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Biomedical subjects

S Lundin

Publications and source records attributed to S Lundin.

At least 163 records · Page 9Linked to original sources
PubMed1981

Central blood volume in spontaneously hypertensive rats and Wistar-Kyoto normotensive rats.

Central blood volume and blood volume were determined in spontaneously hypertensive rats and Wistar Kyoto rats at two ages, 6 and 12 weeks, representing "borderline' hypertension and early "established' hypertension, respectively. A technique was used where plasma and erythrocyte indicators were injected into conscious rats. Blood volume in the cardiopulmonary compartment, present in the 'resting' awake steady-state, could then be estimated by sudden freezing of the entire rat. 12 week-old spontaneously hypertensive rats showed a decreased total blood volume, while the fraction of blood contained in the cardiopulmonary area was significantly increased compared with that of normotensive Wistar Kyoto rats. In 6-week-old spontaneously hypertensive rats, total blood volume was only marginally decreased but also here a tendency towards centralization of the blood was seen. Thus, alone with the development of hypertension in the spontaneously hypertensive rat their decreasing blood volume tends to become increasingly centralized to the cardiopulmonary area. Both neurohormonal influences and structural wall changes in the low-pressure capacitance side may contribute to this.

Animals↗
PubMed1980

Antidiuretic agonism and antagonism of some O-alkylated analogues of vasopressin containing 2-O-alkylated tyrosine.

A series of 2-O-alkylated tyrosine analogues of lysine-vasopressin and desamino-lysine and arginine-vasopressin were synthesized and tested for antidiuretic activity in the water-loaded anaesthetized rat. The analogues displayed only weak antidiuretic activities. When they were infused in the rats together with lysine vasopressin it was found that 1-deamino-[2-O-ethyltyrosine]-lysine-vasopressin inhibited the vasopressin-induced antidiuretic response. The antagonistic properties were further evaluated in long-term experiments on conscious non-hydrated rats with implanted minipumps. The analogues inhibited the vasopressin-induced antidiuresis at antagonist:agonist ratios of 0.5 and 1.0.

Alkylation↗
PubMed1980

Central blood volume in spontaneously hypertensive rats and Wistar-Kyoto normotensive rats.

1. Central blood volume and total blood volume were determined in spontaneously hypertensive rats and Wistar-Kyoto rats at two ages (6 and 12 weeks), representing 'borderline' hypertension and early 'established' hypertension. 2. A technique was used where plasma and erythrocyte indicators were injected into conscious rats. Blood volume in the cardiopulmonary compartment, present in the 'resting' awake steady state, could then be estimated by sudden freezing of the entire rat. 3. Twelve week-old spontaneously hypertensive rats showed a decreased total blood volume, and the fraction of blood contained in the cardiopulmonary area was significantly increased compared with that of normotensive Wistar-Kyoto rats. 4. In 6 week-old spontaneously hypertensive rats, total blood volume was only marginally decreased but here also a tendency towards centralization of the blood was seen. 5. Thus, along with the development of spontaneously hypertensive rat hypertension, a decreasing blood volume tends to become increasingly centralized to the cardiopulmonary area. Both neuro-hormonal influences and structural wall changes in the low-pressure capacitance side may contribute to this.

Aging↗
PubMed1979

Apparent and true vascular resistances to flow in SHR and NCR kidneys as related to the pre/postglomerular resistance ratio.

In maximally vasodilated SHR and NCR kidneys, perfused with filtrable and non-filtrable perfusates, analyses have been performed concerning the extent of average renal tissue pressure (Pt) elevation which occurs upon glomerular filtration and causes passive autoregulation of flow. The results illustrate the great importance of distinguishing between 'apparent' (PA--PV/flow) and 'true' (PA--Pt/flow) renal resistance to flow. This is particularly so when the compared SHR and NCR renal vascular beds differ not only in true total renal resistance but also concerning the structurally determined ratio between the pre- and post-glomerular resistances. The combined results show that this ratio is considerably elevated in adults SHT kidneys because of structural vascular changes, which is perhaps the most efficient way of resetting the 'long term barostat function' of the kidneys in hypertension. It is also illustrated how the altered pre-/post-glomerular ratio in SHR in combination with Pt rises can so markedly distort the results of apparently precise in vitro comparisons of SHR and NCR renal vascular beds as to give entirely misleading results, with underestimations of the structurally based vascular hyperreactivity of the preglomerular section in SHR.

