Altered blood flow regulation in autotransplanted pancreatic islets of rats

1990 ◽  
Vol 259 (1) ◽  
pp. E52-E56 ◽  
Author(s):  
L. Jansson ◽  
S. Sandler
Keyword(s):  
Blood Flow ◽  
Pancreatic Islets ◽  
Blood Perfusion ◽  
Flow Regulation ◽  
Adult Rats ◽  
Partial Pancreatectomy ◽  
Pancreatic Remnant ◽  
Islet Blood Flow ◽  
Blood Flow Regulation ◽  
Other Substances

Adult rats were partially depancreatized, and approximately 500 islets were isolated from each excised pancreas, maintained in tissue culture for 7 days, and subsequently transplanted back to the same animals beneath the renal capsule. Four weeks after transplantation the animals were anesthetized and given an intravenous injection of 1 ml of either saline, 30% (wt/vol) D-glucose, 30% (wt/vol) D-galactose, DL-propranolol (15 mg/kg body wt) dissolved in saline, or terbutaline (1 mg/kg body wt) dissolved in saline. Five minutes later blood perfusion of the islet grafts and the pancreatic remnant were measured with a microsphere technique. Islet blood flow was also measured in animals with pancreas intact and no islet grafts after administration of saline, glucose, or galactose. These animals demonstrated a significant and preferential increase in islet blood flow after glucose administration, whereas galactose caused a selective decrease in islet blood perfusion. Both whole pancreatic blood flow and islet blood flow in the pancreatic remnant were decreased by terbutaline administration, whereas the other substances had no effect. Blood flow to the transplanted islets was decreased by glucose and galactose, whereas propranolol and terbutaline had no effect compared with the saline-injected animals. These results suggest that blood flow regulation differs between transplanted pancreatic islets, islets in the normal pancreas, and islets in the pancreatic remnant after partial pancreatectomy. Whether this reflects lack of innervation or an altered reactivity of the newly formed blood vessels in islet grafts is presently unknown.

Pancreatic and islet blood flow in F1-hybrids of the non-insulin-dependent diabetic GK-Wistar rat

1994 ◽  
Vol 130 (6) ◽  
pp. 612-616 ◽  
Author(s):  
Annika M Svensson ◽  
Samy M Abdel-Halim ◽  
Suad Efendic ◽  
Leif Jansson ◽  
Claes-Göran Östenson
Keyword(s):  
Blood Flow ◽  
Glucose Tolerance ◽  
Pancreatic Islets ◽  
Blood Perfusion ◽  
Wistar Rat ◽  
F1 Hybrids ◽  
Partial Pancreatectomy ◽  
Islet Blood Flow ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

Svensson AM, Abdel-Halim SM, Efendic S, Jansson L, Östenson C-G. Pancreatic and islet blood flow in F1 -hybrids of the non-insulin-dependent diabetic GK-Wistar rat. Eur J Endocrinol 1994:130:612–16. ISSN 0804–4643 Previous studies have indicated that various conditions under which an increased functional load is posed on the pancreatic islets, e.g. partial pancreatectomy and continuous glucose infusions, may influence the microcirculation of the pancreas. To investigate further the effects of elevated functional demand on the islets, the blood perfusion of the whole pancreas and the pancreatic islets was measured with a microsphere technique in an animal model presenting impaired glucose tolerance and mild hyperglycemia, namely F 1-hybrids of the spontaneously non-insulin-dependent diabetic GK-Wistar rat. Normal Wistar rats served as controls. All hybrids had a pathological intraperitoneal glucose tolerance test 1 week before the blood flow measurements, which were performed in 10–12-week-old rats. Both the whole pancreatic and the islet blood flows were increased in the hybrids compared to controls. The fractional islet blood flow, i.e. the fraction of whole pancreatic blood flow diverted through the islets, also was increased in the hybrid rats (12.6 ±0.6% vs 9.8 ±0.5% in controls, p <0.01). A bilateral abdominal vagotomy performed 30 min before the blood flow measurement markedly decreased the blood flow values of the islets and the whole pancreas in both groups of rats. After vagotomy, the islet blood flow in the hybrid rats was similar to that of the vagotomized control animals (8.2 ± 0.8 and 7.5 ± 1.4%, respectively). It is concluded that the increased pancreatic and islet blood perfusion observed in F 1-hybrids of the GK-Wistar rat depends on a mechanism mediated by the vagus nerve. Annika M Svensson, Department of Medical Cell Biology, Biomedical Centre, PO Box 571, S-75123 Uppsala, Sweden

Cerebral vascular autoregulation of blood flow and tissue PO2 in diabetic rats

1985 ◽  
Vol 249 (3) ◽  
pp. H540-H546 ◽  
Author(s):  
M. J. Rubin ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Flow Regulation ◽  
Diabetic Rats ◽  
Adult Rats ◽  
Wall Area ◽  
Normal Limits ◽  
Blood Flow Regulation ◽  
Severe Diabetes ◽  
Tissue Po2 ◽  
Vessel Wall Area

The effect of chronic, severe diabetes mellitus on the morphology, blood flow regulation, and tissue PO2 of the cerebral cortex was evaluated in adult rats. The arterioles of the diabetic animals were enlarged in terms of both lumen diameter and vessel wall area. Although resting blood flow in the diabetic rats was greater than in the normal rats, the autoregulation of cerebral blood flow was very good within an arterial pressure range of 40-150 mmHg, just as in normal rats. The resting tissue PO2 in diabetic rats was 14.9 +/- 0.5 (SEM) compared with 12.7 +/- 0.6 mmHg in normal animals and in both groups remained at or near the resting PO2 at arterial pressures from 40 to 150 mmHg. There was no apparent loss of arterioles on the cortex surface or change in length of individual arterioles in diabetic animals but there was a 20-30% decrease in the number of venules and no change in the length of individual venules. These data indicate that although the arteriolar morphology and number of venules change in the brain during diabetes, physiological function in terms of tissue PO2 and blood flow regulation is maintained within normal limits.

