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Biomedical subjects

G Göthberg

Publications and source records attributed to G Göthberg.

At least 37 records · Page 2Linked to original sources
PubMed1994

Physiology of the renomedullary depressor system.

THE LOCATION OF A DEPRESSOR MECHANISM IN THE RENAL MEDULLA: The late Eric Muirhead was the first to identify a depressor mechanism in the renal medulla. He located it in the renomedullary interstitial cells and was able to extract a lipid substance with the properties of a blood-pressure lowering hormone from papillary tissue, from renomedullary interstitial cells grown as monolayer tissue culture and from the venous outflow of high-pressure perfused kidneys. CHARACTERISTICS OF THE MECHANISM: The reversal of Goldblatt renovascular hypertension induces a reduction in blood pressure associated with an unchanged or slightly decreased heart rate, reduced efferent sympathetic activity and a decrease in vascular resistance in the splanchnic region. If the renal medulla is destroyed chemically by 2-bromoethylamine hydrobromide the blood pressure does not fall to normal levels. Extracorporeal crossperfusion of an isolated normal kidney at high pressure activates the renal depressor mechanism, inducing a decrease in blood pressure, also in association with reduced heart rate and sympathetic nervous activity in the normotensive assay rat. Diuresis and natriuresis are also increased when the mechanism is activated, as when the lipid extracts are given intravenously. FEEDBACK CONTROL: Stimulation of efferent sympathetic activity to the kidney can block the initiation of the depressor mechanism. Also, if nitric oxide synthase is blocked, the depressor mechanism cannot be activated. CONCLUSIONS: The renomedullary depressor mechanism, together with the renin-angiotensin system, provides the kidney with the ability to perfectly control blood pressure homeostasis. The antihypertensive effect of this hormonal system is brought about by sympathetic inhibition (cardioprotective), vascular relaxation (vasoprotective) and increased diuresis/natriuresis (renoprotective), which are the characteristics of modern treatment of hypertension.

Animals↗
PubMed1993

Endoscopic procedures of the upper-thoracic sympathetic chain. A review.

The upsurge of endoscopic surgical procedures now includes procedures of the thoracic sympathetic chain. The number of articles on this issue is rapidly increasing. This article reviews the indications for as well as the technique, complications, side effects, and results of endoscopic upper-thoracic sympathetic ablation. Since 1977, nearly 900 cases have been described in the literature. The main indication is usually hyperhidrosis. The described techniques vary in detail, but the common denominators are simplicity, expedience, minimal surgical trauma, few complications, and low cost compared with standard methods of open surgery. The results are excellent, durable, and stand well compared with results of previous open techniques. Due to the overwhelming advantages of endoscopic methods, we can foresee an increasing adoption of these techniques and a subsequent relegation of the various open surgical procedures of the upper-thoracic sympathetic chain.

Humans↗
PubMed1993

Thoracoscopy for autonomic disorders.

Sympathetic denervation of the arm, the hand, and the heart may now be performed using minimal thoracoscopic procedures. During a 5-year period more than 500 patients were operated on with no major and only a few minor complications. An operation time of 25 minutes, a hospital stay of 1 day, and sick leave of less than 1 week have made the operation suitable for autonomous disorders such as hyperhidrosis. Other conditions such as causalgia, vascular insufficiency, and angina pectoris may be improved or disappear after sympathectomy, but the recurrence rate in Raynaud's disease is high.

Autonomic Nervous System Diseases↗
PubMed1993

Endoscopic electrocautery of the thoracic sympathetic chain. A minimally invasive way to treat palmar hyperhidrosis.

Four hundred and fifty patients with palmar hyperhidrosis have undergone endoscopic thoracic sympathetic electrocautery since 1987 in our department. The procedure requires only minor modifications of standard laparoscopic and urological equipment. The median operating time for a bilateral procedure was 31 minutes (15-120), hospital stay was 1 day postoperatively (1-8), and patients returned to work within 4 (1-40) days. Complications in the whole material were few and mild, pneumothorax (n = 2), haemothorax (n = 1), and Horner's syndrome (n = 1). Five patients required reoperation (four because of primary failure to destroy the nerve and one for recurrent symptoms). The first consecutive 130 of these patients have been followed up by a questionnaire. At follow-up (median 196 days after operation, range 35-1419) all patients but three, who are awaiting reoperation were satisfied with the result. The discomfort and side effects of the operation were in most cases mild and short. This technique makes it possible to widen the indications for operation for people with palmar hyperhidrosis.

Adult↗
PubMed1992

Influence of the renal medulla and early treatment with enalapril upon the development of hypertension in young spontaneously hypertensive rats.