Animals↗
PubMed1978

Plasma volume, blood volume and transcapillary escape rate (TER) of albumin in young spontaneously hypertensive rats (SHR) as compared with normotensive controls (NCR).

A detailed comparison of blood and plasma volumes and of the transcapillary escape rate (TER) of albumin was performed in SHR and matched NCR, particularly during the phase of rapid pressure rise in SHR. Throughout this early phase of life, the relative plasma and blood volumes tend to be lower, and TER higher in SHR, as would be expected when neurogenic mechanisms dominate the initiation of hypertension. Only in late established SHR hypertension, with increasing signs of cardiovascular complications, blood volume tends to be higher in SHR than in NCR. These results are in general agreement with most observations in early essential hypertension in man. They are of interest in contrast to recent findings in another variant of primary hypertension in rats, MHS. Also the apparently quite different initiating mechanisms in SHR and MHS primary hypertension are discussed.

Animals↗
PubMed1976

Hemodynamic consequences of resistance vessel rarification and of changes in smooth muscle sensitivity.

Alterations in resistance vessel design in form of an increased wall/lumen ratio appears to markedly influence the resistance control in primary hypertension (Folkow et al. 1973). The raised resistance has also been suggested to be a consequence of a rarification of resistence vessels or/and to an increased vascular smooth muscle sensitivity. Thus two series paired experiments were performed on matched normotensive rats, utilizing the responses of their hindquarter vascular beds during constant flow perfusion. In the first series, the precapillary resistance vessels section was first "rarified" by graded microplugging, thereby raising resistance at maximal dilatation about 50 per cent. Then the vascular responses to noradrenaline were studied to characterize the dose-response or "resistance curves". In the second series the vascular smooth muscle sensitivity to noradrenaline of one of the hindquarters was changed by infusion of phentolamine. The resistance responses were then recorded and the ensuing "resistance curves" compared. --These changes of resistance vascular architecture and vascular smooth muscle sensitivity, respectively, led to mutually different characters of the "resistance curves". Both of these differ, however, in virtually all important respects from those curves characterizing vascular beds of spontaneously or renal hypertensive rats.

Animals↗
PubMedDate not supplied

Passage of aerosolized BSA and the nona-peptide dDAVP via the respiratory tract in young and adult rats.

The passage of the protein marker, bovine serum albumin (BSA, MW = 67,000), and the nona-peptide, 1-deaminocysteine-8-D-arginine vasopressin (dDAVP, MW = 1067), from the respiratory tract into the blood when applied as an aerosol with a MMAD of 1.7 microns was studied in 14-, 30-, and 100-120-day-old (adult) healthy rats and in adult rats with lung injury. In blood serum of adult rats the levels of immunoreactive BSA reached its maximum 16-24 h after a 1-h aerosol exposure with a calculated total passage of 6.4 +/- 1.8% of the given dose. dDAVP serum levels measured by RIA peaked after 0.5-1 h, giving a total passage of 84.3 +/- 12.9%. With increasing exposure periods from 0.5 to 3 h, which thereby increased the lung burden, the serum levels of BSA and dDAVP increased linearly indicating passive transepithelial transport processes for both molecules. For the young rats, similar serum level-time curves were obtained like those of the adult, with similar total passages of BSA, 4.6 +/- 0.8% for the 14-day-old rats and 5.2 +/- 1.6% for the 30-day-old rats. For dDAVP the total passage was significantly lower in both the 14-day-old rats, 40.9 +/- 12.1%, and the 30-day-old rats, 16.7 +/- 6.1% (p less than .05), as compared to the adult rats. Acute lung inflammation induced in rats by intratracheal instillation of 5 mg ferritin/kg body wt prior to a 1-h marker aerosol exposure increased the passage of BSA (58.7 +/- 18.8%, p less than .05), while the dDAVP passage was less affected (99.2 +/- 25.2%, p greater than .05) as compared to the healthy adult rats. The results indicate that after aerosol exposure the total passage of dDAVP over the respiratory tract was higher than that of the macromolecule BSA, the passage appeared to increase with the maturity of the rats and by inflammatory changes in the lung tissue.

Aerosols↗