Effect of Aminoguanidine on Plasma Nitric Oxide by-Products and Blood Flow During Chronic Peritoneal Sepsis

Alden, Kris J.; Motew, Stephen J.; Sharma, Avadhesh C.; Ferguson, James Henry

doi:10.1097/00024382-199804000-00009

Cited by 25 publications

(26 citation statements)

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“…Of these articles, 52 (38.0%) showed a decreased RVR [25, 28, 30, 31, 32, 33, 34, 36, 45, 46, 47, 51, 52, 53, 58, 62, 63, 68, 69, 70, 71, 72, 73, 74, 75, 78, 84, 85, 87, 92, 95, 98, 99, 100, 101, 109, 111, 112, 114, 115, 120, 122, 124, 125, 126, 130, 131, 135, 143, 144, 154, 155], 16 (11.7%) an unchanged RVR [23, 29, 35, 37, 60, 64, 80, 97, 106, 108, 110, 113, 116, 119, 140, 145,] and 69 (50.3%) an increased RVR [20, 21, 22, 24, 26, 27, 38, 39, 40, 41, 42, 43, 44, 48, 49, 50, 54, 55, 56, 57, 59, 61, 65, …”

Section: Resultsmentioning

confidence: 99%

“…We found 56 experiments performed in small animals [20, 24, 26, 27, 39, 42, 43, 44, 55, 57, 58, 59, 62, 63, 64, 67, 68, 72, 77, 79, 81, 82, 87, 88, 89, 90, 93, 94, 96, 97, 99, 100, 103, 104, 105, 110, 116, 120, 121, 122, 129, 132, 133, 134, 137, 138, 139, 141, 142, 143, 147, 148, 149, 150, 151] and 81 performed in large animals [21, 22, 23, 25, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 40, 41, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 56, 60, 61, 65, 66, 69, 70, 71, 73, 74, ...…”

Section: Resultsmentioning

confidence: 99%

“…Of 59 studies using other methods [20, 29, 30, 33, 34, 36, 37, 38, 39, 40, 43, 44, 46, 47, 48, 55, 57, 59, 61, 64, 67, 68, 70, 76, 77, 79, 82, 84, 87, 88, 93, 94, 96, 97, 98, 101, 103, 104, 105, 107, 116, 120, 122, 123, 125, 129, 130, 132, 133, 134, 136, 137, 138, 139, 147, 148, 149, 150, 151], 16 (27.1%) reported a decreased RVR, 5 (8.5%) an unchanged RVR, and 38 (64.4%) an increased RVR (fig. 3; p =0.017).…”

Section: Resultsmentioning

confidence: 99%

“…Of 29 studies conducted in conscious animals [20, 29, 30, 31, 32, 33, 34, 35, 36, 44, 46, 47, 48, 51, 53, 54, 55, 61, 79, 87, 92, 96, 97, 98, 101, 106, 124, 144, 149], 16 (55.2%) reported a decreased RVR, 4 (13.8%) an unchanged RVR, and 9 (31%) an increased RVR (fig. 4; p = 0.057).…”

Section: Resultsmentioning

confidence: 99%

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Renal Vascular Resistance in Sepsis

et al. 2006

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Aims: To assess changes in renal vascular resistance (RVR) in human and experimental sepsis and to identify determinants of RVR. Methods: We performed a systematic interrogation of two electronic reference libraries using specific search terms. Subjects were animals and patients involved in experimental and human studies of sepsis and septic acute renal failure, in which the RVR was assessed. We obtained all human and experimental articles reporting RVR during sepsis. We assessed the role of various factors that might influence the RVR during sepsis using statistical methods. Results: We found no human studies, in which the renal blood flow (and, therefore, the RVR) was measured with suitably accurate direct methods. Of the 137 animal studies identified, 52 reported a decreased RVR, 16 studies reported no change in RVR, and 69 studies reported an increased RVR. Consciousness of animals, duration of measurement, method of induction of sepsis, and fluid administration had no effect on the RVR. On the other hand, on univariate analysis, size of the animals (p<0.001), technique of measurement (p = 0.017), recovery after surgery (p = 0.004), and cardiac output (p <0.001) influenced the RVR. Multivariate analysis, however, showed that only cardiac output (p = 0.028) and size of the animals (p = 0.031) remained independent determinants of the RVR. Conclusions: Changes in RVR during sepsis in humans are unknown. In experimental sepsis, several factors not directly related to sepsis per se appear to influence the RVR. A high cardiac output and the use of large animals predict a decreased RVR, while a decreased cardiac output and the use of small animals predict an increased RVR.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Renal Vascular Resistance in Sepsis

et al. 2006

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“…This dose regime was selected since it has been reported to produce a substantial inhibition of nNOS within 30 min without altering MAP or the vasodilator response to acetylcholine (Wilcox et al 1998). AG was administered in a continuous infusion at a rate of 1.666 mg kg _1 min _1 , a dose which has previously been shown to significantly decrease plasma nitrate and nitrite without eliciting a pressor response (Alden et al 1998).…”

Section: Experimental Protocolsmentioning

confidence: 99%

Contribution of Endothelial Nitric Oxide Synthase in the Blunted Renal Responses to Volume Expansion in Diabetic Rats

Wongmekiat

Johns

2001

Experimental Physiology

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The renal excretory responses to volume expansion (VE), by 10% body wt, were determined in groups of anaesthetised streptozotocin‐induced diabetic rats with one denervated and one innervated kidney in the presence and absence of nitric oxide synthase (NOS) inhibitors. VE in diabetic rats increased (P < 0.001) cumulative urine sodium excretion (CuUNaV) to 104 ± 9 and 69 ± 6 μmol min−1 (g kidney wt)−1 in the denervated and in the innervated kidneys, respectively, which were both less (P < 0.001) than in the non‐diabetic rats, at 225 ± 14 and 148 ± 14 μmol min−1 (g kidney wt)−1, respectively, in the denervated and the innervated kidney. The non‐selective NOS inhibitor, NG‐nitro‐L‐arginine‐methyl‐ester (L‐NAME) given to the diabetic rats with intact renal innervation enhanced CuUNaV after VE by 43% (P < 0.001), while the combination of L‐NAME and renal denervation restored CuUNaV to a value comparable to that of non‐diabetic rats. In diabetic rats treated with either a relatively selective inhibitor for the neuronal isoform of NOS, 7‐nitroindazole, or a relatively selective inhibitor for the inducible isoform of NOS, aminoguanidine, CuUNaV after VE was similar to the untreated diabetic rats irrespective of whether or not the renal nerves were present. This investigation demonstrated that NO production contributed, at least partly, to the depressed ability to excrete a saline load in diabetes mellitus. The endothelial isoform of NOS was most probably responsible for generating NO which caused the blunted excretory responses. The ability of NO to attenuate the excretory responses to volume expansion was an action independent of the renal innervation status.

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