OBJECTIVE: To investigate the role of the renal medulla in early hypertension in spontaneously hypertensive rats (SHR), and to explore whether the attenuated increase of pressure induced by enalapril treatment is affected by chemical medullectomy. DESIGN: Forty-four male SHR were studied from 5 to 18 weeks of age: 22 remained intact; 22 were medullectomized at 5.5 weeks of age with 2-bromoethylamine hydrobromide; 11 of each of these two groups were treated with enalapril from 6 to 12 weeks of age. Blood pressure, heart rate and body weight were recorded intermittently, and at 18 weeks renal function was also analysed. RESULTS: The results indicate a protective effect of the renal medulla against severe pressure rises in SHR, although even when enalapril also lowered blood pressure in medullectomized SHR, persistent improvements of glomerular filtration rate and renal flow conductance occurred only in intact SHR. Furthermore, after enalapril treatment ended blood pressure rose to higher levels in medullectomized SHR, despite greater sodium-water losses. CONCLUSION: The renal medulla seems to exert a protective role both during and after enalapril treatment.

Animals↗
PubMed1991

Physiological effects of the humoral renomedullary antihypertensive system.

In experiments on rats, the physiological effects of the antihypertensive humoral system of the renal medulla were explored. We studied the parameters of blood pressure, heart rate, efferent sympathetic nervous activity to the splanchnic region, diuresis and natriuresis. The experimental situations included studies on normotensive rats, injected with extracted renomedullary lipids (medullipin), and normotensive rats extracorporally cross-perfusing an isolated kidney at increased pressure levels, to explore the release of renomedullary depressor substances. Spontaneously hyperactive rat (SHR) kidneys were also cross-perfused to study whether the renomedullary mechanism was reset upwards in this type of primary hypertension. Finally, the acute pressure reductions caused by angiotensin converting enzyme (ACE)-inhibitors were studied in intact and chemically medullectomized (2-bromo-ethylamine hydrobromide) rats to explore whether they were at least in part dependent on an intact renal medulla. In normal kidneys the renomedullary depressor system was initiated already at physiological pressure levels (at or above 100 mm Hg), causing the following humorally induced response pattern: the blood pressure fall was associated with decreases in both heart rate and sympathetic activity, while diuresis and natriuresis increased. In SHR kidneys, perfusion pressure had to be raised between 200 and 250 mm Hg before this depressor pattern was activated, revealing an "upward renomedullary resetting" well beyond the prevailing SHR blood pressure. The acute blood pressure decrease initiated in normotensive rats by an ACE-inhibitor (enalaprilat) was abolished in medullectomized rats, indicating an interaction between the renin-angiotensin and the renomedullary antihypertensive systems.

Animals↗
PubMed1991

Is the humoral renal antihypertensive activity of the spontaneously hypertensive rat (SHR) reset to the high blood pressure?

The kidneys have a humoral antihypertensive system, located in the renal medulla and presumably antagonizing the pro-hypertensive renin-angiotensin system. Medullipin I and II and maybe platelet activating factor (PAF), seem to be the mediators of this system, known to be activated after reversal of renovascular hypertension or when the perfusion pressure to a normotensive kidney is suddenly elevated. The present study was undertaken to investigate whether this system is functioning also in the spontaneously hypertensive rat (SHR), and if it is then reset in proportion to the increased mean arterial pressure (MAP). Isolated kidneys from spontaneously hypertensive rats and from Wistar Kyoto rats (WKY) were cross-perfused in vivo from anaesthetized intact Wistar Kyoto rat 'donors'. After 30 min of perfusion at 100 mmHg the perfusion pressure to the isolated kidneys were, for 60 min, either kept unaltered at 100 mmHg or, for the Wistar Kyoto rat kidneys, increased to 150-200 mmHg and, for the spontaneously hypertensive rat kidneys, raised to 200 or 250 mmHg. The results show that the humoral antihypertensive system is present also in spontaneously hypertensive rat kidneys, but is here reset upwards to or even beyond the elevated MAP level. Furthermore, all mean arterial pressure reductions caused by high-pressure perfusion of Wistar Kyoto and spontaneously hypertensive rat kidneys were accompanied by reductions in heart rate (HR) in the 'donors', in agreement with previous observations after reversing renal hypertension and after i.v. medullipin I injection. In fact, in spontaneously hypertensive rat kidneys, the 'incretory' depressor mechanism appears to be more markedly reset upwards than is the 'excretory' depressor mechanism inherent in pressure diuresis with consequent salt-volume elimination. In conclusion spontaneously hypertensive rats, like Wistar Kyoto rats and Wistar rats, have a humoral antihypertensive system in the kidneys, but it is reset upwards even beyond the elevated mean arterial pressure level in spontaneously hypertensive rats. The combination of a depressor response and reduced heart rate in the 'donors' renders further evidence that the medullipins are the principal, though probably not the only, humoral antihypertensive factors released from the cross-circulated kidneys.

