Sustainable utilization of the vegetable oil manufacturing waste product in the formulation of eco-friendly emulsifiable cutting fluids.

The conventional Metal cutting fluids (MCFs) used are mineral-based petroleum oils that perform well but are toxic and difficult to dispose of; therefore, these are hazardous to human health as well as the environment. This issue can be solved by using natural vegetable oil-based MCF, which are readily available, environment and human-friendly, and renewable. Therefore, we synthesized various types of emulsifiers (anionic, and nonionic with different ethylene oxide units as well as mono and gemini cationic surfactants as corrosion inhibitors and biocides) based on recycled vegetable oil (RO) from spent bleaching earth (SBE), and elucidated their chemical structures by different spectroscopic techniques. The individually synthesized emulsifiers (anionic, and nonionic with different ethylene oxide units) at different ratios (8-15 by wt.%) and mixed emulsifiers (anionic/nonionic, nonionic/nonionic with different degrees of ethylene oxide) at different ratios (8-12 by wt.%) were utilized as additives in the preparation of different vegetable residual oil-based MCF formulations. The mixed emulsifiers at different ratios of nonionic/nonionic with hydrophilic-lipophilic balance (HLB) value 10 (Formulas I, II, III, and IV), and anionic/nonionic (Formula V, and VI) exhibited stable emulsions compared to individual emulsifiers. Formulas (I and VI) displayed good protection effectiveness in corrosion tests. Formula VI had better wettability (25.22 on CS, 23.68 on Al, and 22.28 on WC) and a smaller particle size (63.97 nm). Tribological properties of Formula VI were also performed. The results exhibit that Formula VI is consistent with the commercial sample. As a result, this study contributed to the resolution of one of the industry's problems.

Effect of beta adrenergic blockade on renin response to renal nerve stimulation.

The ability of d,l-propranolol to block renin secretion in response to various extrarenal stimuli, such as hemorrhage and hypoglycemia, has been interpreted to indicate the presence of an intrarenal beta receptor regulating renin release. However, two problems complicate this interpretation: (a) the stimuli have effects outside the kidney, and (b) d,l-propranolol has a local anesthetic, as well as a beta adrenergic blocking, action. In the present study, the effects of a purely intrarenal stimulus, in the form of renal nerve stimulation (RNS), on renin secretion was examined. The effects of d,l-propranolol (anesthetic and beta-blocking activity), l-propranolol (beta-blocking activity only), and d-propranolol (local anesthetic activity only) on the renin response to RNS were examined. In a control group of animals, two sequential RNS increased mean renin secretion from 401 to 1,255 U/min (P less than 0.25) and from 220 to 2,179 U/min (P less than 0.01). In a second group the first RNS increased renin secretion from 201 to 1,181 U/min (P less than 0.01), but after d,l-propranolol was given RNS did not significantly alter renin secretion (33 to 55 U/min). In a third group the initial RNS increased renin secretion from 378 to 1,802 U/min (P less than 0.025), but after l-propranolol was given RNS had no significant effect on renin secretion (84 to 51 U/min). A fourth group of dogs showed a rise in renin secretion from 205 to 880 U/min (P less than 0.001) in response to the first RNS, while the second RNS, given after an infusion of d-propranolol, caused a rise in renin secretion from 80 to 482 (P less than 0.005). The nature of the electrical stimulus was consistent in all groups and caused no detectable changes in renal or systemic hemodynamics or in urinary electrolyte excretion. The results, therefore, indicate that renin secretion can be stimulated through intrarenal beta receptors independent of changes in systemic or renal hemodynamics or in tubular sodium reabsorption. Hence the effect of beta stimulation on renin secretion would appear to result from a direct action on the renin-secreting cells of the juxtaglomerular apparatus.

Effect of beta-adrenergic blockade and inhibitors of angiotensin II and prostaglandins on renal autoregulation.

The role of the renin-angiotensin system and prostaglandins in renal autoregulation was investigated in dog kidneys in situ. Renal autoregulation during decreases in renal arterial pressure (RAP) was examined in animals pretreated with a competitive antagonist of angiotensin ii, [1-sarcosine, 8-glycine] angiotensin II, or one of two chemically dissimilar inhibitors of prostaglandin synthetase, indomethacin and meclofenamate. Because of recent evidence suggesting a role for an intrarenal beta receptor in regulating renin release, renal autoregulation was also examined in animals treated with the beta-adrenergic blocking agent propranolol. In all groups of animals constancy of glomerular filtration rate (GFR) and renal blood flow (RBF) was observed after substantial decreases in RAP to a range of 70-90 mmHg. These studies therefore do not provide evidence in support of a role for angiotensin II, prostaglandins, or an intrarenal beta receptor as mediators of the renal autoregulation of GFR or total RBF.