Perivascular Macrophages Regulate Blood Flow Following Tissue Damage

2021 ◽  
Author(s):  
Evelina Vågesjö ◽  
Kristel Parv ◽  
David Ahl ◽  
Cédric Seignez ◽  
Carmen Herrera Hidalgo ◽  
...  
Keyword(s):  
Blood Flow ◽  
Tissue Damage ◽  
Blood Perfusion ◽  
Tissue Perfusion ◽  
Flow Regulation ◽  
Dependent Manner ◽  
Mortality And Morbidity ◽  
Blood Flow Regulation ◽  
Hind Limb Muscle ◽  
Tissue Restoration

Rationale: Ischemic injuries remain a leading cause of mortality and morbidity worldwide, and restoration of functional blood perfusion is vital to limit tissue damage and support healing. Objective: To reveal a novel role of macrophages in reestablishment of functional tissue perfusion following ischemic injury that can be targeted to improve tissue restoration. Methods and Results: Using intravital microscopy of ischemic hind limb muscle in mice, and confocal microscopy of human tissues from amputated legs, we found that macrophages accumulated perivascularly in ischemic muscles, where they expressed high levels of iNOS. Genetic depletion of iNOS specifically in macrophages (Cx3cr1-CreERT2;Nos2fl/fl or LysM-Cre;Nos2fl/fl) did not affect vascular architecture but highly compromised blood flow regulation in ischemic but not healthy muscle, which resulted in aggravated ischemic damage. Thus, the ability to upregulate blood flow was shifted from eNOS (endothelial)-dependence in healthy muscles to completely rely on macrophage-derived iNOS during ischemia. Macrophages in ischemic muscles expressed high levels of CXCR4 and CCR2, and local overexpression by DNA plasmids encoding the corresponding chemokines CXCL12 or CCL2 increased macrophage numbers, while CXCL12 but not CCL2 induced their perivascular positioning. As a result, CXCL12-overexpression increased the number of perfused blood vessels in the ischemic muscles, improved functional muscle perfusion in a macrophage-iNOS-dependent manner, and ultimately restored limb function. Conclusions: This study establishes a new function for macrophages during tissue repair, as they regulate blood flow through the release of iNOS-produced NO. Further, we demonstrate that macrophages can be therapeutically targeted to improve blood flow regulation and functional recovery of ischemic tissues.

LOCAL BLOOD FLOW REGULATION IN TRANSPLANTED RAT PANCREATIC ISLETS

2000 ◽  
Vol 70 (2) ◽  
pp. 280-287 ◽  
Author(s):  
Richard Olsson ◽  
Leif Jansson ◽  
Arne Andersson ◽  
Per-Ola Carlsson
Keyword(s):  
Blood Flow ◽  
Pancreatic Islets ◽  
Flow Regulation ◽  
Local Blood Flow ◽  
Rat Pancreatic Islets ◽  
Blood Flow Regulation

Impact of intrinsic blood flow regulation in cirrhosis: maintenance of hepatic arterial buffer response

2000 ◽  
Vol 279 (2) ◽  
pp. G454-G462 ◽  
Author(s):  
Sven Richter ◽  
Isabella Mücke ◽  
Michael D. Menger ◽  
Brigitte Vollmar
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Blood Perfusion ◽  
Flow Regulation ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Total Blood ◽  
Arterial Blood ◽  
Blood Flow Regulation ◽  
The Impact

The hepatic arterial buffer response (HABR) effectively controls total blood perfusion in normal livers, but little is known about blood flow regulation in cirrhosis. We therefore studied the impact of HABR on blood perfusion of cirrhotic livers in vivo. After 8-wk CCl4 treatment to induce cirrhosis, 18 anesthetized rats (and 18 noncirrhotic controls) were used to simultaneously assess portal venous and hepatic arterial inflow with miniaturized ultrasonic flow probes. Stepwise hepatic arterial blood flow (HAF) or portal venous blood flow (PVF) reduction was performed. Cirrhotic livers revealed a significantly reduced total hepatic blood flow (12.3 ± 0.9 ml/min) due to markedly diminished PVF (7.3 ± 0.8 ml/min) but slightly increased HAF (5.0 ± 0.6 ml/min) compared with noncirrhotic controls (19.0 ± 1.6, 15.2 ± 1.3, and 3.8 ± 0.4 ml/min). PVF reduction caused a significant HABR, i.e., increase of HAF, in both normal and cirrhotic livers; however, buffer capacity of cirrhotic livers exceeded that of normal livers ( P < 0.05) by 1.7- to 4.5-fold (PVF 80% and 20% of baseline). Persistent PVF reduction for 1, 2, and 6 h demonstrated constant HABR in both groups. Furthermore, HABR could be repetitively provoked, as analyzed by intermittent PVF reduction. HAF reduction did not induce changes of portal flow in either group. Because PVF is reduced in cirrhosis, the maintenance of HAF and the preserved HABR must be considered as a protective effect on overall hepatic circulation, counteracting impaired nutritive blood supply via the portal vein.

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