Animals↗
PubMed1990

Do angiotensin converting enzyme inhibitors lower blood pressure in the rat partly via the humorally mediated antihypertensive system of the renal medulla?

It has been suggested that there is a negative-feedback interaction between the humoral renomedullary antihypertensive system and angiotensin II. If so, the acute blood pressure-lowering effects of angiotensin converting enzyme (ACE) inhibitors might be due, in part, to an increased secretion of renomedullary depressor substances. Groups of anaesthetized Wistar-Kyoto rats (WKY) with an intact or chemically destroyed renal medulla received either saline or the ACE inhibitor enalapril, and mean arterial pressure (MAP), heart rate and renal function were measured. MAP was clearly decreased after enalapril administration in the WKY controls with an intact renal medulla, but was not changed in the medullectomized group. In one WKY control group, where the prostaglandin and kallikrein-kinin systems had also been acutely blocked, the MAP reduction after enalapril was even more marked than in the intact controls. Thus, the acute blood pressure-lowering effect of enalapril is clearly dependent on an intact renal medulla, further suggesting that the renomedullary antihypertensive system is important to normal blood pressure homeostasis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Renal and circulatory effects of medullipin I, as studied in the in-vivo cross-circulated isolated kidney and intact Wistar-Kyoto (WKY) rat.

The renal medulla harbours powerful humoral antihypertensive mechanisms, as earlier explored in unclipping experiments on renal hypertensive rats or in normotensive isolated kidneys cross-circulated at increased perfusion pressures from 'donor rats', in which renal function also seemed to be affected. Injection of the renomedullary factor medullipin I (Med I; formerly ANRL) mimics these haemodynamic responses, and Med I seems to be one of the most important mediators of the depressor effects. The present study was performed to analyse further the haemodynamic and, particularly, the renal effects of Med I, using anaesthetized intact WKY rats and constant-pressure perfused (90 mmHg) isolated WKY kidneys, cross-circulated by these intact 'donor' rats. Mean arterial pressure (MAP), heart rate (HR) and renal function were followed for one 30-min period before and two 30-min periods after injection of 1 mg Med I (M; n = 7) or an equal volume of saline as control (C; n = 13). In the intact 'donor' WKY, MAP and HR remained largely constant in C during the three periods, being 126 +/- 5, 125 +/- 5, and 120 +/- 5 mmHg, while MAP fell in the M group after Med I, from 121 +/- 5 to 107 +/- 7 and 107 +/- 5 mmHg (P less than 0.05), and also HR tended to decrease in M. Renal resistance (RR) fell while renal plasma flow (RPF) and glomerular filtration rate (GFR) increased significantly (P less than 0.05) after Med I in the M donor rats despite their MAP reduction. However, in the constant-pressure perfused, cross-circulated kidneys the RR, RPF and GFR changes were clearly more pronounced (P less than 0.01) and also diuresis, natriuresis, osmolar excretion and osmolar clearance increased significantly after Med I (P less than 0.01). In conclusion, the present results support the view that Med I not only has important and long-lasting depressor effects but also affects renal function in important ways, inducing vasodilatation and increasing GFR, RPF, diuresis and sodium-osmolar excretion.

Animals↗
PubMed1988

The humoral renal antihypertensive system: nervous and hemodynamic effects in normotensive and unclipped renal hypertensive rats.

A series of studies of the humoral renal antihypertensive system in normotensive and 2K 1C-renal antihypertensive rats is outlined. The rapid structural upward resetting of the cardiovascular system in renal hypertensive rats was associated with a structural downward resetting in the vasculature of the hypotensive clipped kidney. Unclipping of this kidney caused a pronounced release of renomedullary depressor agents, explaining the rapid normalization of pressure seen after unclipping. This normalization of pressure masks a state of pronounced functional hypotension in a structurally still hypertensive cardiovascular system, characterized by marked splanchnic vasodilatation and a lack of neurogenic counter-regulation. Only when this state has lasted long enough to normalize the structural upward resettings, characteristic of hypertension does the cardiovascular system return to normal. Further, cross-circulation techniques have shown that the humoral antihypertensive agents suppress tonic sympathetic activity, thereby inhibiting normal reflex counter-regulation of their vasodilator effects. Presumably this occurs via both vagal cardiac afferents and central actions. Further, behavior and awareness become depressed during intense and prolonged renomedullary release. Finally, experiments for which a normotensive kidney is cross-circulated from a normotensive rat suggest that the humoral renomedullary antihypertensive system has its threshold of release set so low as to contribute to normal blood pressure regulation, presumably in reciprocal balance with the renocortical renin-angiotensin system. Stepwise pressure elevations increasingly enhance release of the depressor agents from the cross-perfused kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