassay. The hormone participates in body fluid homeostasis through its effect on renal sodium excretion and by inducing a shift of circulating fluid to the interstitial space. Release of ANF is mainly regulated by mechanical changes in the left and right atrial wall. It has been demonstrated that ANF release is related to changes in atrial wall tension occurring during each atrial cycle, and therefore, release of ANF will increase with increasing heart rate. Not only the increase in wall tension during passive atrial distension (v wave), but also the increase in tension during atrial systole (a wave) are determinants of ANF release. The mechanochemical transducer is most likely located in the atrial myocytes, but its nature is unknown. There is no evidence to suggest that efferent cardiac nerves are essential in the regulation of ANF release. Humoral factors have been suggested as regulators of ANF release, particularly catecholamines and angiotensin II. A receptor-mediated direct stimulatory effect of alpha-adrenergic stimulation and an inhibitory effect of beta-adrenergic stimulation have been demonstrated, but these direct effects are small compared to the effect of changes in atrial wall tension. Circulating catecholamines and angiotensin II stimulate ANF release mainly through their haemodynamic effects.

Angiotensin II↗
PubMed1993

An epidemiologic and economic study of respiratory diseases in two conventional Danish swine herds. I: Prevalence of respiratory lesions at slaughter and their effects on growth.

A total of 578 slaughter pigs from 2 Danish conventional farrow-to-finish operations (Herds A and B) were followed from an age of 14 days to slaughter. Pigs were weighted at 3 weeks intervals and at slaughter and an extended post mortem examination of the plucks was done. Comparison of growth rates in pigs with and without specific types of lesions by the t-test and those with multiple lesions with regression models demonstrated that Mycoplasma-like pneumonia, complicated pneumonia, anterio-ventral pleuritis, fissures and atrophic rhinitis significantly reduced mean daily gain and increased the time required to reach slaughter weight. The total impact of the lesions in Herd A was an estimated reduction in mean daily gain of 27 grams and a 2 day increase in the interval from 14 days of age until slaughter (MDG14). Decreases in MDG14 in Herd B were more substantial, 98 grams and 16.7 days. Reductions in mean daily gains during the interval from the fourth weighing until slaughter were 31 grams in Herd A and 137 grams in Herd B. Chronic dorso-caudal and parietal pleuritis, without other lesions present, had no significant adverse effects on growth rates in either herd. Interactions between lesions did not significantly alter the estimates. The R2 values obtained for the regression models showed that the presence, absence or extent of lesions at slaughter explained only 13-27% of the variations in growth rates in the 2 herds.

Abattoirs↗
PubMed1993

An epidemiologic and economic study of respiratory diseases in two conventional Danish swine herds. II: Associations between lesions present at slaughter and mean daily gains during specific intervals of the growth period.

A total of 578 slaughter pigs from 2 Danish conventional farrow-to-finish operations (Herds a and B) were followed from an age of 14 days to slaughter. Pigs were weighted at 3 weeks intervals and at slaughter and extended post mortem examination of the plucks was done. Regression models with second and third order interaction terms demonstrated that Mycoplasma-like pneumonia, complicated pneumonia, anterior-ventral pleuritis, pericarditis, fissures and atrophic rhinitis, separately and through interactions with other lesions, significantly reduced mean daily gains during specific intervals of the growth period in 2 conventional swine herds. It is likely that the periods of reduced growth reflect the times when the diseases were in the acute and early recovery stages. Maximum estimated reductions in daily gains associated with the combined lesions were 82 grams and 283 grams during the interval 120-140 days in Herds A and B, respectively. Although dorso-caudal pleuritis and parietal pleuritis had minor negative effects during 2 intervals neither had a significant adverse effect on total growth rate in either herd (Paisley et al. 1993). R2 values for the regression models were less than 0.27 showing that the lesions present at slaughter explained less than 27% of the variation in herd mean daily gains during any interval.

Abattoirs↗
PubMed1993

Pathological lesions in the right and left porcine lung: evaluation of an alternative method for scoring pneumonic lesions based on right lung examination.

Plucks from 2,372 sows, gilts and slaughterswine (originating from 3 independent sources) were evaluated for presence and severeness of 6 different pathological entities. Results were calculated for each of the lungs separately and compared to the combined findings of both lungs. Both qualitatively (comparing relative test sensitivities) and quantitatively (comparing lung scores), the right lung results were more optimal than the left lung outcomes and relatively consistent among the 3 data sets. The over-all right lung relative sensitivities for the detection of catarrhal pneumonia or chronic pleuritis were 81.3% and 72.0%, respectively. The over-all differences in the right minus left lung scores for the 2 lesions were +13.0% and +9.0%, respectively. The necessary sample size of right lungs to detect at least 1 lung with catarrhal pneumonia or chronic pleuritis is presented along with a method for calculating confidence intervals.

Animals↗